Vein Thrombosis In Cirrhotic Patients Research Articles

Role of Elevated International Normalized Ratio as a Predictor for Portal Vein Thrombosis in Cirrhotic Patients

Role of Elevated International Normalized Ratio as a Predictor for Portal Vein Thrombosis in Cirrhotic Patients

Serum Protein C and D-Dimer as Predictors of Portal Vein Thrombosis in Cirrhotic Patients without Hepatocellular Carcinoma

Serum Protein C and D-Dimer as Predictors of Portal Vein Thrombosis in Cirrhotic Patients without Hepatocellular Carcinoma

Serum Protein C and D-Dimer as Predictors of Portal Vein Thrombosis in Cirrhotic Patients without Hepatocellular Carcinoma

Serum Protein C and D-Dimer as Predictors of Portal Vein Thrombosis in Cirrhotic Patients without Hepatocellular Carcinoma

Prevalence of chronic venous insufficiency and deep vein thrombosis in cirrhotic patients.

People with cirrhosis of the liver are at risk for complications that can worsen their quality of life and increase morbidity and mortality. Contrary to previous beliefs, cirrhosis does not protect against the development of thromboembolic events, and cirrhotic patients may have higher rates of deep vein thrombosis (DVT). The study of chronic venous disease and its impact on patients with cirrhosis is unknown in the literature and may be an important fact since this condition also had impact on quality of life and morbidity. The aim of this study is to evaluate the prevalence of DVT (Deep Venous thrombosis) in outpatients with cirrhosis and the degree of chronic venous insufficiency, evaluating possible correlations between clinical and laboratory aspects of cirrhotic patients with these pathologies. Patients with cirrhosis were evaluated in the outpatient clinic of the Liver Transplantation and Hepatology Service of HC-FMUSP from November 2018 to November 2022, with clinical evaluation, venous disease questionnaires, data collection of imaging and laboratory tests, and venous color Doppler ultrasound. The information was analyzed by the University of São Paulo (USP) Statistics Department. There was a prevalence of 7.6% of DVT in studied patients, VCSS score 6.73 and severe CEAP classification (C4-6) 32.1%. There was no association of DVT with qualitative variables by the Fisher test such as Child Turcotte Pugh Scale (CTP) (p = 0.890), dichotomized INR values (p = 0.804), etiology of cirrhosis (p = 0.650) and chronic kidney disease (p > 0.999), nor with quantitative variables by t-student's such as age (p = 0.974), Body Mass Index (BMI) (p = 0.997), MELD score (p = 0.555), Albumin (p = 0.150) and Platelets (p = 0.403). We found that as the severity of ascites increases, there is an increase in the proportion of patients classified in the category indicating more severe clinical manifestations of chronic venous disease (C4 to C6). The mean age (54 years) was higher in patients with DVT than in those without. The mean BMI of patients without DVT (25.7 kg/m2) is lower than that of patients with DVT (27.0 kg/m2). The prevalence of DVT is higher in patients with thrombophilia (20.0%) than in those without (7.0%). This suggests an association between the two variables. The descriptive measures of the MELD score, the cirrhosis scale used for liver transplant waiting lists, did not indicate an association of this scale with the occurrence of DVT. The incidence of VTE (Venous Thromboembolic Events) and CVD (Chronic Venous Disease) within the sample surpassed that of the general population; nevertheless, more studies are required to validate these results. Concerning venous thromboembolism, no correlation was observed between the variables within the sample and the augmented risk of VTE. Regarding chronic venous disease, studies have shown that edema and orthostatism are correlated with increased severity of CVD on the VCSS scales. Statistical dispersion methods suggest that patients with higher BMI and more severe liver disease (according to the Child-Pugh score) are more likely to experience worsening of CVD. About chronic venous disease, studies have shown that edema and orthostatism are correlated with increased severity of CVD on the VCSS scales.

Approach to different thrombolysis techniques and timing of thrombolysis in the management of portal vein thrombosis in cirrhotic patients.

