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Update in the treatment of cirrhotic patients with portal vein thrombosis

Jialin Wu1,2,3,4, Xinyi Deng5, Junyang Luo4, Zaibo Jiang4, Fuda Xie1,2,3, Bonan Chen1,2,3, Hoi Wing Leung1,2,3, Ge Zhang6, Ka Fai To1, Wei Kang1,2,3orcid
Clinical and Molecular Hepatology 2025;31(4):1139-1166.
Published online: June 24, 2025

1Department of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Sir Y.K. Pao Cancer Center, Prince of Wales Hospital, The Chinese University of Hong Kong, China

2Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, Hong Kong, China

3CUHK-Shenzhen Research Institute, Shenzhen, China

4Department of Interventional Radiology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China

5Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China

6Law Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases (TMBJ), School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China

Corresponding author : Wei Kang Department of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Sir Y.K. Pao Cancer Center, Prince of Wales Hospital, The Chinese University of Hong Kong, 30-32 Ngan Shing Street, Shatin, Hong Kong 999077, China Tel: +852-35051505, Fax: +852-26497286, E-mail: weikang@cuhk.edu.hk

Editor: Moon Young Kim, Yonsei University Wonju College of Medicine, Korea

• Received: April 12, 2025   • Revised: May 19, 2025   • Accepted: June 19, 2025

Copyright © 2025 by The Korean Association for the Study of the Liver

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • Portal vein thrombosis (PVT) is characterized by the formation of a thrombus (blood clot) within the portal vein system, including main portal vein and its intrahepatic portal vein branches, and may extend to the superior mesenteric vein or splenic vein. The emergence of PVT is linked to diverse risk factors, encompassing liver conditions with cirrhosis, abdominal infections, previous abdominal surgeries, malignancies, inherited or acquired thrombophilias, and systemic hypercoagulable conditions. Recent studies revealed a possible connection between the occurrence of PVT and either contracting corona virus disease 2019 (COVID-19) or receiving a COVID-19 vaccination. Current treatment strategies were primarily based on symptom management, extent, and progression of thrombosis, but their efficacy was inconsistent and suboptimal. Untimely or inadequate treatment can lead to the progression of the thrombus and increase the risk of complications, such as portal hypertension, variceal bleeding, and hepatic decompensation, posing a significant risk to the patient’s life. Thus, early and appropriate initiation of pharmacologic and interventional treatments, as well as more aggressive strategies, is crucial for the management and prevention of PVT progression and recurrence. This review focuses on the literature on the recent advancements in the treatment of PVT using various therapeutic modalities, including anticoagulant therapy, thrombolysis, thrombectomy, interventional therapy and liver transplant in cirrhotic patients. In addition, we discuss pearls and pitfalls of these strategies for PVT, highlighting recent progress, identifying knowledge gaps, and proposing avenues towards precision management.
  • Keywords: Portal vein thrombosis; Cirrhosis; Anticoagulation; Thrombolysis; Transjugular intrahepatic portosystemic shunt
Portal vein thrombosis (PVT) refers to thrombosis in the main portal vein and/or the left and right branches of the portal vein, with or without thrombosis in the mesenteric vein and splenic vein. PVT unrelated to solid malignancy is prevalent in cirrhotic patients, demonstrating a 5-year incidence rate of 11% [1,2]. Although the risk factors and pathogenesis of PVT have been extensively studied over decades (Table 1), recent evidence suggests a potential association between PVT and both corona virus disease 2019 (COVID-19) infection and COVID-19 vaccination [3,4]. A cross-sectional observational study by Hassnine and Elsayed [5] investigated the incidence of acute PVT in patients with liver cirrhosis and COVID-19. The study included 70 cirrhotic patients, stratified into two groups: Group A comprised 28 patients with cirrhosis and COVID-19, while Group B consisted of 42 age- and sex-matched cirrhotic controls without COVID-19. Notably, acute PVT was detected in 10.7% (3/28) of COVID-19–associated cirrhosis cases, compared to only 2.3% (1/42) in the non-COVID-19 cohort (P<0.05), suggesting that in cirrhotic patients infected with COVID-19, PVT may be a potential complication even in the absence of hepatocellular carcinoma. Furthermore, emerging studies have documented significant hepatic microvascular alterations in COVID-19 patients, characterized by increased portal vein branch formation, lumen dilatation, various degrees of luminal thrombosis in both portal and sinusoidal veins, and portal tract fibrosis [3,6,7]. Concurrently, evidence of coagulopathy and the presence of antiphospholipid antibodies underscore the complex systemic effects of the virus, contributing to substantial derangement of the intrahepatic vascular network as well as heightened thrombotic risks [8,9]. In addition, recent findings indicate a potential association between portal venous system thrombosis and COVID-19 vaccination, specifically with the ChAdOx1 nCoV-19 vaccine (AstraZeneca), Ad26.COV2.S vaccine (Johnson & Johnson/Janssen), and BNT162b2 mRNA vaccine (BioNTech/Pfizer) [10,11]. This underscores the risks of vaccine-induced thrombosis, particularly vaccine-induced immune thrombotic thrombocytopenia [12,13].
PVT treatment strategies mainly include observation, anticoagulation, thrombolysis, thrombectomy, or endovascular approaches such as transjugular intrahepatic portosystemic shunt (TIPS) (Fig. 1) [14]. At present, anticoagulation is considered the first-line option for treating PVT, but its efficacy may vary due to differences in coagulation status between patients with and without cirrhosis, as well as variations in the extent and severity of the thrombotic embolization among individuals [15]. If anticoagulation therapy fails to produce a response in patients with recent and extensive PVT and signs of intestinal ischemia or infarction, alternative treatment options such as local or systemic thrombolytic therapy, as well as more aggressive intervention procedures should be considered [16]. Although significant advances have been made in treatment, particularly for chronic PVT or portal cavernoma, challenges remain, including ensuring long-term transparency of portal vein lumen and maintaining stent patency [4,17]. This review aims to summarize current evidence-based understanding of therapeutic advances in PVT among cirrhotic patients, focus on the status of ongoing interventions, and present potential future directions for therapy.
Cirrhosis is a chronic liver disease characterized by progressive liver damage and fibrosis. It can eventually lead to a decompensated stage, which is associated with complex alterations in the hemostatic system. The pathogenesis of PVT in cirrhosis is probably multifactorial, primarily arising from alterations in the various components of Virchow’s triad, including decreased portal vein flow, hypercoagulability, and injury to the vessel wall [18,19]. These alterations involve both procoagulant and anticoagulant factors, which can theoretically lead to both thrombotic and bleeding complications [20]. However, the onset of PVT in individuals with liver cirrhosis is often gradual and subtle during the natural course, thus, its symptoms such as abdominal discomfort and fatigue are often masked [21,22]. Especially, in patients with cirrhosis who already have complications such as ascites, hypersplenism and esophageal varices, the symptoms of PVT may be more undetectable. PVT can lead to the development of portal hypertension and collateral vessels, known as porto-portal collaterals, which serve as alternative pathways for blood to bypass the obstructed portal vein [23]. However, the presence of these collaterals can result in the development of portal cavernoma, further exacerbating portal hypertension and leading to complications such as variceal bleeding, ascites, hepatic encephalopathy, and an increased risk of mortality [22,24].
Increasing evidence demonstrated that PVT can spontaneously regress without any antithrombotic therapy, which is referred to as “transient PVT” [2,25]. Studies report varying rates of spontaneous resolution in cirrhotic PVT, with partial thrombosis resolution observed in up to 47.6% of cases [26-29]. Qi et al. [30] conducted a proportion meta-analysis among the 14 cohort studies or randomized controlled trials (RCTs) to evaluate transient PVT. Their results revealed a pooled incidence of transient PVT of 39.8%, which was comparable to the rate observed in a prior meta-analysis reporting 42% spontaneous recanalization in untreated patients [31]. By contrast, other studies reported that none had recanalization among patients who did not receive anticoagulation [32,33]. The reasons for this heterogeneity in reported spontaneous recanalization rates warrant further analysis. Data regarding predictors for spontaneous PVT recanalization remain scarce, except for the ultrasound parameters identified by Maruyama et al. [26]. They reported that the diameter and flow volume in the largest collateral vessel at the time of thrombus detection were significantly smaller in patients who showed improvement compared to those who did not. Furthermore, neither the degree nor the extension of PVT was significantly associated with changes in PVT status [26]. Similarly, evidence from an Italian cohort indicates that while the incidence of spontaneous portal vein recanalization was higher in patients with a thrombus occupancy of less than 50% (57.6%, 8 out of 14) compared to those with over 75% occupancy (33%, 5 out of 15), this difference was not statistically significant (P=0.198) [34]. Current potential explanations for spontaneous recanalization in transient PVT may include improvements in liver function and variations in the severity and natural history of partial PVT [4,35].
The association between regression or progression of thrombus and clinical outcome remains unclear [27]. Some studies have demonstrated that spontaneous resolution or unchanged PVT in liver cirrhosis has little or no impact on prognosis [26-28]. It appeared to be rational that the worsened PVT and deteriorated liver function synergistically increased the mortality. However, Ghabril and colleagues identified 48,570 patients undergoing their first liver transplantation (LT), and simple and multiple logistic regression analysis showed that PVT at LT is associated with early (90 days) mortality and graft failure [36]. Such divergent conclusions could potentially be attributed to differences in study design, patient demographics, liver function at baseline, and the severity of PVT. Although these patients can “wait and see” to avoid the potential risks of anticoagulation therapy and serious hemorrhagic events, it is crucial to closely monitor the patency of the portal vein so that timely treatment can be given in case of thrombosis progression or recurrence [2,26]. Stotts et al. [37] proposed that in individuals without contraindications, who are asymptomatic and not eligible for transplantation, it may be appropriate to postpone elective anticoagulation initially and instead opt for confirmatory imaging after 3 to 6 weeks, considering the potential for spontaneous recanalization.
Traditional anticoagulation
Recent advancements in anticoagulant therapy have significantly enhanced the clinical management of PVT [4]. Individuals who undergo anticoagulant therapy appear to exhibit a higher rate of recanalization, as well as a reduced risk of thrombotic progression. Cumulative evidence from meta-analysis evaluating anticoagulation in cirrhotic PVT reveals critical efficacy-safety patterns [31,38-40]. The pooled rates of PVT recanalization in patients receiving anticoagulant therapy ranged from 53% to 71.5%, while the pooled rates of complete PVT recanalization ranged from 40.8% to 53%. On the contrary, the rate of PVT recanalization in patients who did not undergo anticoagulant therapy ranged between 25.2% and 42%, with the rate of complete PVT recanalization being approximately 33%. What’s more, the incidence of PVT progression was 6.9–9% in anticoagulant-treated patients versus 33% in untreated controls [31]. Furthermore, it has been observed that anticoagulation therapy is associated with enhanced survival outcomes among individuals diagnosed with cirrhosis. Guerrero et al. [41] in their recent research evaluate the effect of anticoagulation on all-cause mortality in cirrhotic patients with PVT, including individual data on 500 patients from five studies, of whom 205 (41%) received anticoagulation and 295 did not. The findings indicated that anticoagulation can not only effectively decrease all-cause mortality in patients with cirrhosis but also reduce PVT independently of recanalization [41]. Another study, using propensity score matching, demonstrated a significant improvement in overall survival among patients receiving anticoagulation therapy compared to the control group (P=0.041), and exhibited a notable reduction in the size of PVT (53.3% vs. 108.2%, P=0.009). Additionally, the anticoagulation group also has a low rate of incidence of over encephalopathy (P=0.041) [42].
The conventional therapeutic armamentarium primarily comprises vitamin K antagonists (VKAs), heparins (including unfractionated heparin and low molecular weight heparins (LMWH) such as enoxaparin/dalteparin/nadroparin), and the synthetic pentasaccharide fondaparinux [43]. VKAs, particularly warfarin, and LMWH remain the standard anticoagulants for preventing and managing venous thromboembolism in cirrhotic patients, despite their indirect coagulation factor modulation and variable efficacy in this population [44,45]. A recent multicenter RCT provided critical insights into warfarin efficacy in cirrhotic patients. The study demonstrated that anticoagulation therapy significantly improved PVT recanalization rates compared to no treatment (71.9% vs. 34.4% intention-to-treat analysis, P=0.004; 76.7% vs. 32.4% per-protocol analysis, P<0.001) [46]. Multivariate Cox regression analysis identified anticoagulation as an independent predictor of recanalization. Notably, while bleeding complications and mortality rates showed no significant difference between groups, untreated patients exhibited a substantially higher incidence of ascites progression (3.3% vs. 26.5%, P=0.015) [46].
Fondaparinux, a synthetic selective factor Xa inhibitor, has a unique mechanism of action involving high-affinity binding to antithrombin, potentiating the inhibition of activated factor X without directly targeting thrombin or platelet factor IV, thereby minimizing the risk of heparin-induced thrombocytopenia compared to LMWH [1,47]. This pharmacodynamic profile, coupled with a fixed daily dosing regimen, simplifies clinical management while maintaining efficacy in thrombus resolution. Evidence from a retrospective cohort study of 124 cirrhotic patients with PVT demonstrated fondaparinux’s superiority over LMWH [48]. At 36 months, the probability of complete thrombus resolution was significantly higher in the fondaparinux group (77% vs. 51%, P=0.001), an effect that persisted even with reduced dosing. In a multivariate analysis, fondaparinux therapy (hazard ratio [HR] 2.38; P=0.002) and full-dose administration (HR 1.78; P=0.035) were found to be independent predictors of portal vein recanalization. Notably, while the bleeding rate was numerically higher in the fondaparinux group (27% vs. 13%), this did not reach statistical significance (P=0.06). In summary, fondaparinux can serve as a viable anticoagulation strategy in cirrhotic patients with PVT, particularly those with contraindications to LMWH or heparin-induced thrombocytopenia history.
