Surgical treatment of a large portopulmonary venous anastomosis in a patient with portal vein thrombosis.
Ontology highlight
ABSTRACT:
SUBMITTER: Ochi T
PROVIDER: S-EPMC10859668 | biostudies-literature | 2024 Feb
REPOSITORIES: biostudies-literature
Publications
Surgical treatment of a large portopulmonary venous anastomosis in a patient with portal vein thrombosis.
Ochi Takahiro T Sakairi Yuichi Y Yusa Jotaro J Sata Yuki Y Toyoda Takahide T Inage Terunaga T Tanaka Kazuhisa K Suzuki Hidemi H Ota Joji J Kondo Takayuki T Kato Naoya N Yoshino Ichiro I
JTCVS techniques 20231213
Similar Datasets
Project description:Portal vein thrombosis is an important cause of portal hypertension. PVT occurs in association with cirrhosis or as a result of malignant invasion by hepatocellular carcinoma or even in the absence of associated liver disease. With the current research into its genesis, majority now have an underlying prothrombotic state detectable. Endothelial activation and stagnant portal blood flow also contribute to formation of the thrombus. Acute non-cirrhotic PVT, chronic PVT (EHPVO), and portal vein thrombosis in cirrhosis are the three main variants of portal vein thrombosis with varying etiological factors and variability in presentation and management. Procoagulant state should be actively investigated. Anticoagulation is the mainstay of therapy for acute non-cirrhotic PVT, with supporting evidence for its use in cirrhotic population as well. Chronic PVT (EHPVO) on the other hand requires the management of portal hypertension as such and with role for anticoagulation in the setting of underlying prothrombotic state, however data is awaited in those with no underlying prothrombotic states. TIPS and liver transplant may be feasible even in the setting of PVT however proper selection of candidates and type of surgery is warranted. Thrombolysis and thrombectomy have some role. TARE is a new modality for management of HCC with portal vein invasion.
| S-EPMC4415192 | biostudies-other
Project description:BackgroundPortal vein thrombosis (PVT) and venous thromboembolism (VTE) are fearsome complications of liver cirrhosis.ObjectivesTo assess the prevalence and the main risk factors for venous thrombotic complications in hospitalized cirrhotic patients.Patients/methodsWe retrospectively reviewed electronic administrative discharge data of 19461 cirrhotic patients hospitalized over a 35-year period; univariate and multivariate logistic regression was used to asses risk factors for PVT or VTE and their impact on hospital stay and mortality.Results382 out of 7445 patients (5.1%) were diagnosed with PVT and 95 (1.3%) with VTE. Liver cirrhosis complications were observed in 45% of patients. Hepatic encephalopathy (HE) (OR 13.88 [10.76-17.98] p < 0.0001), endoscopic signs of portal hypertension (OR 1.33 [1.02-1.75] p = 0.02), hepatocellular carcinoma (HCC) (OR 4.59 [3.6-5.84] p < 0.0001), diabetes (OR 1.68 [1.27-2.22] p = 0.0001), abdominal surgery/invasive procedures (OR 2.03 [1.56-2.64] p < 0.0001) emerged as independent predictors of PVT. Higher risk of VTE was observed in patients with HE (OR 3.21 [1.78-5.79] p < 0.0001), HCC (OR 1.98 [1.23-3.19] p = 0.002) or other tumors (OR 2.48 [1.42-4.32] p = 0.001), acute illnesses (infections OR 3.01 [1.84-5.05] p = 0.0001; cardiac/respiratory insufficiency OR 2.4 [1.27-4.53] p = 0.003; acute myocardial infarction/stroke OR 7.86 [1.76-35.12] p = 0.003). VTE was the only independent predictor of in-hospital mortality (OR 4.45 [1.05-18.81] p = 0.042).ConclusionsLiver disease complications related to portal hypertension, HCC or other tumors, diabetes, acute illnesses (i.e. infections, cardiac/pulmonary insufficiency, acute myocardial infarction/stroke) and abdominal interventions are associated with increased risk of PVT or VTE in hospitalized cirrhotic patients, and should be considered to define personalized preemptive approaches.
| S-EPMC9352602 | biostudies-literature
Project description:BackgroundThere are concerns about a link between the ChAdOx1 nCoV-19 and Ad26.COV2.S vaccines against COVID-19 and cerebral venous thrombosis (CVT) and other thrombotic events. One key missing component of the risk-benefit analysis of using such vaccines is the risk of these severe thrombotic events following COVID-19.MethodsUsing a retrospective cohort study based on electronic health records primarily in the USA, the absolute risks of CVT and portal vein thrombosis (PVT) in the two weeks following a diagnosis of COVID-19 (made between January 20, 2020 and March 25, 2021) were calculated. The risks were compared to cohorts of patients with influenza (diagnosed within the same period) and people receiving an mRNA vaccine (i.e. not the ChAdOx1 nCoV-19 and Ad26.COV2.S vaccines) against COVID-19 (matched for demographics and the main risk factors for CVT and PVT).FindingsA total of 537,913 patients with a COVID-19 diagnosis were included. The incidence of CVT in the two weeks after a COVID-19 diagnosis was 42.8 per million people (95% CI 28.5-64.2). This was significantly higher than in a matched cohort of people who received an mRNA vaccine (RR = 6.33, 95% CI 1.87-21.40, P = 0.00014) and patients with influenza (RR = 2.67, 95% CI 1.04-6.81, P = 0.031). The incidence of PVT after COVID-19 diagnosis was 392.3 per million people (95% CI 342.8-448.9). This was significantly higher than in a matched cohort of people who received an mRNA vaccine (RR=4.46, 95% CI 3.12-6.37, P < 0.0001) and patients with influenza (RR=1.43, 95% CI 1.10-1.88, P = 0.0094).