Thrombolysis is not currently recommended in cirrhotic patients with acute portal vein thrombosis (PVT) in most guidelines, because of the exceedingly limited data and the perceived high risk of bleeding adverse events. However, in the few studies including patients with cirrhosis, the rate of success was high and that of adverse events was similar in patients with or without cirrhosis. Hence, thrombolysis might be a rescue therapeutic option in patients with cirrhosis and acute, symptomatic thrombosis of the portal venous system, unresponsive to anticoagulation, provided a suitable timing is kept, less than 30 days and, if possible, less than 14 days from the acute onset of portal vein thrombosis. In this review perspective article, I discuss the several potential approaches of thrombolysis, either local or systemic, alone or combined with mechanical procedures for thrombus removal, or as a complement to Transjugular Intrahepatic Portosystemic Shunt placement, with a focus on the more suitable timing of thrombolysis. However, the very limited available data preclude from performing firm recommendations, and decision to carry out thrombolysis must take into account both the occurrence of major contraindications and the current critical clinical setting. In the next future, large high-quality multicentre studies will hopefully be able to settle more firm indications and preferable techniques.

Prevalence and clinical characteristics of advanced portal vein thrombosis in cirrhotic patients with gastroesophageal variceal hemorrhage.

Portal venous thrombosis (PVT) in cirrhotic patients is usually asymptomatic and diagnosed incidentally. In this study we aimed to investigate the prevalence and characteristics of advanced PVT in cirrhotic patients with a recent episode of gastroesophageal variceal hemorrhage (GVH). Cirrhotic patients with recent GVH at one month before their admission for further treatment to prevent rebleeding were retrospectively recruited. Hepatic venous pressure gradient (HVPG) measurements, contrast-enhanced computed tomography (CT) scan of the portal vein system, and endoscopy were performed. PVT was diagnosed by CT examination and classified as none, mild and advanced. Of the 356 patients enrolled, 80 (22.5%) had advanced PVT. Elevated levels of white blood cells (WBC) and serum D-dimer were observed in advanced PVT patients compared with those with no or mild PVT. Moreover, HVPG was lower in patients with advanced PVT, with fewer patients having HVPG exceeding 12 mmHg, while grade III esophageal varices and varices with red signs were more prevalent. Multivariate analysis showed that WBC count (odds ratio [OR] 1.401, 95% confidence interval [CI] 1.171-1.676, P < 0.001), D-dimer level (OR 1.228, 95% CI 1.117-1.361, P < 0.001), HVPG (OR 0.942, 95% CI 0.900-0.987, P = 0.011), and grade III esophageal varices (OR 4.243, 95% CI 1.420-12.684, P = 0.010) were associated with advanced PVT. Advanced PVT, which is associated with a more severe hypercoagulable and inflammatory status, causes severe prehepatic portal hypertension in cirrhotic patients with GVH.

Presence of Hepatocellular Carcinoma Does Not Affect Course and Response to Anticoagulation of Bland Portal Vein Thrombosis in Cirrhotic Patients.

Malignancies are generally considered a risk factor for deep vein thrombosis and may hamper the recanalisation of thrombosed veins. We investigate whether the natural course and response to anticoagulant treatment of bland portal vein thrombosis (PVT) in patients with cirrhosis complicated by hepatocellular carcinoma (HCC) differ from those without HCC. Retrospective study in two hepatology referral centres, in Italy and Romania where patients with a diagnosis of PVT on cirrhosis and follow-up of at least 3 months with repeated imaging were included. A total of 162 patients with PVT and matching inclusion and exclusion criteria were identified: 30 with HCC were compared to 132 without HCC. Etiologies, Child-Pugh Score (7 vs 7) and MELD scores (11 vs 12, p=0.3679) did not differ. Anticoagulation was administered to 43% HCC vs 42% nonHCC. The extension of PVT in the main portal trunk was similar: partial/total involvement was 73.3/6.7% in HCC vs 67.4/6.1% in nonHCC, p=0.760. The remainder had intrahepatic PVT. The recanalization rate was 61.5% and 60.7% in HCC/nonHCC in anticoagulated patients (p=1). Overall PVT recanalisation, including treated and untreated patients, was observed in 30% of HCC vs 37.9% of nonHCC, p=0.530. Major bleeding incidence was almost identical (3.3% vs 3.8%, p=1). Progression of PVT after stopping anticoagulation did not differ (10% vs 15.9%, respectively, HCC/nHCC, p=0.109). The course of bland non-malignant PVT in cirrhosis is not affected by the presence of active HCC. Treatment with anticoagulation in patients with active HCC is safe and as effective as in nonHCC patients, this can potentially allow us to use otherwise contraindicated therapies (ie TACE) if a complete recanalization is achieved with anticoagulation.