Although the efficacy of anticoagulation in cirrhotic patients remains controversial due to its narrow therapeutic window and bleeding risk, the potential benefits of anticoagulation therapy in alleviating portal hypertension may outweigh gastrointestinal bleeding complications. Several studies show that anticoagulation therapy did not increase the incidence of bleeding complications [40,49]. Two independent RCTs demonstrated that sequential combination therapy with nadroparin calcium followed by warfarin was both effective and safe in cirrhotic patients with PVT, with no significant between-group difference in bleeding rate compared with non-anticoagulated controls [50,51]. Prior studies and the American Gastroenterological Association (AGA) Update Clinical Practice also confirmed that the use of warfarin or heparin-derived medications was associated with higher recanalization rates and greater safety in cirrhotic patients [1,41,52,53]. Moreover, patients receiving anticoagulation demonstrated improved liver reserve indices, as evidenced by better Child–Pugh classification scores, MELD scores, and serum albumin levels compared to non-anticoagulated controls [50,51].
Physician should be noted that the efficacy of anticoagulation can be influenced by various factors, including the potential biases inherent in retrospective studies, the age of the thrombus, etiology and severity of liver disease, the degree of thrombus burden, treatment strategies, and the time interval between estimated thrombus onset and initiation of anticoagulation [15,54]. At the same time, individual anticoagulation requires rigorous assessment of bleeding history, fall risk, frailty, thrombocytopenia, and hepatic or renal function.
Direct oral anticoagulants
Recent studies have accumulated substantial evidence supporting the preferential use of new direct oral anticoagulants (DOACs) in cirrhotic patients with PVT, offering pharmacokinetic advantages including rapid onset, fixed dosing regimens, and elimination of routine coagulation monitoring. Current Food and Drug Administration approved agents comprise direct thrombin inhibitor (dabigatran) and four factor Xa inhibitors (rivaroxaban, apixaban, edoxaban, betrixaban, and dabigatran) [55]. Prior meta-analyses demonstrate that DOAC-based regimens achieve superior recanalization rates compared to conventional therapy, with comparable major bleeding risks [45,56]. Despite the lack of standardized response criteria for PVT in cirrhotic patients across studies [57-68], DOACs achieve higher recanalization rates (48–63%) and lower thrombus progression rates (12–18%) compared with conventional anticoagulants, with comparable variceal bleeding and death risk in chronic PVT patients (Table 2). These studies were conducted in the United States [57,58,61,63,68], Japan [60], China [62,64-66], India [67], and international Vascular Liver Disease Interest Group Consortium [59], with the number of cirrhotic patients in the samples ranging from 36 to 396 who were treated with DOACs for the treatment of PVT. However, it is important to acknowledge the heterogeneity among case series, which includes variations in the stage and severity of PVT, as well as differences in the types and doses of anticoagulants used. Particularly, most previous studies focus on compensation population and are limited by non-standard definitions of bleeding [59,62,65,66]. In a recent study, Mort et al. [63] reported the rates of bleeding and discontinuation of DOACs in patients with decompensated cirrhosis. They found that Child–Pugh classification B and C patients exhibited a significantly higher risk of major bleeding or clinically relevant non-major bleeding, with an incidence of 25.8% (24 out of 93 patients). Of note, some studies also involve varied conditions such as Budd–Chiari syndrome, atrial fibrillation, splanchnic vein thrombosis, or non-cirrhotic PVT [58,59].
A 2024 meta-analysis demonstrated that DOACs significantly reduced risks of rates of all-cause death, major bleeding, intracranial hemorrhage and gastrointestinal bleeding in cirrhotic patients compared to warfarin, though no mortality difference was observed [45]. As shown in Table 2, several studies compared the rates of bleeding in cirrhosis patients treated with DOACs to those in cirrhosis patients treated with traditional anticoagulation [57,58,60,61,68]. In general, DOACs have been shown to be either non-inferior or superior to conventional anticoagulants regarding the incidence of bleeding and recurrent embolic events. These findings align with a large US retrospective cohort study showing DOACs, especially apixaban, were associated with lower composite risks of venous thromboembolism recurrence and major bleeding hospitalization than warfarin in patients with chronic liver disease [69].
Another systematic review comparing the use of DOACs with VKAs to treat PVT in patients with cirrhosis revealed superior clinical outcomes with DOACs, including higher pooled rates of PVT recanalization and reduced risks of thrombus progression [70]. These observations are corroborated by recent findings from Xiao et al. [56], whose study underscores edoxaban’s efficacy in achieving significant reductions in PVT volume, superior complete response rates, and sustained long-term thrombus improvement, when compared to traditional therapies. Similarly, Nagaoki et al. [60] conducted a comparative analysis of PVT volume changes in cirrhotic patients receiving either edoxaban or warfarin after receiving a 2-week initial course of danaparoid sodium therapy. Their findings indicated that treatment with edoxaban for a duration of 6 months resulted in a significant reduction in PVT volume, whereas warfarin treatment during the same period was associated with a significant worsening of PVT volume (P<0.001). Importantly, the safety profile of DOACs remained favorable, with no statistically significant increase in gastrointestinal bleeding or other adverse effects relative to VKAs [15].
Compared to traditional VKAs, which rely on vitamin K, prothrombin complex concentrates, or fresh frozen plasma with associated risks of volume overload and thrombosis, DOACs provide targeted reversal agents (idarucizumab for dabigatran; andexanet alfa for rivaroxaban and apixaban), achieving rapid hemostasis with reduced thrombotic risk [71,72]. Notably, although DOACs eliminate routine monitoring and lower intracranial hemorrhage risk compared to VKAs, challenges persist in determining optimal dosing for PVT management in Child–Pugh B and C cirrhosis. Per current practical guidelines [72-75], DOACs are considered safe in Child–Pugh A cirrhosis but require caution in Child–Pugh B cirrhotic patients or those with creatinine clearance <30 mL/min. All DOACs are not recommended in Child–Pugh C cirrhosis [75]. Clinicians should exercise caution when managing cirrhotic individuals with PVT on DOACs, as therapeutic doses may interfere with coagulation diagnostics, leading to significant international normalized ratio (INR) elevations and model for end-stage liver disease (MELD) score increases. A recent study confirmed that DOACs at peak plasma levels may cause profound increases in the MELD score in cirrhotic patients due to their effects on INR, underscoring the necessity of precautions to prevent artificial inflation of the MELD score in this population [76].
Up to date, the optimal duration and dosing of anticoagulation therapy for PVT remain unclear, and there is a lack of definitive standardized clinical guidelines. Recanalization of the PVT may not be observed in all patients within the initial 3 or 6 months of anticoagulation therapy. The AGA clinical practice guidelines recommended that anticoagulation is indicated for acute (<6 months) non-ischemic PVT with >50% luminal occlusion or involvement of main portal/mesenteric veins [1]. Optimal candidates demonstrate thrombus progression, multivessel involvement, inherited thrombophilia, or LT eligibility [77]. Conversely, anticoagulation is not recommended for chronic PVT (>6 months) with complete occlusion and established cavernous transformation due to minimal recanalization potential [1]. However, current management strategies endorsed by the European Association for the Study of the Liver (EASL), Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis, and Baveno VI consensus advocate long-term anticoagulation in chronic PVT patients and symptomatic PVT following gastrointestinal bleeding prophylaxis, contingent upon individualized thrombotic risk assessment and prior thrombotic history [21,72,75]. In a prospective cohort study involving 81 cirrhotic patients with PVT, anticoagulation demonstrated time-dependent recanalization efficacy [78]. The study showed complete portal recanalization in 46 patients (56.8%), with cases distributed as follows: 60.9% (28/46) achieved recanalization at 3-month follow-up, 28.3% (13/46) at 6 months, and 10.8% (5/46) at 12 months post-initiation. From experience at our center, we suggest anticoagulation should not be discouraged in cirrhotic PVT patients lacking absolute contraindications, and extended therapeutic durations may be warranted even in initially non-responsive cases.
The role of thrombolysis in PVT management remains controversial due to limited data from small-scale studies. However, it appears to be a specialized intervention for acute PVT, particularly in cases with thrombus extension into the superior mesenteric vein (SMV) and signs of mesenteric ischemia [79,80]. Endovascular thrombolysis should be considered if no clinical improvement, thrombus extension into the SMV and signs of mesenteric ischemia are observed with anticoagulation. Multiple minimally invasive techniques are available for PVT intervention in cirrhotic patients, including TIPS with mechanical thrombectomy with or without direct thrombolysis, percutaneous transhepatic thrombectomy/thrombolysis, and indirect transarterial thrombolysis via the superior mesenteric artery (SMA) [1,81,82]. This synergistic strategy incorporates two principal delivery methods: one involving transcatheter direct thrombolysis via catheter-based infusion of fibrinolytic agents into the thrombotic core, and the other utilizing pharmacomechanical thrombolysis that combines pharmacological dissolution with mechanical fragmentation devices to optimize thrombus penetration [83]. Moreover, transcatheter SMA urokinase infusion therapy may be a safe and effective option for both acute PVT and fresh mesenteric thrombus [82]. Current thrombolytic agents include streptokinase, urokinase or recombinant tissue plasminogen activator (rt-PA). While these approaches theoretically enable targeted thrombolysis, its clinical adoption remains limited due to insufficient evidence and heightened bleeding risks in cirrhotic patients with inherent coagulopathy and portal hypertension.
Existing evidence suggests that systemic or catheter-directed thrombolysis achieves higher recanalization rates compared to anticoagulation [79,81,84]. Gao et al. [79] performed a systematic meta-analysis to evaluate the efficacy and safety of thrombolysis for portal venous system thrombosis. Their subgroup analysis focused on cirrhotic patients and revealed a pooled overall response rate of 99%, a complete recanalization rate for PVT of 46%, a 28% incidence of bleeding complications during therapy, a 3% rate of thrombosis recurrence, and a 3% short-term mortality rate [79]. Furthermore, the analysis indicated that catheter-directed thrombolysis demonstrates a significantly higher efficacy, with a response rate of 94%, compared to systemic thrombolysis, which showed an 84% response rate. Additionally, bleeding patterns differed between the two approaches, revealing that the local catheter-directed technique was associated with 50% major bleeding events, in contrast to a 100% occurrence of major bleeding events associated with systemic thrombolysis [79]. But this discrepancy should be noted by physicians as previous anticoagulation studies often include chronic PVT cases with inherently lower recanalization potential, whereas thrombolysis is predominantly reserved for acute thromboses with recent onset.
Nowadays, thrombolytic therapy is not recommended as routine management for cirrhotic PVT in current guidelines due to insufficient data and concerns over procedure-related hemorrhage. Based on existing evidences [79,85,86], strict monitoring parameters are mandatory for thrombolysis, including dynamic assessment of D-dimer levels, fibrinogen, and other coagulation parameters to mitigate hemorrhagic risks, with treatment duration typically restricted to not exceed 2 weeks and vascular patency evaluated within 3–5 days of initiation. Future large, multicenter RCTs should prioritize standardized protocols, including drug type, dosage, and delivery methods to evaluate safety, optimal timing, and long-term outcomes in cirrhotic PVT populations.
TIPS establishment for PVT, particularly chronic PVT, involves a multimodal approach, including transcatheter thrombus localization, balloon angioplasty, thrombolytic infusion, mechanical thrombectomy, and stent placement to restore portal venous patency and mitigate portal hypertension [24]. While early reports dismissed PVT as a contraindication for TIPS due to technical challenges and theoretical risks of hepatic decompensation, recent advancements in interventional radiology have transformed TIPS into a viable therapeutic option [17,87]. Over the past three decades, numerous clinical studies and case series have investigated the efficacy of TIPS in the management of PVT among patients with cirrhosis (Table 3) [64,82,85,88-113]. The variability in the success rates of TIPS procedures and the recanalization rates of PVT among these studies may be attributed to the heterogeneity of portal vein conditions and operator’s skills. In general, patients with chronic PVT and portal cavernoma pose significant technical challenges during TIPS placement, resulting in a relatively lower procedural success rate compared to those without these conditions [90-92,96]. A meta-analysis reveals that TIPS can be successfully performed in 75–100% of cases, achieving partial recanalization in 84% and complete recanalization in 73% of patients, with 95% maintaining long-term portal vein patency [114]. TIPS long-term patency may vary across studies because post-TIPS coagulation profiles or genetic prothrombotic factors can impact outcomes. AGA clinical practice guidelines highlight that portal vein revascularization via TIPS (PVR-TIPS) warrants consideration in select cirrhotic individuals with PVT who exhibit concurrent indications for TIPS placement, such as persistent ascites refractory to medical therapy or recurrent variceal bleeding. Moreover, the presence of spontaneous portosystemic shunts (SPSS) is an often-overlooked risk factor that may reduce hepatic perfusion and contribute to the development of overt hepatic encephalopathy [115,116]. Studies well documented that embolisation of large SPSS during TIPS creation reduced the risk of overt hepatic encephalopathy, which is associated with an increased risk of long-term, but not short-term, mortality in cirrhotic patients with portal hypertension [117-119]. Thus, such scenarios should be cautiously evaluated during TIPS-assisted portal vein revascularization procedures, and should be conducted by interventional radiologists with substantial experience. Furthermore, in liver transplant candidates, portal vein recanalization may be considered as a preoperative bridge to transplantation when it demonstrates potential to improve procedural feasibility by restoring portal trunk patency and reestablishing physiological blood flow subsequent to end-to-end anastomosis [1,4].