| S-EPMC8324974 | biostudies-literature
Project description:To construct a stable rat portal vein thrombosis (PVT) model and explore the time window of urokinase thrombolytic therapy on this basis. Constructing a rat PVT model by combining anhydrous ethanol disruption of portal endothelium with stasis of blood flow. Forty-eight rats after PVT modeling were divided into control group and experimental group, with 24 rats in each group. The experimental and control groups were given urokinase treatment and saline tail vein injection, respectively. The two groups of rats were observed and compared for PVT formation at 1, 3 and 5 days after modeling, respectively. A stable rat PVT model was successfully constructed. No significant differences were found in PVT length, portal vein wet weight, and percentage of luminal occlusion area in the control rats at 1, 3, and 5 days after successful modeling (P > 0.05). Compared with control rats 1 day after modeling, the percentage of non-organized thrombus luminal area was significantly decreased (P < 0.0001), and the percentage of organized thrombus luminal area was significantly increased (P < 0.0001) in the PVTs of control rats at 3 and 5 days after modeling. After thrombolytic treatment with urokinase, plasma fibrinogen (FBG) levels were significantly decreased in the experimental group of rats compared with the control group (P < 0.0001), and plasma D-dimer (D2D) levels were significantly increased in the experimental group of rats compared with the control group (P < 0.0001). In addition, we observed prolongation of prothrombin time (PT) in the experimental group at 1, 3 and 5 days after modeling compared to the control group (P = 0.0001). Compared with the control group, portal vein wet weight and PVT length were significantly decreased in the experimental group of rats at 1 day after modeling (P < 0.05), whereas these differences were not found in the two groups of rats at 3 and 5 days after modeling (P > 0.05). The percentage of non-organized thrombus area in the experimental group was significantly decreased compared with that in the control group at 1, 3, and 5 days after modeling (P < 0.05), whereas there was no significant difference in the percentage of lumen area of organized thrombus between the two groups (P > 0.05). The method of producing a rat PVT model by destroying the endothelium of the portal vein by anhydrous ethanol combined with blood flow stasis is feasible and reproducible. In addition, the optimal time window for thrombolysis in the treatment of PVT in rats using urokinase is the early stage of thrombosis, when the fibrin content is highest.
| S-EPMC11296622 | biostudies-literature
Project description:ObjectiveSplenectomy is one crucial solution for hypersplenism with portal hypertension. However, portal vein system thrombosis (PVST) caused by hemodynamic changes affects the prognosis of patients. We analyze the changes in portal vein hemodynamics following splenectomy for Wilson's disease combined with portal hypertension and the influencing factors that lead to PVST.MethodsA retrospective cohort study was conducted, in which 237 Wilson's disease patients with hypersplenism underwent splenectomy. The hemodynamic indices of the portal vein were monitored before surgery and on the 1st, 7th, and 14th days around surgery. The patients were divided into PVST and non-PVST groups. The clinical factors were identified by univariate and multivariate logistic regression. The Logit P was calculated according to the logistic regression prediction model, and the ROC curve for each independent factor was plotted.ResultsThe portal vein velocity, flow, and inner diameter showed a downward trend around surgery, with statistically significant differences between each time point (P < 0.01). The PVST incidence rate was 55.7%. Univariate analysis revealed that the platelet (PLT) levels on the postoperative 3rd and 7th days (P = 0.001; P < 0.001), D-dimer (D-D) on the postoperative 7th and 14th days (P = 0.002; P < 0.001), preoperative portal vein velocity, flow, diameter (P < 0.001), and splenic vein diameter (P < 0.001) were all statistically and significantly different between the two groups. Multivariate logistic regression revealed a significant increase in PLT on the postoperative 7th day (OR = 1.043, 95% CI, 1.027-1.060, P < 0.001) and D-D on the postoperative 14th day (OR = 1.846, 95% CI, 1.400-2.435, P < 0.001). Preoperative portal and splenic vein diameters (OR = 1.565, 95% CI, 1.213-2.019, P = 0.001; OR = 1.671, 95% CI, 1.305-2.140, P < 0.001) were the risk factors for PVST. However, preoperative portal vein velocity and flow (OR = 0.578, 95% CI, 0.409-0.818, P = 0.002; OR = 0.987, 95% CI, 0.975-0.990, P = 0.046) were protective factors for PVST. Logit P was calculated using a logistic regression prediction model with a cut-off value of -0.32 and an area under receiver operating characteristic curve of 0.952 with 88.61% accuracy.ConclusionsSplenectomy relieves portal hypertension by reducing the hemodynamics index. PVST is linked to multiple factors, including preoperative portal vein diameter, velocity, flow, and splenic vein diameter, especially PLT on the postoperative 7th day and D-D on the postoperative 14th day. The predictive model is accurate in predicting PVST.