Beyond the Guidelines: Anticoagulant Treatment of Patients with Recent Portal Vein Thrombosis in the Setting of Liver Cirrhosis

Abstract Portal vein thrombosis, in the clinical setting of liver cirrhosis, is a complication which increases mortality rate by leading to specific complications. Its presence also serves as a negative prognostic factor for these patients. Specialized literature, although rich in papers on this subject, presents loose and sometimes contradictory information regarding its prognosis and specific treatment. This paper brings into discussion the issue of recent portal vein thrombosis in cirrhotic patients, with emphasis on indications for initiation of anticoagulant therapy and the optimal drug of choice. It also highlights the utility of using correct terminology for facilitating clinical approach of guideline recommendations as well as increasing the quality of published scientific papers. The coagulation homeostasis of the cirrhotic patient presents many particularities that can make the optimal therapeutic choice extremely difficult when portal vein thrombosis is established. Absence of randomized clinical trials and lack of consensus regarding anticoagulant treatment in these patients leaves it up to the clinician to decide when and what anticoagulant to use. Analysis of the newest guidelines and recent meta-analysis made it possible to identify the right context for initiating therapy with the most used anticoagulants currently: low molecular weight heparin, vitamin K antagonists and direct oral anticoagulants.

Metabolic Disorders and Risk of Portal Vein Thrombosis in Liver Cirrhosis: A Systematic Review and Meta-Analysis.

Portal vein thrombosis is considered to be an indicator of worse outcomes in patients with hepatic cirrhosis. More and more evidence shows that metabolic disorders are noticeable pro-thrombotic factors. However, whether or not metabolic disorders increase the risk of cirrhotic portal vein thrombosis is controversial. We aim to quantify the magnitude of the association between metabolic disorders and the risk of cirrhotic portal vein thrombosis. Databases were searched for papers to identify studies in which metabolic disorders were compared in liver cirrhosis with or without portal vein thrombosis. Based on data from the eligible studies, metabolic disorders related to portal vein thrombosis included diabetes mellitus, nonalcoholic fatty liver disease, hypercholesterolemia, and body mass index. Pooled adjusted odds ratios with 95% CIs were calculated. Data for 22 studies with a total of 57 371 portal vein thrombosis cases and 3 979 015 participants were included. Statistically significant pooled odds ratios for portal vein thrombosis were obtained for diabetes mel- litus (odds ratio 1.80, 95% CI 1.42-2.28), nonalcoholic fatty liver disease (odds ratio 1.61, 95% CI 1.34-1.95), and hypercholesterolemia (odds ratio 3.59, 95% CI 1.83-7.03). Body mass index was likely irrelevant with cirrhotic portal vein thrombosis (odds ratio 1.01, 95% CI 0.87-1.17), both in overall and subgroup meta-analyses. Significant heterogeneities among studies were observed, except for the hypercholesterolemia group. Metabolic disorders, such as diabetes mellitus, nonalcoholic fatty liver disease, and hypercholesterolemia, increased the risk of portal vein thrombosis in cirrhotic patients by 1.80-fold, 1.61-fold, and 3.59-fold, respectively. Body mass index did not appear to be a risk predictor of cirrhotic portal vein thrombosis. Further, well-designed clinical and mechanistic studies are required to strengthen the arguments, especially in obese patients.

Bacterial infections as a predisposing factor for the development of portal vein thrombosis in cirrhotic patients: a prospective study

Bacterial infections as a predisposing factor for the development of portal vein thrombosis in cirrhotic patients: a prospective study

A Dynamic Nomogram Predicting Portal Vein Thrombosis in Cirrhotic Patients During Primary Prophylaxis for Variceal Hemorrhage.