As outlined in the EASL Clinical Practice Guidelines [115], in patients with cirrhosis who present with complete PVT or cavernoma that progresses despite anticoagulation, TIPS creation and PVR are recommended to facilitate access to LT and enable physiological portal vein anastomosis. However, in patients with chronic cavernous transformation of the portal vein (CTPV), the creation of TIPS poses significant technical challenges for interventional radiologists due to the characteristic replacement of the portal vein by tortuous collateral vessels. The inability to visualize the intrahepatic portal trunk or its branches, combined with the absence of a well-defined portal venous structure, substantially complicates procedural planning and execution. While these interventions remain technically demanding and require prolonged radiation exposure, growing operator experience has enabled successful TIPS placement in select cases. Our previous studies demonstrate that the percutaneous transluminal sharp recanalization (PTR) technique can be used as an alternative and facilitate recanalization after the failure of conventional percutaneous catheterization [17,113]. In cases where TIPS fails due to the inability to recanalize the original main portal vein, utilizing large, cavernous collateral vessels to establish portosystemic shunts may serve as a viable alternative [24,120]. This paradigm shift is attributed to innovations such as PTR, balloon-assisted, percutaneous transhepatic or transsplenic access, and percutaneous TIPS recanalization techniques, which enable thrombus traversal in cases of chronic occlusion or cavernoma (Fig. 2) [109,113]. Based on our institutional experience with CTPV [17,109,113], the middle hepatic access route may represent an effective alternative to right hepatic vein access during TIPS shunt creation, though these findings require further validation. Moreover, in such scenarios, revascularization of persistent portal venous channels should be prioritized over stent deployment in collateral pathways, given that collateral vessel stenting demonstrates suboptimal portal decompressive efficacy and is associated with a higher incidence of procedure-related hemoperitoneum [18,120].
The role of anticoagulation following TIPS placement in PVT management remains debated. While TIPS demonstrates distinct clinical advantages in high-risk populations, particularly through rapid symptom resolution and reduced bleeding risk in variceal bleeding, the rationale for withholding anticoagulation post-procedure primarily stems from the premise that portal flow restoration through shunt creation may inherently maintain vascular patency by counteracting the cirrhotic hypercoagulable state and venous stasis [121]. However, this paradigm warrants critical re-evaluation in patients with chronic portal cavernoma, where technical constraints often necessitate stent deployment in selective intrahepatic portal branches or collateral vessels. In such cases, the hemodynamic efficacy of non-stented portal channels for thrombus prevention remains unverified, particularly given documented instances of de novo PVT formation post-TIPS that may adversely impact clinical outcomes. Although anticoagulation therapy shows limited impact on short-term shunt patency, emerging evidence supports its potential role in mitigating thrombotic recurrence, higher probability of recanalization and improving long-term prognosis [1,64]. We propose long-term systematic anticoagulation should be considered for cirrhotic patients undergoing TIPS without contraindications, balancing the procedural hemodynamic benefits against hypercoagulable state of advanced liver disease and non-physiological portal vein reconstruction.
Complications following TIPS placement, including stenosis, hepatic encephalopathy, and liver failure, remain critical considerations in post-procedural management. Therefore, the decision to perform TIPS in high-risk patients should involve a multidisciplinary team comprising gastroenterologists, hepatologists, intensivists, and interventional radiologists [122,123]. When feasible, patients should be fully informed of these potential complications.
In cases of extensive PVT, mechanical or pharmacological thrombectomy represents a valuable rescue therapeutic approach for achieving portal vein recanalization [121,124]. This technique involves physical disruption and aspiration of thrombus using specialized devices such as the AngioJet system (Boston Scientific), which employs retrograde saline jet streams to generate a vacuum effect (Venturi-Bernoulli principle) for clot maceration and aspiration, thereby minimizing the need for high-dose thrombolytics [83]. Other mechanical thrombectomy devices, such as the Arrow-Trerotola system (Arrow International), Trellis Peripheral Infusion system (Covidien), and Amplatzer Thrombectomy Device system (Microvena), employ rotational mechanisms for clot fragmentation but lack integrated aspiration functionality or capacity for concurrent localized thrombolytic administration [83,125,126].
Mota et al. [81] reported three cases of symptomatic acute/subacute PVT with concurrent mesenteric vein thrombosis. All patients underwent mechanical thrombectomy combined with catheter-directed thrombolysis. The procedures were technically successful in all cases, and patients were discharged without complications. Moreover, in patients with ‘complex PVT’, partial or complete thrombosis may be confined to the portal vein trunk and/or the distal parts of the splenic vein and/or the SMV [127]. These instances can be addressed through thrombectomy combined with standard porto-portal reconstruction or an interposition vein graft from the SMV to the graft portal vein, yielding favorable outcomes [86]. Another study compared the clinical outcomes of patients with and without PVT who underwent LT [128]. The authors suggested that extensive thrombectomy combined with shunt ligation is a legitimate strategy for establishing stable inflow in living donor LT, even in cases of advanced PVT. These results suggest that thrombectomy may represent a viable alternative to conventional therapies for high-risk PVT patients and LT candidates. Nonetheless, emerging evidence indicates that percutaneous transhepatic thrombectomy, while demonstrating efficacy in achieving rapid thrombus clearance in acute PVT, carries a risk of endothelial injury and transmural vascular trauma that may potentiate thrombogenic pathways and increase the likelihood of recurrent thrombosis [126,129]. Current evidence suggests that mechanical thrombectomy may be particularly beneficial in high-bleeding-risk patients or those with contraindications to thrombolytic agents, as it reduces thrombolytic exposure while achieving rapid thrombus debulking [83,130]. However, chronic or organized thrombi demonstrate diminished responsiveness to mechanical thrombectomy alone, frequently necessitating adjunctive procedures such as balloon angioplasty or targeted stenting. In such scenarios, a thrombectomy approach combining thrombolytic agents with TIPS stent deployment can synergistically enhance recanalization efficacy while reducing thrombolytic infusion duration [1,16].
Management of PVT in cirrhotic individuals undergoing LT lacks standardized protocols, with outcomes heavily influenced by thrombus severity, surgical strategies, and postoperative care [131]. Complete PVT is associated with a significant poor outcome in post transplantation survival [32]. Rodríguez-Castro et al. [132] and Zanetto et al. [133] in their studies indicate that complete PVT (Yerdel grades III–IV) significantly reduces 30-day and 1-year post-transplant survival, with a 5.65-fold increase in early mortality risk. This heightened risk is partly attributable to early post-transplant re-thrombosis, particularly in advanced Yerdel grades, necessitating meticulous preoperative evaluation [132,133]. In LT candidates, detailed contrast-enhanced computed tomography or magnetic resonance imaging is mandatory during the evaluation for LT eligibility, with particular attention to portal and mesenteric vein patency [4]. A multidisciplinary team should thoroughly evaluate all potential portal vein reconstruction strategies in patients with PVT before considering them ineligible for transplantation, particularly when complete portal vein obstruction extends into the SMV, precluding standard portal-to-portal anastomosis [18,87].
During LT, intraoperative strategies should prioritize physiological portal inflow restoration to mitigate graft dysfunction and thrombosis. Technical attention should be directed toward avoiding anastomotic strictures and excessive venous length [4]. Meanwhile, physiological reconstruction represents the preferred surgical approach, while non-physiological techniques serve as bailout procedures when anatomical constraints preclude standard anastomosis [127]. The optimal postoperative anticoagulation strategy remains controversial and should be determined through multidisciplinary consensus involving both hepatologists and transplant surgeons. A systematic review demonstrated that 13% of patients developed early posttransplant thrombotic recurrence when postoperative anticoagulation was omitted, with this complication being associated with significantly increased morbidity and mortality [132]. Therefore, long-term anticoagulation may be recommended for patients with comorbid hypercoagulable states, non-anatomic portal vein reconstructions, or interposition grafts.
Nonoperative management remains the standard approach for uncomplicated PVT. In cases of acute PVT with concurrent mesenteric venous thrombosis involvement manifesting as abdominal pain, hematochezia, and peritoneal signs, particularly when complicated by suspected intestinal necrosis or perforation, immediate multidisciplinary consultation and surgical evaluation are warranted [134,135]. If acute mesenteric ischemia is left untreated, this process may progress to life-threatening intestinal necrosis and is associated with 60–80% mortality [134,136]. Early diagnosis and timely surgical intervention are the cornerstones of modern treatment to reduce the high mortality associated with this entity [134]. In 1997, Klempnauer et al. [137] reported on a series of 31 patients who underwent surgical treatment. Of these, 11 underwent open surgical thrombectomy, and among them, 5 received additional local thrombolysis with rt-PA delivered via a catheter placed in a distal mesenteric vein and all survived [137]. Inhospital mortality of these 11 patients was 27% (3/11). Since then, no series on open surgical thrombectomy of the portomesenteric venous system has been published [138]. Consequently, the role of open surgical thrombectomy in contemporary clinical practice remains uncertain.
Based on existing practice guidelines and studies [1,18,115,139], we propose an exploratory algorithm for the management of PVT in patients with liver cirrhosis (Fig. 3). The initial assessment should consider the stage, grade, extent, and changes in PVT, along with clinical manifestations, complications of portal hypertension, and risks of bleeding. Patients exhibiting intestinal ischemia require urgent inpatient care for anticoagulation and gastrointestinal decompression, and should undergo a comprehensive multidisciplinary evaluation to prevent ischemic necrosis.
For asymptomatic cases without intestinal ischemia, recent (<6 months) non-occlusive thrombus (<50% lumen) without extension to the SMV may be monitored with close imaging surveillance at 3-month intervals, unless the patient is on the LT waitlist. In contrast, recent extensive thrombus exhibiting more than 50% occlusion of the main portal vein with or without SMV involvement warrants immediate initiation of anticoagulation therapy. TIPS is typically reserved for patients who do not respond to 6 months of anticoagulation therapy, especially transplantation candidates with complete PVT, with or without mesenteric vein involvement, who may benefit from PVR-TIPS [1,18]. Additionally, it is imperative to implement prophylaxis for gastroesophageal variceal bleeding or high-risk gastroesophageal varices before initiating anticoagulation therapy. In patients with recurrent gastroesophageal variceal bleeding or refractory ascites to conventional pharmacological and endoscopic therapy, TIPS should be considered. Furthermore, in cases of chronic portal cavernoma PVT, multidisciplinary consultation is essential. In selected patients without TIPS contraindications, options such as PTR or combined techniques including transhepatic/transsplenic thrombectomy and thrombolysis may be considered. However, these approaches are supported by limited data and should be performed by experienced interventional specialists.
Recently, the emerging concept of “liver vasomics” has gained attention in the field of medical research [140]. Vasomics represents an innovative omics discipline that systematically analyzes and models the vascular system by integrating various aspects, including anatomical structure, disease pathophysiology, biomechanics, medical imaging, computational science, and artificial intelligence (AI) [16,140-142]. By harnessing the capabilities of advanced medical imaging technology and AI methodologies, liver vasomics may enable early detection of PVT and personalized therapeutic strategies in cirrhosis, potentially revolutionizing PVT management.
PVTs are common in cirrhotic patients and are associated with progression of portal hypertension and mortality. While anticoagulation remains first-line therapy, its optimal duration and efficacy require validation in multinational prospective RCTs, particularly to evaluate the safety, dosing regimens, and long-term outcomes of DOACs in cirrhotic patients. For chronic CTPV, there remains a paucity of literature evaluating the efficacy of combined therapeutic strategies incorporating anticoagulation agents and interventional procedures to develop evidence-based algorithms. Research should prioritize comparative assessment of different access routes (transjugular, transhepatic, transsplenic, PTR, and balloon-assisted techniques) with or without thrombectomy, focusing on recanalization success rates, procedural safety profiles, and long-term patency outcomes in this population. In transplant settings, perioperative management of PVT mandates comprehensive protocols integrating preoperative imaging, intraoperative techniques focused on physiological portal flow restoration, and postoperative anticoagulation regimens tailored through multidisciplinary consensus, guided by thrombus burden and surgical reconstruction complexity. Given the current paucity of robust predictive models for PVT outcomes across therapeutic modalities, future investigations should focus on establishing validated risk-stratification frameworks and universal PVT classification systems through the integration of AI and multi-omics biomarkers, enabling precise quantification of thrombus burden, real-time monitoring of therapeutic responses, and data-driven optimization of individualized management strategies.