| S-EPMC9189385 | biostudies-literature
Project description:Surgical strategies for graft portal vein flow restoration vary from termino-terminal portal vein anastomosis to more complex bypass reconstructions. Although the surgical strategy strongly influences the post-operative outcome, the Yerdel grading is still commonly used to determine the prognosis of patients with portal vein thrombosis (PVT) undergoing liver transplantation (LT). We retrospectively reviewed the cases of LT performed on recipients with complex PVT at two high-volume transplantation centres. We stratified the patients by the type of portal vein reconstruction, termino-terminal portal vein anastomosis (TTA) versus bypass reconstruction (bypass group), and assessed a multivariable survival analysis. The rate of mortality at 90 days was 21.4% for the bypass group compared to 9.8% in the TTA group (p = 0.05). In the multivariable correlation analysis, only a trend for greater risk of early mortality was confirmed in the bypass groups (HR 2.5; p = 0.059). Yerdel grade was uninfluential in the rate of early complications. A wide range of surgical options are available for different situations of PVT which yield an outcome unrelated to the Yerdel grading. An algorithm for PVT management should be based on the technical approach and should include a surgically oriented definition of PVT extension.
| S-EPMC10095520 | biostudies-literature
Project description:There are several conditions that can lead to portal vein thrombosis (PVT), including including infection, malignancies, and coagulation disorders. Anew condition of interest is protein C and S deficiencies, associated with hypercoagulation and recurrent venous thromboembolism. We report the case of a non-cirrhotic 63-year-old male diagnosed with acute superior mesenteric vein thrombosis and PVT and combined deficiencies in proteins C and S, recanalized by short-term low molecular heparin plus oral warfarin therapy.
| S-EPMC4110546 | biostudies-literature
Project description:Portal vein thrombosis (PVT) is associated with inferior pretransplantation and posttransplantation outcomes. We aimed to create a predictive model to risk stratify transplant candidates for PVT. Data on adult transplants in the United States during the Model for End-Stage Liver Disease (MELD) era through September 2016 were reviewed. We constructed and validated a scoring system composed of routine, readily available clinical information to predict the development of incident PVT at 12 months from transplantation listing. A total of 66,568 liver transplant candidates were dichotomized into 2 groups to construct (n = 34,751) and validate (n = 31,817) a scoring system. In general, the derivation and validation cohorts were clinically similar. Although nonalcoholic steatohepatitis was a significant predictor of incident PVT (hazard ratio, 1.29; 95% confidence interval, 1.08-1.54; P < 0.001), age, MELD score, and moderate-to-severe ascites were also associated with increased risk. African American race was associated with decreased risk. A scoring system (PVT risk index [RI]) of these 5 variables had an area under the curve of 0.71 and 0.70 in both derivation and validation cohorts, respectively. By applying the low cutoff score of 2.6, incident PVT could be accurately excluded (negative predictive value 94%). Using the high cutoff score of 4.6 (positive predictive value 85%), PVT could be diagnosed with high accuracy. The PVT-RI predicts which candidates awaiting lifesaving liver transplantation will and will not develop future PVT. Although this scoring system will require prospective validation, it provides a powerful new tool for the clinician when risk stratifying cirrhosis patients prior to liver transplantation for future PVT development.
| S-EPMC6864229 | biostudies-literature
Project description:Portal vein tumor thrombosis is a strong poor indication of HCC. Characterizing the molecular alterations of these metastatic HCCs is important for understanding the molecular mechanisms during HCC progression and metastasis. Previous genomic studies mainly focus on single molecular layer, such as gene expressions or exonic mutations. In this study, we systematically examined the copy number variation (CNV), DNA methylation, miRNA and transcriptome of matched adjacent normal tissues, primary tumors and PVTTs from 19 HCC patients. Based on the integrative multi-omics profiles, we established the molecular landscape of the metastatic HCCs and identified a set of the recurrent genomic alterations and candidate driver genes.
2017-02-17 | GSE77275 | GEO
Project description:Portal vein thrombosis (PVT) is an uncommon, but potentially devastating complication of portal vein embolization (PVE). Its occurrence relates to both local and systemic risk factors. In the setting of PVE, precipitating factors include injury to the vessel wall and reduced portal flow. Contributory factors include portal hypertension, hypercoagulopathy, inflammatory processes, malignancy, pregnancy, oral contraceptive use, and asplenia. The goal of therapy is to prevent thrombus progression and lyse existing clot. Hepatectomy is impossible if adequate recanalization has not occurred and/or overt portal hypertension develops. The mechanisms for thrombus development, its diagnosis, management, and prognosis are discussed.
| S-EPMC3193332 | biostudies-other