BackgroundPortal vein thrombosis (PVT) would exert a further increase in resistance to portal blood flow, resulting in worsening portal hypertension and poor outcome. This study aimed to identify risk factors and develop an clinically applicable dynamic nomogram predicting the occurrence of PVT in cirrhotic patients during primary prophylaxis for variveal hemorrhage (VH).MethodsThe multi-center retrospective study enrolled cirrhotic patients with high-risk varices, which were further divided into training and validation cohorts for 3 years follow-up. A dynamic nomogram based on the Cox proportional hazard regression model was developed with the cutoff value calculated by X-title analysis. The performance of the nomogram was evaluated with Harrell’s concordance index (C-index), calibration curve and decision curve analysis.Results91 (34.0%) of the whole cohort were diagnosed with PVT during 3-year follow-up. Variables including carvedilol (P < 0.001), low portal vein velocity (P < 0.001), increased size of esophageal varices (P = 0.005), and high HbA1c (P < 0.001) and procalcitonin (P = 0.015) were identified to be independently associated with PVT, which were further incorporated into the dynamic nomogram with optimal cutoff (8.8 and 14.6) for risk-stratification. The C-indexes (0.894 of internal validation and 0.892 of external validation) and calibration curves demonstrated ideal discrimination and calibration. The thresholds for more reasonable application of the nomogram were 0–0.27, 0–0.66, and 0.04–1.00 at 1, 2, and 3-year, respectively.ConclusionThe dynamic nomogram could be accurately and reliably used for clinical risk-stratification of PVT in cirrhotic patients during primary prophylaxis for VH.

Direct oral anticoagulant administration in cirrhotic patients with portal vein thrombosis: What is the evidence?

In recent years, the traditional concept that cirrhosis-related coagulopathy is an acquired bleeding disorder has evolved. Currently, it is known that in cirrhotic patients, the hemostatic system is rebalanced, which involves coagulation factors, fibrinolysis and platelets. These alterations disrupt homeostasis, skewing it toward a procoagulant state, which can lead to thromboembolic manifestations, especially when hemodynamic and endothelial factors co-occur, such as in the portal vein system in cirrhosis. Portal vein thrombosis is a common complication of advanced liver cirrhosis that negatively affects the course of liver disease, prognosis of cirrhotic patients and success of liver transplantation. It is still debated whether portal vein thrombosis is the cause or the consequence of worsening liver function. Anticoagulant therapy is the mainstay treatment for acute symptomatic portal vein thrombosis. In chronic portal vein thrombosis, the role of anticoagulant therapy is still unclear. Traditional anticoagulants, vitamin K antagonists and low-molecular-weight heparin are standard-of-care treatments for portal vein thrombosis. In the last ten years, direct oral anticoagulants have been approved for the prophylaxis and treatment of many thromboembolic-related diseases, but evidence on their use in cirrhotic patients is very limited. The aim of this review was to summarize the evidence about the safety and effectiveness of direct oral anticoagulants for treating portal vein thrombosis in cirrhotic patients.

Bacterial infection as a predisposing factor for the development of portal vein thrombosis in cirrhotic patients: a prospective study

Background and Aims: Non-malignant portal vein thrombosis (PVT) is one of the complications of liver cirrhosis. The predisposing factors for PVT in cirrhotic patients are not entirely clear. The aim of this study was to identify possible clinical risk factors related to the development of PVT in patients with liver cirrhosis.

The Predictive Role of Variceal Band Ligation in the Development of Portal Vein Thrombosis in Cirrhotic Patients