Authors’ contributions

WK conceptualized the study, provided direction and guidance on the whole project. JW, XD, and JL wrote and edited the manuscript. BC and FX performed the literature search. JW and XD generated the figures and tables. FX and HWL revised the manuscript. ZJ, GZ, and KFT gave professional comments on the study. All authors reviewed and approved the final version of the manuscript.

Acknowledgements

This study is supported by the National Natural Science Foundation of China (NSFC) (2022, No. 82272990), NSFCRGC Joint Research Scheme (N_CUHK448/23), CUHK direct research grant (2024.066).

Conflicts of Interest

The authors have no conflicts to disclose.

Figure 1.
Management strategies for portal vein thrombosis in patients with cirrhosis.
cmh-2025-0411f1.jpg
Figure 2.
Illustration for transjugular intrahepatic portosystemic shunt placement via transjugular, transhepatic, and transsplenic routes.
cmh-2025-0411f2.jpg
Figure 3.
Algorithm for management of nonmalignant PVT in cirrhosis. CTPV, cavernous transformation of the portal vein; ET, endoscopic therapy; LT, liver transplantation; LVP, large volume paracentesis; PVT, portal vein thrombosis; SMV, superior mesenteric vein; TIPS, transjugular intrahepatic portosystemic shunt.
cmh-2025-0411f3.jpg
Table 1.
Common risk factors of portal vein thrombosis in cirrhosis
Table 1.
Systemic disorder
 Advanced portal hypertension with reduced portal blood flow velocity
 Steal syndrome from large spontaneous portosystemic shunts
 Non-selective beta-blockers
 Plasma D-dimer concentrations
 Malignancy
Inherited thrombophilia
 Factor V Leiden, FactorⅡgene mutation
 Prothrombin gene G20210A mutation
 Anticardiolipin antibodies
 Lupus anticoagulant
Acquired thrombophilia
 Increased Factor VIII levels
 Protein C and S deficiency, antithrombin deficiency
Other systemic risk factors
 metabolic syndrome (MASH, diabetes, obesity)
 COVID-19, COVID-19 vaccine
 Other extrinsic factors
Local vascular damage
 Inflammatory disorders (pylephlebitis, pancreatitis, intraabdominal infections)
 Splenectomy, abdominal trauma, TIPS
 Intra-abdominal surgery (sclerotherapy, hepatectomy, surgical shunt)
 Abdominal malignancy (HCC, pancreatic cancer, gastric cancer, colorectal cancer)
 Local regional therapy for HCC (TACE, radioembolization)

COVID-19, corona virus disease 2019; HCC, hepatocellular carcinoma; MASH, metabolic dysfunction–associated steatohepatitis; TACE, transcatheter arterial chemoembolization; TIPS, transjugular intrahepatic portosystemic shunt.

Table 2.
Anticoagulation with DOACs in patients with cirrhosis and portal vein thrombosis
Table 2.
Study Study design Patients Baseline liver function Drugs Treatment (dose, duration) Main results Complications
Intagliata et al. [57] (2016) Retrospective Anticoagulated patients (n=39, splanchnic thrombosis [46%], non-splanchnic VTE [41%], and AF [13%]) DOACs group: DOACs group (n=20), apixaban [55%] and rivaroxaban [45%]); DOACs group: NA Bleeding: 4/20 in DOACs vs. 3/19 in traditional group, P=0.9
CP (A/B): 9/11; apixaban 5 mg BID or 2.5 mg BID;
MELD score: 12 (10–15) Traditional group (n=19), warfarin [68%] and enoxaparin [32%]) rivaroxaban 20 mg QD or 10 mg QD;
Traditional group: Traditional group:
CP (A/B): 9/10; LMWH 1 mg/kg BID or 40 mg/d;
MELD score: 14 (11–17) warfarin variable with INR
Hum et al. [58] (2017) Retrospective Anticoagulated patients (n=45) DOACs group: DOACs group (n=27, rivaroxaban [63%] and Apixaban [47%]); DOACs group: Improve: Bleeding: 8/27 in DOACs vs. 10/18 in traditional group, P=0.12
PVT (20%), DVT (44%), AF (53%), and other (2%) CP (A/B/C): 11/12/4; apixaban 5 mg BID, with or without a 10 mg BID load; DOACs group (n=26 [96%]);
MELD-XI: 8.9±3.4; Traditional group (n=18, warfarin [83%] and enoxaparin [17%]) rivaroxaban 15 mg daily, with or without a 20 mg daily load; traditional group (n=17 [94%])
Traditional group: Traditional group: Progress:
CP (A/B/C): 7/9/2; enoxaparin 1 mg/kg BID or 1.5 mg/kg/d; DOACs group (n=1 [4%]);
MELD-XI score: 10.1±3.8 warfarin dosed to an INR goal of 2–3 or an INR 1 unit greater than baseline traditional group (n=1 [6%])
De Gottardi et al. [59] (2017) Retrospective Anticoagulated patients (n=36) All are DOACs group: DOACs group (n=36, rivaroxaban [83%], apixaban [11%] and dabigatran [5%]) DOACs group: Recurrent: n=1 (3%) Major bleeding: 1/36;
PVT (61%), Bud-Chiari Syndrome (14%), cardiac arrhythmia (14%), DVT (5%) and other (5%) CP score: 6 (5–8); rivaroxaban 5–20 mg/d; Minor bleeding: 4/36
MELD score: 10.2 apixaban 2.5–10 mg/d;
dabigatran 110–220 mg/d
Nagaoki et al. [60] (2018) Retrospective Cirrhotic patients (n=50) DOACs group: DOACs group (n=20, edoxaban [100%]); DOACs group: Complete improve: Gastrointestinal bleeding:
CP (A/B): 15/5; Traditional group (n=30, warfarin [100%]) edoxaban 60 mg QD or 30 mg QD; DOACs group (n=14 [70%]), traditional group (n=6 [20%]), P<0.001; 3/20 in DOACs group vs. 2/30 in traditional group, P=0.335
Traditional group: Traditional group: Progress:
CP (A/B/C):15/10/5 warfarin dosed to an INR goal of 2–3 DOACs group (n=1 [5%]),
traditional group (n=14 [47%]),
P<0.001
Davis et al. [61] (2020) Retrospective Anticoagulated patients (n=167) DOACs group: DOACs group (n=57, apixaban [52.6%], dabigatran [1.8%] and rivaroxaban [45.6%]); NA After 3 months, recurrent: After 3 months, major bleeding: 3/57 in DOACs vs. 10/110 in traditional group, P=0.381;
PVT (13%), DVT (25%), AF (31%), PE (16%) and other (20%) CP (A/B/C): 35/11/3; DOACs group (n=1 [1.8%]),
MELD score: 11 (8–14); traditional group (n=2 [1.8%]), Stroke: 1/57 in DOACs vs. 0/110 in traditional group, P=0.341
Traditional group: Traditional group (n=110, warfarin [100%]) P=0.731
CP (A/B/C): 43/53/7;
MELD score: 13 (8–17);
Ai et al. [62] (2020) Prospective Cirrhotic patients (n=80) DOACs group: DOACs group (n=40, rivaroxaban [65%], dabigatran [35%]) DOACs group: After 3 months, improve: Bleeding: 3/40 in DOACs vs. 1/40 in untreated group, P>0.05
CP score: 7.2±1.5; rivaroxaban 20 mg QD; DOACs group (n=5 [13%]),
Untreated group: dabigatran 150 mg BID untreated group (n=0 [0%]),
CP score: 7.4±1.7 P<0.05;
After 6 months, improve:
DOACs group (n=11 [28%]),
untreated group (n=1 [3%]),
P<0.05
Mort et al. [63] (2021) Retrospective Anticoagulated patients (n=138) DOACs group: DOACs group (n=57, apixaban [68.1%], dabigatran [8.7%] and rivaroxaban [23.2%]) NA NA Major bleeding: 11/138
PVT (28%), DVT (34%), AF (32%) and other (6%) CP (A/B/C): 45/70/23;
MELD score: 13.6±5.4
Lv et al. [64] (2021) Prospective Cirrhotic patients (n=396) Untreated group: Untreated group (n=48 [12.1%]); DOACs group: Improve: Gastrointestinal bleeding: 20/136 in non-anticoagulant group vs. 6/42 in DOACs group vs. 31/218 in warfarin group, P=0.131;
CP (A/B/C):13/25/10; Anticoagulant group (n=63 [15.9%]); rivaroxaban 10 mg/d; untreated group (n=5 [12.2%]);
MELD: 12.6±3.8; TIPS group (n=88 [22.2%]) Traditional group: anticoagulant group (n=23 [39.7%]);
Anticoagulant group: TIPS and anticoagulant group (n=197 [49.8%]); warfarin initially 2.5 mg and gradually reached INR 2–3; TIPS group (n=88 [100%]) Non-gastrointestinal bleeding: 0/136 vs. 0/42 vs. 7/218, P=0.055;
CP (A/B/C): 33/27/3; Anticoagulant therapy: TIPS and anticoagulant group (n=296 [99.5%]); Minor bleeding: 0/136 vs. 2/42 vs. 19/218, P=0.002
MELD score: 10.3±2.9; warfarin (n=218 [83.8%]); enoxaparin 4,000–8,000 IU/d Stable:
TIPS group: enoxaparin (n=20 patients [7.7%]); untreated group (n=35 [85.4%]);
CP (A/B/C): 22/51/15; rivaroxaban (n=22 patients [8.5%]) anticoagulant group (n=32 [55.2%]);
MELD: 12.5±3.5; TIPS and anticoagulant group (n=1 [0.5%]);
TIPS+anticoagulant group: Progress:
CP (A/B/C): 67/113/17; untreated group (n=1 [2.4%]);
MELD score: 11.5±2.9 anticoagulant group (n=3 [5.2%])
Zhou et al. [65] (2023) Retrospective Cirrhotic patients (n=94) Rivaroxaban group: DOACs group (n=94, rivaroxaban [55%] and dabigatran [45%]) DOACs group: Complete improve: Major bleeding: 3/52 in rivaroxaban group vs. 1/42 in dabigatran group, P=0.646;
CP score: 7.1±1.1; rivaroxaban 15 mg BID in the first 20 days, 20 mg QD in the following days; rivaroxaban group (n=39 [75%]),
MELD score: 9.0 (7.0–0.5); dabigatran group (n=33 [79%]) Minor bleeding: 6/52 in
Dabigatran group: dabigatran 150 mg BID or 110 mg BID rivaroxaban group vs. 5/42 in dabigatran group, P=0.691
CP score: 6.9±1.2;
MELD score: 8.4 (7.4–0.7)
Zhang et al. [66] (2024) Prospective Cirrhotic patients (n=60) All patients are CP (A) LMWH-Ca+DOACs group (n=30, rivaroxaban [100%]); LMWH-Ca+DOACs group: Complete improve: Gastrointestinal bleeding: 0/30 in LMWHCa+DOACs group vs. 2/30 in LMWHCa+traditional group, P=0.317
LMWH-Ca+traditional group (n=30, warfarin [100%]) nadroparin calcium 4,100 AXaIU/d in the first 14 days, rivaroxaban 20 mg QD in the following days; LMWH-Ca+DOACs group (n=21 [70%]),
LMWH-Ca+traditional group (n=6 [20%]), P<0.001;
LMWH-Ca+traditional group: Progress:
nadroparin calcium 4,100 AXaIU/d in the first 14 days, warfarin dosed to an INR goal of 2–3 in the following days LMWH-Ca+DOACs group (n=1 [3%]),
LMWH-Ca+traditional group (n=14 [47%]), P<0.001
Premkumar et al. [67] (2025) Prospective Cirrhotic patients (n=72) DOACs group: DOACs group (n=72, dabigatran [100%]) DOACs group: Improve: 34 patients (47.2%) HE: 3 patients (4.2%);
CP (A/B/C): 27/43/2; enoxaparin based weight in the first 3–5 days, dabigatran 150 mg BID in the following days Ascites: 5 patients (7.0%);
MELD score: 11.8±2.1 Acute variceal bleeding: 1 patient (1.3%);
Spontaneous bacterial peritonitis: 3 patients (4.1%)
Niu et al. [68] (2025) Retrospective Cirrhotic patients (n=275) Untreated group: Untreated group (n=143 [52%]); DOACs group: Mortality rate: Gastrointestinal bleeding:
CP (A/B/C):39/54/38; Anticoagulant group (n=132 [48%]) rivaroxaban 15 mg/d or apixaban 2.5–5 mg BID; untreated group (n=77 [55.4%]) vs. anticoagulant group (n=52 [39.7%]), P=0.01 61.0% in untreated group vs. 59.2% in anticoagulant group, P=0.765
Anticoagulant group: Traditional group:
CP (A/B/C): 51/49/28 warfarin was titrated to an INR goal of 2–3;
LMWH followed weightbased dosing (1 mg/kg twice daily)

AF, atrial fibrillation; BID, twice daily; CP, Child–Pugh class; DOACs, direct oral anticoagulants; DVT, deep vein thrombosis; HE, hepatic encephalopathy; INR, international normalized ratio; LMWH-Ca, low-molecular-weight heparin calcium; MELD, model for end-stage liver disease; MELD-XI score, MELD score excluding INR; PVT, portal vein thrombosis; QD, once daily; VTE, venous thromboembolism; TIPS, Transjugular Intrahepatic Portosystemic Shunt; PE, pulmonary embolism; NA, not available.