Abstract Introduction. It is well known that portal vein thrombosis (PVT) can accelerate liver decompensation, reducing overall survival(1). In the literature, the topic whether PVT is a risk factor for variceal bleeding or it influences the effectiveness of variceal band ligation (VBL) remains of great interest The aim of this study was to assess if VBL is a potential risk factor for PVT development. An observational and retrospective study was conducted in a single tertiary center from 2010 to 2021 and included data from 285 patients with liver cirrhosis. Results. Of the 285 patients, gender distribution described 47.32% female (n =135) and 52.8% male (n =150) with a mean age of 55 years (range =23-79). The average MELD score was 12.5 (range 7-27). Of the total number of patients, 48.8% (n=139) had previous VBL: 20% (n=57) underwent primary prophylactic VBL and 34.7% (n=99) underwent secondary prophylaxis. Thus, 285 VBL procedures had been performed and the average number of VBL session was 2 (range 1-10) The mean time follow up was 92.55 months (range 22-230. During the follow up period PVT was diagnosed in 41.4% of patients (n =118) of which 67.77% (n =80) had at least one previous session of VBL: 33% of patients (n =39) had performed primary prophylaxis and 34.74% (n =41) secondary. A logistic regression was conducted to assess if VBL (primary and/or secondary prophylaxis) are risk factors for PVT development. The model was significant for primary prophylaxis (p =0.002, OR 3.28, CI 1.53-7.02) resulting that the risk of PVT is increasing around 3 times after primary prophylactic VBL. Conclusion. Our study showed a certain predisposition for cirrhotic patients to develop PVT after VBL performed as primary prophylaxis thus raising the question: does VBL impact the occurrence of PVT in cirrhotic patients? Furthermore, to our knowledge, this is the first study in the literature that focuses on this topic. More studies should be performed to evaluate and describe the relationship between VBL and the risk of PVT.

S1117 Efficacy and Safety of Direct Oral Anticoagulants in Treatment of Splanchnic Vein Thrombosis in Cirrhotic Patients: Systematic Review and Meta-analysis

S1117 Efficacy and Safety of Direct Oral Anticoagulants in Treatment of Splanchnic Vein Thrombosis in Cirrhotic Patients: Systematic Review and Meta-analysis

Management of portal vein thrombosis in cirrhotic patients enlisted for liver transplantation: From diagnosis to treatment (Review).

Portal vein thrombosis (PVT) commonly occurs in patients with cirrhosis. Several classification systems of PVT have been proposed over the years reflecting the challenge in establishing a widely accepted system. To date, PVT has been considered an absolute contraindication for orthotopic liver transplantation (OLT) since it is associated with decreased graft survival and increased patient mortality. Nevertheless, the development of modern surgical techniques has enabled the inclusion of these candidates in OLT waiting lists, since their postoperative results are shown to be comparable to those of patients without PVT. The aim of the present review was to critically appraise the available treatment options for cirrhotic patients enlisted for liver transplantation in the setting of PVT.

Prevalence and clinical significance of portal vein thrombosis in cirrhotic patients with acute decompensation

Prevalence and clinical significance of portal vein thrombosis in cirrhotic patients with acute decompensation

Protein S for Portal Vein Thrombosis in Cirrhotic Patients Waiting for Liver Transplantation.

Portal vein thrombus (PVT) is a challenge in liver transplantation. How PVT develops in cirrhotic patients who already have coagulopathy is unclear. This study aimed to investigate possible contributing factors to PVT in cirrhotic patients. A total of 349 cirrhotic patients who waited liver transplantation were included in this study and 48 of them had PVT. For all the patients, the mean age was 53.5 ± 9.0 year old, and 75.9% of the patients were male. There were 233 (66.8%) patients who had either hepatitis B or C. The mean Model For End-Stage Liver Disease (MELD) score was 16.4 ± 7.5. Eighteen of 48 patients with PVT and 145 of 301 patients without PVT received liver transplantation. Multivariate analysis showed that low protein S level (hazard ratio = 2.46, p = 0.017) was the only independent risk factor for PVT development. Protein S deficiency also demonstrated prognostic value on short-term survival, not only for cirrhotic patients awaiting liver transplantation (69.9% versus 84.1% at 1 year survival, p = 0.012), but also for the patients having liver transplantation (70.4% versus 84.8% at 1 year survival, p = 0.047). In conclusion, protein S level was an independent risk factor for PVT development in decompensated cirrhotic patients, and protein S deficiency was also a prognostic factor for the patients waiting for liver transplantation.

Systemic inflammation and portal vein thrombosis in cirrhotic patients with gastroesophageal varices.

Cirrhotic patients with gastroesophageal varices and non-tumoral portal vein thrombosis have a higher risk of re-bleeding and poor prognosis. This study aimed to analyze inflammatory biomarkers and thromboelastography in cirrhotic patients with portal vein thrombosis. A total of 385 consecutive cirrhotic patients with gastroesophageal varices were prospectively enrolled between 1 December 2016, and 31 August 2017. Of these, 231 were eligible for analysis and were divided into portal vein thrombosis (n = 103) and non-portal vein thrombosis (n = 128) groups based on computerized tomography angiography findings. Patients with portal vein thrombosis generally had higher Child-Pugh scores than those without portal vein thrombosis (6.38 ± 0.12 vs. 5.81 ± 0.09, P < 0.001). The serum albumin levels were significantly lower in patients with portal vein thrombosis (35.90 ± 0.52 vs. 38.52 ± 0.43, P < 0.001). The portal vein thrombosis group had significant higher serum levels of interleukin 6 [4.85 (3.15-6.99) vs. 3.09 (2.06-5.20) pg/ml, P < 0.001] and tumor necrosis factor alpha [10.70 (7.60-15.20) vs. 9.07 (7.03-11.60) pg/ml, P = 0.020]. The interleukin 6 level was 2.5-fold higher in patients with portal vein thrombosis (adjusted odds ratio: 2.574; 95% confidential interval: 1.248-5.310). Thromboelastography showed that TEG-R, the reaction time, was significantly lower in the portal vein thrombosis group [5.20 (4.80-6.30) vs. 6.00 (5.20-6.95), P = 0.009], indicating enhanced coagulation activity. This study confirmed the important role of systemic inflammation in portal vein thrombosis. Interleukin 6, an important inflammatory cytokine, is independently associated with portal vein thrombosis. The correlation between the interleukin 6 level and portal vein thrombosis requires further investigation.

3:27 PM Abstract No. 320 Management of portal vein thrombosis in cirrhotic patients

To compare the efficacy of transjugular intrahepatic portosystemic shunt (TIPS) to anticoagulation and no treatment in cirrhotic patients with portal vein thrombosis (PVT). This single-center retrospective study evaluated 64 consecutive cirrhotic patients with imaging diagnosis of PVT between November 2005 and July 2019. 15 patients were excluded due to lack of adequate follow-up imaging. Of the remaining 49 patients, 11 (22%) were female. The median age was 61.5 (range, 24-80) years. 9 (18%) patients were treated with TIPS, 12 (24%) with anticoagulation, and 28 (57%) received no treatment. Demographic and clinical data were collected by reviewing the electronic medical record. PVT was evaluated using contrast-enhanced CT or MRI. Thrombus burden in the main portal (MPV), superior mesenteric (SMV), and splenic (SV) vein was graded as follows: grade 1, < 25%; grade 2, 26-50%; grade 3, 51-75%; and grade 4, > 75% of the luminal diameter. Yerdel scoring system was also used to evaluate the extent of portomesenteric thrombus. Thrombus burden at 6 and 12 months was compared to baseline imaging. Patient survival was estimated using Kaplan-Meier analysis. The extent of baseline thrombus was compared using Kruskal-Wallis test. Treatment response was analyzed by chi square test. There was no statistically significant difference in baseline thrombus burden between the 3 groups (MPV, P = 0.345; SMV, P = 0.244; SV, P = 0.541; Yerdel grade, P = 0.230). At 6 months, 87.5%, 58.3%, and 4.8% patients demonstrated complete or partial recanalization in the TIPS, anticoagulation, and no treatment groups respectively (TIPS/no treatment, P <0.0001; TIPS/anticoagulation, P = 0.163). At 12 months, 100%, 57.1%, 11.1% patients demonstrated complete or partial recanalization in the TIPS, anticoagulation, and no treatment groups respectively (TIPS/no treatment, P <0.0001; TIPS/ anticoagulation, P = 0.051). The overall survival between the 3 groups was not significantly different (P = 0.788) TIPS has significantly higher recanalization rate compared to no treatment and has a trend towards higher recanalization rate than that of anticoagulation at 6 and 12 months in cirrhotic patients with PVT.