Table 3.
Studies on transjugular intrahepatic portosystemic shunt for portal vein thrombosis in cirrhosis
Table 3.
Study Study design Patients TIPS indication PVT occlusion Baseline liver function TIPS success rate TIPS assistant techniques PVT recanalization Main outcome
Jiang et al. [82] (2017) RCTs 20 VB (90%) 10% Complete main PV occlusion CP (A/B/C)*: (1/9/10); 20/20 (100%) NA 55% Complete HE:13/20 (65%)
MELD score: 9.1±5.1 15% Partial Shunt dysfunction: 3/20 (15%)
Blum et al. [85] (1995) Retrospective 7 VB (100%) 100% PV Complete main PV occlusion; CP class (B/C): (2/5) 7/7 (100%) NA 100% Recanalization Shunt dysfunction: 1/7 (14%)
57% Extension into SMV Death: 1/7 (14%)
Bauer et al. [88] (2006) Retrospectives 9 Pre-liver transplant (100%) 67% Complete main PV occlusion; NA 9/9 (100%) NA 88.8% Recanalization NA
78% Extension into SMV;
44% Portal cavernoma
Senzolo et al. [89] (2006) Retrospective 19 NA 74% Complete main PV occlusion; CP score: 9 (median) 19/19 (100%) NA NA HE: 1/19 (5%)
53% Extension into SMV; Death: 1/19 (5%)
32% Portal cavernoma
Van Ha et al. [90] (2006) Retrospective 15 VB (69%) 54% Complete main PV occlusion; CP (B/C): (10/3) 13/15 (87%) NA NA Shunt dysfunction: 1/13 (8%)
Ascites (23%) 8% Extension into SMV; Death: 2/13 (15%)
Pleural effusion (8%) 23% Portal cavernoma
Perarnau et al. [91] (2010) Retrospective 34 VB (79%) 23% Complete main PV occlusion; CP (A/B/C): (3/11/7) 27/34 (79%) NA HE: 4/27 (14%)
Ascites (15%) Long-term patency 28%
Other (6%) 56% Portal cavernoma
Han et al. [92] (2011) Retrospective 57 VB (100%) 19% Complete main PV occlusion; CP (A/B/C): (21/18/4) 43/57 (75%) TH (26%) 100% Recanalization The 1- and 2-year cumulative HE rate was 25% and 27%; The 1- and 2-year cumulative shunt dysfunction rate was 21% and 32% (bare stent).
70% Extension into SMV; TS (5%)
37% Portal cavernoma
Luo et al. [93] (2011) Retrospective 13 VB (54%) 92% Complete main PV occlusion; CP (A/B/C): (4/5/4) 13/13 (100%) TH (31%) 92% Recanalization Shunt dysfunction: 2/13 (15%)
Abdominal pain (46%) 85% Extension into SMV; TS (8%) Death: 2/13 (15%)
62% Portal cavernoma
Luca et al. [94] (2011) Retrospective 70 VB (69%) 34% Complete main PV occlusion; CP (A/B/C): (17/42/11) 70/70 (100%) NA 57% Complete The rate of encephalopathy at 12 and 24 months was 27% and 32%;
Ascites (26%) 79% Extension into SMV; 30% Partial The rate of TIPS dysfunction at 12 and 24 months was 38% and 85% for bare stent, and 21% and 29% for covered stent.
pre-liver transplant (5%) 0% Portal cavernoma Death: 10/70 (14%)
D’Avola et al. [95] (2012) Retrospective 15 Pre-liver transplant (54%) 100% Chronic PV occlusion CP score: 8±3 15/15 (100%) NA 100% Complete Shunt dysfunction: 3/15 (20%)
VB (40%) MELD score: 14±4
Ascites (6%)
Chen et al. [96] (2015) Retrospective 18 VB (100%) 100% Complete main PV occlusion; CP class: (A/B/C) (4/9/1) 14/18 (78%) TH (78%) 78% Recanalization HE: 1/14 (7%); Shunt dysfunction: 1/14 (7%)
100% Extension into SMV; TH+TM (22%) Death:11/14 (7%)
100% Portal cavernoma
Habib et al. [97] (2015) Prospective 11 Pre-liver transplant (100%) 73% Complete main PV occlusion; NA 11/11 (100%) TS (100%) 55% Complete Transient HE: 1/11 (10%)
55% Portal cavernoma 45% Partial Transplant: 3/11 (27%)
Luo et al. [98] (2015) RCTs 37 VB (100%) 35% Complete main PV occlusion CP (B/C): (25/12) 37/37 (100%) NA 65% Complete The 1- and 2-year probability of HE was 16.2% and 38.5% respectively; The 1- and 2-year probability of TIPS patency was 91.7% and 71.3% respectively.
MELD score: 14.2±6.5 Death: 12/37 (32%)
Salem et al. [99] (2015) Retrospective 44 Pre-liver transplant (100%) 39% Complete main PV occlusion; NA 43/44 (98%) TH (26%) 76% Complete HE: 9/43 (21%)
50% Extension into SMV TS (7%) 24% Partial Shunt dysfunction: 12/43 (28%)
30% Portal cavernoma
Wang et al. [100] (2015) Retrospective 25 VB (100%) 8% Complete main PV occlusion; CP (A/B/C): (3/20/2) 25/25 (100%) NA 87% Complete Shunt dysfunction: 5/25 (20%)
16% Extension into SMV MELD score: 1.96±2.37 Death: 5/25 (20%)
Rosenqvist et al. [101] (2016) Retrospective 11 VB (73%) 27% Extension into SMV NA 11/11 (100%) TS (9%) 82% Complete Shunt dysfunction: 3/11 (27%)
Ascites (9%) 18% Partial Death: 5/11 (45%)
Others (18%)
Lakhoo and Gaba [102] (2016) Retrospective 12 Prevention of PVT progression (66%) 8% Complete main PV occlusion; CP (A/B/C): (4/5/3) 12/12 (100%) NA 58% Complete HE: 3/12 (25%)
Ascites (17%) 75% Extension into SMV 33% Partial Death: 3/12 (25%)
VB (17%)
Qi et al. [103] (2016) Prospective 51 VB (100%) 35% Complete main PV occlusion; CP (A/B/C): (7/28/8); 43/51 (84%) TH (58%) 100% Recanalization The cumulative rates free of HE at the 6th, 12th and 24th month: 51%, 43%, and 40%;
74% Extension into SMV; MELD score: 8.22±4.00 TS (2%)
42% Portal cavernoma The cumulative rates free of the first episode of shunt dysfunction at the 6th, 12th and 24th month was 79%, 76% and 69% respectively.
Zhao et al. [104] (2016) Retrospective 191 VB (87%) 26% Complete main PV occlusion; CP (A/B/C): (43/78/62); 183/191 (95.8%) TH (23%) 51% Complete HE was developed in 56 patients (30.6%).
Ascites (13%) 48% Extension into SMV; MELD score: 12.8±5.7 44% Partial The1-, 2-, 3-, 4-and 5- year primary shunt patency rate was 78.7%, 68.9%, 58.5%, and 47.5%, respectively.
Thornburg et al. [105] (2017) Retrospective 61 Pre-liver transplant (100%) 56% Complete main PV occlusion; MELD: 14 (range, 7–42) 60/61 (98%) TH (3%) 72% Complete HE: 11/60 (18%)
30% Extension into SMV; TS (33%) 19% Partial Shunt dysfunction: 5/60 (8%)
48% Portal cavernoma Death: 2/60 (3%)
Wang et al. [106] (2017) Retrospective 98 VB (91%) 100% Complete main PV occlusion; CP (A/B/C): (21/46/31) 89/98 (91%) TH (72.4%) 100% Recanalization HE 36 (36.7%);
Ascites (18%) 60% Extension into SMV; The cumulative rate of restenosis was 19.4%, 31.6%, 39.8%, 52.0%, and 61.2% at 1, 2, 3, 4, and 5 years, respectively.
17% Portal cavernoma
Lv et al. [107] (2017) Retrospective 212 VB (92%) 29% Complete main PV occlusion; CP (A/B/C): (64/115/33) 212/212 (100%) THa 100% Recanalization The cumulative incidence of overt HE at 1 year, 3 years and 5 years was 33%, 39%, and 40%;
Ascites (8%) 52% Extension into SMV; MELD score: 9.8±4.1 TSa
22% Portal cavernoma The cumulative incidence of the first episode of shunt dysfunction at 1 year, 3 years and 5 years of follow-up was 11%, 19%, and 21%, respectively.
Lv et al. [108] (2018) RCTs 24 VB (100%) 33% Complete main PV occlusion; CP (A/B/C): (9/13/2) 23/24 (96%) THa 86% Complete The 1-year and 2-year actuarial probability of overt HE was 23% and 28%;
90% Extension into SMV; MELD score: 12 (range, 9–13) TSa 9% Partial The 1-year and 2-year shunt patency rate was 85% and 80%.
46% Portal cavernoma
Luo et al. [109] (2018) Retrospective 24 VB (100%) 100% Complete main CP (A/B/C): (7/14/3) 22/24 (91.7%) TH (100%) 100% Recanalization HE 4/22 (18%);
PV occlusion; 13% Extension into MELD score: 10.7±3.2 Shunt dysfunction 5/22 (23%)
SMV; 5% Portal cavernoma Death: 3/22 (14%)
Merola et al. [110] (2018) Retrospective 65 VB (39%) 75% Complete main MELD score: 14.9±5.5 65/65 (100%) NA 92.3% Recanalization HE: 19 (29%)
Ascites (37%) PV occlusion; 15% Portal cavernoma
Hydrothorax (3%)
Li et al. [111] (2019) Prospective 25 VB (100%) 100% Complete main PV occlusion; CP (A/B/C): 12/8/5 21/25 (84%) TH (56%) TS (28%) 100% Recanalization HE 3/21 (14.3%); shunt dysfunction 2/21 (9.5)
100% Portal cavernoma
Lv et al. [64] (2021) Prospective 88 VB (91%) 16% Complete main PV occlusion; CP (A/B/C): 22/51/15 88/88 (100%) TH (7%) 90% Complete HE 23/88 (26%);
Ascites (9%) 60% Extension into SMV; MELD score: 12.5±3.5 TS (5%) 10% Partial Death 24/88 (27%)
22% Cavernous The cumulative incidences of OHE at 1 year and 3 years of HE was 25.0% and 26.1%.
The 1-year and 3-year cumulative incidences of shunt dysfunction were 15.9% and 27.3%.
Wang et al. [112] (2021) Retrospective 75 VB (97%) 6% Complete main PV occlusion; CP (A/B/C): 29/40/3 72/75 (96%) NA 100% Recanalization HE 14/72 (19.4%);
Ascites (4%) 54% Extension into SMV MELD score: 10.9±3.0 Shunt dysfunction 7/72 (9.7%)
Luo et al. [113] (2024) Retrospective 106 VB (82%) 100% Complete main PV occlusion; CP score: 6 (5–7.75) 100/106 (94%) TH (83%) 100% Recanalization HE: 17/100 (17%)
Ascites (10%) TS (12%) Shunt dysfunction 37/100 (37%)

CP, Child–Pugh class; HE, hepatic encephalopathy; MELD, model for end-stage liver disease; PVT, portal vein thrombosis; RCTs, randomized controlled trials; TH, transsplenic approach; TS, transsplenic access; VB, Varices bleeding; SMV, superior mesenteric vein; NA, not available; TM, thrombolytic therapy.

*CP or MELD score are expressed as median (interquartile range) or mean±standard deviation from the original article.

aProportional percentages not available.

AGA

American Gastroenterological Association

AI

artificial intelligence

CTPV

cavernous transformation of the portal vein

DOACs

direct oral anticoagulant

EASL

European Association for the Study of the Liver

INR

international normalized ratio

LMWH

low molecular weight heparins

LT

liver transplantation

MELD

model for end-stage liver disease

PTR

percutaneous transluminal sharp recanalization

PVR-TIPS

portal vein revascularization via TIPS

PVT

portal vein thrombosis

rt-PA

recombinant tissue plasminogen activator

SMA

superior mesenteric artery

SMV

superior mesenteric vein

SPSS

spontaneous portosystemic shunts

TIPS

transjugular intrahepatic portosystemic shunt

VKA

vitamin K antagonist
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Update in the treatment of cirrhotic patients with portal vein thrombosis
Clin Mol Hepatol. 2025;31(4):1139-1166.   Published online June 24, 2025
DOI: https://doi.org/10.3350/cmh.2025.0411
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Update in the treatment of cirrhotic patients with portal vein thrombosis
Clin Mol Hepatol. 2025;31(4):1139-1166.   Published online June 24, 2025
DOI: https://doi.org/10.3350/cmh.2025.0411
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Update in the treatment of cirrhotic patients with portal vein thrombosis
Image Image Image
Figure 1. Management strategies for portal vein thrombosis in patients with cirrhosis.
Figure 2. Illustration for transjugular intrahepatic portosystemic shunt placement via transjugular, transhepatic, and transsplenic routes.
Figure 3. Algorithm for management of nonmalignant PVT in cirrhosis. CTPV, cavernous transformation of the portal vein; ET, endoscopic therapy; LT, liver transplantation; LVP, large volume paracentesis; PVT, portal vein thrombosis; SMV, superior mesenteric vein; TIPS, transjugular intrahepatic portosystemic shunt.

Figure 1.

Figure 2.

Figure 3.

Update in the treatment of cirrhotic patients with portal vein thrombosis
Systemic disorder
 Advanced portal hypertension with reduced portal blood flow velocity
 Steal syndrome from large spontaneous portosystemic shunts
 Non-selective beta-blockers
 Plasma D-dimer concentrations
 Malignancy
Inherited thrombophilia
 Factor V Leiden, FactorⅡgene mutation
 Prothrombin gene G20210A mutation
 Anticardiolipin antibodies
 Lupus anticoagulant
Acquired thrombophilia
 Increased Factor VIII levels
 Protein C and S deficiency, antithrombin deficiency
Other systemic risk factors
 metabolic syndrome (MASH, diabetes, obesity)
 COVID-19, COVID-19 vaccine
 Other extrinsic factors
Local vascular damage
 Inflammatory disorders (pylephlebitis, pancreatitis, intraabdominal infections)
 Splenectomy, abdominal trauma, TIPS
 Intra-abdominal surgery (sclerotherapy, hepatectomy, surgical shunt)
 Abdominal malignancy (HCC, pancreatic cancer, gastric cancer, colorectal cancer)
 Local regional therapy for HCC (TACE, radioembolization)
Study Study design Patients Baseline liver function Drugs Treatment (dose, duration) Main results Complications
Intagliata et al. [57] (2016) Retrospective Anticoagulated patients (n=39, splanchnic thrombosis [46%], non-splanchnic VTE [41%], and AF [13%]) DOACs group: DOACs group (n=20), apixaban [55%] and rivaroxaban [45%]); DOACs group: NA Bleeding: 4/20 in DOACs vs. 3/19 in traditional group, P=0.9
CP (A/B): 9/11; apixaban 5 mg BID or 2.5 mg BID;
MELD score: 12 (10–15) Traditional group (n=19), warfarin [68%] and enoxaparin [32%]) rivaroxaban 20 mg QD or 10 mg QD;
Traditional group: Traditional group:
CP (A/B): 9/10; LMWH 1 mg/kg BID or 40 mg/d;
MELD score: 14 (11–17) warfarin variable with INR
Hum et al. [58] (2017) Retrospective Anticoagulated patients (n=45) DOACs group: DOACs group (n=27, rivaroxaban [63%] and Apixaban [47%]); DOACs group: Improve: Bleeding: 8/27 in DOACs vs. 10/18 in traditional group, P=0.12
PVT (20%), DVT (44%), AF (53%), and other (2%) CP (A/B/C): 11/12/4; apixaban 5 mg BID, with or without a 10 mg BID load; DOACs group (n=26 [96%]);
MELD-XI: 8.9±3.4; Traditional group (n=18, warfarin [83%] and enoxaparin [17%]) rivaroxaban 15 mg daily, with or without a 20 mg daily load; traditional group (n=17 [94%])
Traditional group: Traditional group: Progress:
CP (A/B/C): 7/9/2; enoxaparin 1 mg/kg BID or 1.5 mg/kg/d; DOACs group (n=1 [4%]);
MELD-XI score: 10.1±3.8 warfarin dosed to an INR goal of 2–3 or an INR 1 unit greater than baseline traditional group (n=1 [6%])
De Gottardi et al. [59] (2017) Retrospective Anticoagulated patients (n=36) All are DOACs group: DOACs group (n=36, rivaroxaban [83%], apixaban [11%] and dabigatran [5%]) DOACs group: Recurrent: n=1 (3%) Major bleeding: 1/36;
PVT (61%), Bud-Chiari Syndrome (14%), cardiac arrhythmia (14%), DVT (5%) and other (5%) CP score: 6 (5–8); rivaroxaban 5–20 mg/d; Minor bleeding: 4/36
MELD score: 10.2 apixaban 2.5–10 mg/d;
dabigatran 110–220 mg/d
Nagaoki et al. [60] (2018) Retrospective Cirrhotic patients (n=50) DOACs group: DOACs group (n=20, edoxaban [100%]); DOACs group: Complete improve: Gastrointestinal bleeding:
CP (A/B): 15/5; Traditional group (n=30, warfarin [100%]) edoxaban 60 mg QD or 30 mg QD; DOACs group (n=14 [70%]), traditional group (n=6 [20%]), P<0.001; 3/20 in DOACs group vs. 2/30 in traditional group, P=0.335
Traditional group: Traditional group: Progress:
CP (A/B/C):15/10/5 warfarin dosed to an INR goal of 2–3 DOACs group (n=1 [5%]),
traditional group (n=14 [47%]),
P<0.001
Davis et al. [61] (2020) Retrospective Anticoagulated patients (n=167) DOACs group: DOACs group (n=57, apixaban [52.6%], dabigatran [1.8%] and rivaroxaban [45.6%]); NA After 3 months, recurrent: After 3 months, major bleeding: 3/57 in DOACs vs. 10/110 in traditional group, P=0.381;
PVT (13%), DVT (25%), AF (31%), PE (16%) and other (20%) CP (A/B/C): 35/11/3; DOACs group (n=1 [1.8%]),
MELD score: 11 (8–14); traditional group (n=2 [1.8%]), Stroke: 1/57 in DOACs vs. 0/110 in traditional group, P=0.341
Traditional group: Traditional group (n=110, warfarin [100%]) P=0.731
CP (A/B/C): 43/53/7;
MELD score: 13 (8–17);
Ai et al. [62] (2020) Prospective Cirrhotic patients (n=80) DOACs group: DOACs group (n=40, rivaroxaban [65%], dabigatran [35%]) DOACs group: After 3 months, improve: Bleeding: 3/40 in DOACs vs. 1/40 in untreated group, P>0.05
CP score: 7.2±1.5; rivaroxaban 20 mg QD; DOACs group (n=5 [13%]),
Untreated group: dabigatran 150 mg BID untreated group (n=0 [0%]),
CP score: 7.4±1.7 P<0.05;
After 6 months, improve:
DOACs group (n=11 [28%]),
untreated group (n=1 [3%]),
P<0.05
Mort et al. [63] (2021) Retrospective Anticoagulated patients (n=138) DOACs group: DOACs group (n=57, apixaban [68.1%], dabigatran [8.7%] and rivaroxaban [23.2%]) NA NA Major bleeding: 11/138
PVT (28%), DVT (34%), AF (32%) and other (6%) CP (A/B/C): 45/70/23;
MELD score: 13.6±5.4
Lv et al. [64] (2021) Prospective Cirrhotic patients (n=396) Untreated group: Untreated group (n=48 [12.1%]); DOACs group: Improve: Gastrointestinal bleeding: 20/136 in non-anticoagulant group vs. 6/42 in DOACs group vs. 31/218 in warfarin group, P=0.131;
CP (A/B/C):13/25/10; Anticoagulant group (n=63 [15.9%]); rivaroxaban 10 mg/d; untreated group (n=5 [12.2%]);
MELD: 12.6±3.8; TIPS group (n=88 [22.2%]) Traditional group: anticoagulant group (n=23 [39.7%]);
Anticoagulant group: TIPS and anticoagulant group (n=197 [49.8%]); warfarin initially 2.5 mg and gradually reached INR 2–3; TIPS group (n=88 [100%]) Non-gastrointestinal bleeding: 0/136 vs. 0/42 vs. 7/218, P=0.055;
CP (A/B/C): 33/27/3; Anticoagulant therapy: TIPS and anticoagulant group (n=296 [99.5%]); Minor bleeding: 0/136 vs. 2/42 vs. 19/218, P=0.002
MELD score: 10.3±2.9; warfarin (n=218 [83.8%]); enoxaparin 4,000–8,000 IU/d Stable:
TIPS group: enoxaparin (n=20 patients [7.7%]); untreated group (n=35 [85.4%]);
CP (A/B/C): 22/51/15; rivaroxaban (n=22 patients [8.5%]) anticoagulant group (n=32 [55.2%]);
MELD: 12.5±3.5; TIPS and anticoagulant group (n=1 [0.5%]);
TIPS+anticoagulant group: Progress:
CP (A/B/C): 67/113/17; untreated group (n=1 [2.4%]);
MELD score: 11.5±2.9 anticoagulant group (n=3 [5.2%])
Zhou et al. [65] (2023) Retrospective Cirrhotic patients (n=94) Rivaroxaban group: DOACs group (n=94, rivaroxaban [55%] and dabigatran [45%]) DOACs group: Complete improve: Major bleeding: 3/52 in rivaroxaban group vs. 1/42 in dabigatran group, P=0.646;
CP score: 7.1±1.1; rivaroxaban 15 mg BID in the first 20 days, 20 mg QD in the following days; rivaroxaban group (n=39 [75%]),
MELD score: 9.0 (7.0–0.5); dabigatran group (n=33 [79%]) Minor bleeding: 6/52 in
Dabigatran group: dabigatran 150 mg BID or 110 mg BID rivaroxaban group vs. 5/42 in dabigatran group, P=0.691
CP score: 6.9±1.2;
MELD score: 8.4 (7.4–0.7)
Zhang et al. [66] (2024) Prospective Cirrhotic patients (n=60) All patients are CP (A) LMWH-Ca+DOACs group (n=30, rivaroxaban [100%]); LMWH-Ca+DOACs group: Complete improve: Gastrointestinal bleeding: 0/30 in LMWHCa+DOACs group vs. 2/30 in LMWHCa+traditional group, P=0.317
LMWH-Ca+traditional group (n=30, warfarin [100%]) nadroparin calcium 4,100 AXaIU/d in the first 14 days, rivaroxaban 20 mg QD in the following days; LMWH-Ca+DOACs group (n=21 [70%]),
LMWH-Ca+traditional group (n=6 [20%]), P<0.001;
LMWH-Ca+traditional group: Progress:
nadroparin calcium 4,100 AXaIU/d in the first 14 days, warfarin dosed to an INR goal of 2–3 in the following days LMWH-Ca+DOACs group (n=1 [3%]),
LMWH-Ca+traditional group (n=14 [47%]), P<0.001
Premkumar et al. [67] (2025) Prospective Cirrhotic patients (n=72) DOACs group: DOACs group (n=72, dabigatran [100%]) DOACs group: Improve: 34 patients (47.2%) HE: 3 patients (4.2%);
CP (A/B/C): 27/43/2; enoxaparin based weight in the first 3–5 days, dabigatran 150 mg BID in the following days Ascites: 5 patients (7.0%);
MELD score: 11.8±2.1 Acute variceal bleeding: 1 patient (1.3%);
Spontaneous bacterial peritonitis: 3 patients (4.1%)
Niu et al. [68] (2025) Retrospective Cirrhotic patients (n=275) Untreated group: Untreated group (n=143 [52%]); DOACs group: Mortality rate: Gastrointestinal bleeding:
CP (A/B/C):39/54/38; Anticoagulant group (n=132 [48%]) rivaroxaban 15 mg/d or apixaban 2.5–5 mg BID; untreated group (n=77 [55.4%]) vs. anticoagulant group (n=52 [39.7%]), P=0.01 61.0% in untreated group vs. 59.2% in anticoagulant group, P=0.765
Anticoagulant group: Traditional group:
CP (A/B/C): 51/49/28 warfarin was titrated to an INR goal of 2–3;
LMWH followed weightbased dosing (1 mg/kg twice daily)
Study Study design Patients TIPS indication PVT occlusion Baseline liver function TIPS success rate TIPS assistant techniques PVT recanalization Main outcome
Jiang et al. [82] (2017) RCTs 20 VB (90%) 10% Complete main PV occlusion CP (A/B/C)*: (1/9/10); 20/20 (100%) NA 55% Complete HE:13/20 (65%)
MELD score: 9.1±5.1 15% Partial Shunt dysfunction: 3/20 (15%)
Blum et al. [85] (1995) Retrospective 7 VB (100%) 100% PV Complete main PV occlusion; CP class (B/C): (2/5) 7/7 (100%) NA 100% Recanalization Shunt dysfunction: 1/7 (14%)
57% Extension into SMV Death: 1/7 (14%)
Bauer et al. [88] (2006) Retrospectives 9 Pre-liver transplant (100%) 67% Complete main PV occlusion; NA 9/9 (100%) NA 88.8% Recanalization NA
78% Extension into SMV;
44% Portal cavernoma
Senzolo et al. [89] (2006) Retrospective 19 NA 74% Complete main PV occlusion; CP score: 9 (median) 19/19 (100%) NA NA HE: 1/19 (5%)
53% Extension into SMV; Death: 1/19 (5%)
32% Portal cavernoma
Van Ha et al. [90] (2006) Retrospective 15 VB (69%) 54% Complete main PV occlusion; CP (B/C): (10/3) 13/15 (87%) NA NA Shunt dysfunction: 1/13 (8%)
Ascites (23%) 8% Extension into SMV; Death: 2/13 (15%)
Pleural effusion (8%) 23% Portal cavernoma
Perarnau et al. [91] (2010) Retrospective 34 VB (79%) 23% Complete main PV occlusion; CP (A/B/C): (3/11/7) 27/34 (79%) NA HE: 4/27 (14%)
Ascites (15%) Long-term patency 28%
Other (6%) 56% Portal cavernoma
Han et al. [92] (2011) Retrospective 57 VB (100%) 19% Complete main PV occlusion; CP (A/B/C): (21/18/4) 43/57 (75%) TH (26%) 100% Recanalization The 1- and 2-year cumulative HE rate was 25% and 27%; The 1- and 2-year cumulative shunt dysfunction rate was 21% and 32% (bare stent).
70% Extension into SMV; TS (5%)
37% Portal cavernoma
Luo et al. [93] (2011) Retrospective 13 VB (54%) 92% Complete main PV occlusion; CP (A/B/C): (4/5/4) 13/13 (100%) TH (31%) 92% Recanalization Shunt dysfunction: 2/13 (15%)
Abdominal pain (46%) 85% Extension into SMV; TS (8%) Death: 2/13 (15%)
62% Portal cavernoma
Luca et al. [94] (2011) Retrospective 70 VB (69%) 34% Complete main PV occlusion; CP (A/B/C): (17/42/11) 70/70 (100%) NA 57% Complete The rate of encephalopathy at 12 and 24 months was 27% and 32%;
Ascites (26%) 79% Extension into SMV; 30% Partial The rate of TIPS dysfunction at 12 and 24 months was 38% and 85% for bare stent, and 21% and 29% for covered stent.
pre-liver transplant (5%) 0% Portal cavernoma Death: 10/70 (14%)
D’Avola et al. [95] (2012) Retrospective 15 Pre-liver transplant (54%) 100% Chronic PV occlusion CP score: 8±3 15/15 (100%) NA 100% Complete Shunt dysfunction: 3/15 (20%)
VB (40%) MELD score: 14±4
Ascites (6%)
Chen et al. [96] (2015) Retrospective 18 VB (100%) 100% Complete main PV occlusion; CP class: (A/B/C) (4/9/1) 14/18 (78%) TH (78%) 78% Recanalization HE: 1/14 (7%); Shunt dysfunction: 1/14 (7%)
100% Extension into SMV; TH+TM (22%) Death:11/14 (7%)
100% Portal cavernoma
Habib et al. [97] (2015) Prospective 11 Pre-liver transplant (100%) 73% Complete main PV occlusion; NA 11/11 (100%) TS (100%) 55% Complete Transient HE: 1/11 (10%)
55% Portal cavernoma 45% Partial Transplant: 3/11 (27%)
Luo et al. [98] (2015) RCTs 37 VB (100%) 35% Complete main PV occlusion CP (B/C): (25/12) 37/37 (100%) NA 65% Complete The 1- and 2-year probability of HE was 16.2% and 38.5% respectively; The 1- and 2-year probability of TIPS patency was 91.7% and 71.3% respectively.
MELD score: 14.2±6.5 Death: 12/37 (32%)
Salem et al. [99] (2015) Retrospective 44 Pre-liver transplant (100%) 39% Complete main PV occlusion; NA 43/44 (98%) TH (26%) 76% Complete HE: 9/43 (21%)
50% Extension into SMV TS (7%) 24% Partial Shunt dysfunction: 12/43 (28%)
30% Portal cavernoma
Wang et al. [100] (2015) Retrospective 25 VB (100%) 8% Complete main PV occlusion; CP (A/B/C): (3/20/2) 25/25 (100%) NA 87% Complete Shunt dysfunction: 5/25 (20%)
16% Extension into SMV MELD score: 1.96±2.37 Death: 5/25 (20%)
Rosenqvist et al. [101] (2016) Retrospective 11 VB (73%) 27% Extension into SMV NA 11/11 (100%) TS (9%) 82% Complete Shunt dysfunction: 3/11 (27%)
Ascites (9%) 18% Partial Death: 5/11 (45%)
Others (18%)
Lakhoo and Gaba [102] (2016) Retrospective 12 Prevention of PVT progression (66%) 8% Complete main PV occlusion; CP (A/B/C): (4/5/3) 12/12 (100%) NA 58% Complete HE: 3/12 (25%)
Ascites (17%) 75% Extension into SMV 33% Partial Death: 3/12 (25%)
VB (17%)
Qi et al. [103] (2016) Prospective 51 VB (100%) 35% Complete main PV occlusion; CP (A/B/C): (7/28/8); 43/51 (84%) TH (58%) 100% Recanalization The cumulative rates free of HE at the 6th, 12th and 24th month: 51%, 43%, and 40%;
74% Extension into SMV; MELD score: 8.22±4.00 TS (2%)
42% Portal cavernoma The cumulative rates free of the first episode of shunt dysfunction at the 6th, 12th and 24th month was 79%, 76% and 69% respectively.
Zhao et al. [104] (2016) Retrospective 191 VB (87%) 26% Complete main PV occlusion; CP (A/B/C): (43/78/62); 183/191 (95.8%) TH (23%) 51% Complete HE was developed in 56 patients (30.6%).
Ascites (13%) 48% Extension into SMV; MELD score: 12.8±5.7 44% Partial The1-, 2-, 3-, 4-and 5- year primary shunt patency rate was 78.7%, 68.9%, 58.5%, and 47.5%, respectively.
Thornburg et al. [105] (2017) Retrospective 61 Pre-liver transplant (100%) 56% Complete main PV occlusion; MELD: 14 (range, 7–42) 60/61 (98%) TH (3%) 72% Complete HE: 11/60 (18%)
30% Extension into SMV; TS (33%) 19% Partial Shunt dysfunction: 5/60 (8%)
48% Portal cavernoma Death: 2/60 (3%)
Wang et al. [106] (2017) Retrospective 98 VB (91%) 100% Complete main PV occlusion; CP (A/B/C): (21/46/31) 89/98 (91%) TH (72.4%) 100% Recanalization HE 36 (36.7%);
Ascites (18%) 60% Extension into SMV; The cumulative rate of restenosis was 19.4%, 31.6%, 39.8%, 52.0%, and 61.2% at 1, 2, 3, 4, and 5 years, respectively.
17% Portal cavernoma
Lv et al. [107] (2017) Retrospective 212 VB (92%) 29% Complete main PV occlusion; CP (A/B/C): (64/115/33) 212/212 (100%) THa 100% Recanalization The cumulative incidence of overt HE at 1 year, 3 years and 5 years was 33%, 39%, and 40%;
Ascites (8%) 52% Extension into SMV; MELD score: 9.8±4.1 TSa
22% Portal cavernoma The cumulative incidence of the first episode of shunt dysfunction at 1 year, 3 years and 5 years of follow-up was 11%, 19%, and 21%, respectively.
Lv et al. [108] (2018) RCTs 24 VB (100%) 33% Complete main PV occlusion; CP (A/B/C): (9/13/2) 23/24 (96%) THa 86% Complete The 1-year and 2-year actuarial probability of overt HE was 23% and 28%;
90% Extension into SMV; MELD score: 12 (range, 9–13) TSa 9% Partial The 1-year and 2-year shunt patency rate was 85% and 80%.
46% Portal cavernoma
Luo et al. [109] (2018) Retrospective 24 VB (100%) 100% Complete main CP (A/B/C): (7/14/3) 22/24 (91.7%) TH (100%) 100% Recanalization HE 4/22 (18%);
PV occlusion; 13% Extension into MELD score: 10.7±3.2 Shunt dysfunction 5/22 (23%)
SMV; 5% Portal cavernoma Death: 3/22 (14%)
Merola et al. [110] (2018) Retrospective 65 VB (39%) 75% Complete main MELD score: 14.9±5.5 65/65 (100%) NA 92.3% Recanalization HE: 19 (29%)
Ascites (37%) PV occlusion; 15% Portal cavernoma
Hydrothorax (3%)
Li et al. [111] (2019) Prospective 25 VB (100%) 100% Complete main PV occlusion; CP (A/B/C): 12/8/5 21/25 (84%) TH (56%) TS (28%) 100% Recanalization HE 3/21 (14.3%); shunt dysfunction 2/21 (9.5)
100% Portal cavernoma
Lv et al. [64] (2021) Prospective 88 VB (91%) 16% Complete main PV occlusion; CP (A/B/C): 22/51/15 88/88 (100%) TH (7%) 90% Complete HE 23/88 (26%);
Ascites (9%) 60% Extension into SMV; MELD score: 12.5±3.5 TS (5%) 10% Partial Death 24/88 (27%)
22% Cavernous The cumulative incidences of OHE at 1 year and 3 years of HE was 25.0% and 26.1%.
The 1-year and 3-year cumulative incidences of shunt dysfunction were 15.9% and 27.3%.
Wang et al. [112] (2021) Retrospective 75 VB (97%) 6% Complete main PV occlusion; CP (A/B/C): 29/40/3 72/75 (96%) NA 100% Recanalization HE 14/72 (19.4%);
Ascites (4%) 54% Extension into SMV MELD score: 10.9±3.0 Shunt dysfunction 7/72 (9.7%)
Luo et al. [113] (2024) Retrospective 106 VB (82%) 100% Complete main PV occlusion; CP score: 6 (5–7.75) 100/106 (94%) TH (83%) 100% Recanalization HE: 17/100 (17%)
Ascites (10%) TS (12%) Shunt dysfunction 37/100 (37%)
Table 1. Common risk factors of portal vein thrombosis in cirrhosis

COVID-19, corona virus disease 2019; HCC, hepatocellular carcinoma; MASH, metabolic dysfunction–associated steatohepatitis; TACE, transcatheter arterial chemoembolization; TIPS, transjugular intrahepatic portosystemic shunt.

Table 2. Anticoagulation with DOACs in patients with cirrhosis and portal vein thrombosis

AF, atrial fibrillation; BID, twice daily; CP, Child–Pugh class; DOACs, direct oral anticoagulants; DVT, deep vein thrombosis; HE, hepatic encephalopathy; INR, international normalized ratio; LMWH-Ca, low-molecular-weight heparin calcium; MELD, model for end-stage liver disease; MELD-XI score, MELD score excluding INR; PVT, portal vein thrombosis; QD, once daily; VTE, venous thromboembolism; TIPS, Transjugular Intrahepatic Portosystemic Shunt; PE, pulmonary embolism; NA, not available.

Table 3. Studies on transjugular intrahepatic portosystemic shunt for portal vein thrombosis in cirrhosis

CP, Child–Pugh class; HE, hepatic encephalopathy; MELD, model for end-stage liver disease; PVT, portal vein thrombosis; RCTs, randomized controlled trials; TH, transsplenic approach; TS, transsplenic access; VB, Varices bleeding; SMV, superior mesenteric vein; NA, not available; TM, thrombolytic therapy.

CP or MELD score are expressed as median (interquartile range) or mean±standard deviation from the original article.

Proportional percentages not available.

Table 1.

Table 2.

Table 3.

CMH : Clinical and Molecular Hepatology
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