• Advanced cirrhosis
• Ascites
• D-dimers

• Humans
• Fibrin Fibrinogen Degradation Products/analysis
• Fibrin Fibrinogen Degradation Products/metabolism
• Liver Cirrhosis/blood
• Liver Cirrhosis/complications
• Liver Cirrhosis/diagnosis
• Biomarkers/blood
• Venous Thromboembolism/blood
• Venous Thromboembolism/diagnosis
• Venous Thromboembolism/etiology
• Disseminated Intravascular Coagulation/diagnosis
• Disseminated Intravascular Coagulation/blood
• Disseminated Intravascular Coagulation/etiology

• contrast-enhanced ultrasound
• hepatocellular carcinoma
• portal cavernoma
• portal vein thrombosis
• thrombophilia

• Hepatocellular carcinoma
• Liver transplantation
• Portal vein thrombosis

• anaemia
• cirrhosis
• coagulopathy
• decompensated liver disease
• portal vein thrombosis

• 5-fluorouracil
• Advanced colon cancer
• Cetuximab
• Decompensated cirrhosis
• Portal vein thrombosis

• Humans
• Fluorouracil/adverse effects
• Cetuximab/adverse effects
• Portal Vein
• Positron Emission Tomography Computed Tomography
• Colonic Neoplasms/drug therapy
• Liver Diseases
• Liver Cirrhosis/complications
• Thrombosis

• PZ2023010 Beijing Municipal Administration of Hospitals Incubating Program

• Cirrhosis
• Portal hypertension
• Portal vein recanalization
• Portal vein thrombosis
• TIPS

• Humans
• Portal Vein/surgery
• Portasystemic Shunt, Transjugular Intrahepatic/adverse effects
• Retrospective Studies
• Ascites/drug therapy
• Venous Thrombosis/diagnostic imaging
• Venous Thrombosis/etiology
• Venous Thrombosis/therapy
• Liver Cirrhosis/pathology
• Thrombosis/drug therapy
• Hemorrhage
• Treatment Outcome
• Anticoagulants/adverse effects

• graft failure
• liver transplant
• portal venous thrombosis
• survival

• Budd-Chiari syndrome
• Hepatobiliary cancer
• Pancreatic cancer
• Portal vein thrombosis
• Splanchnic vein thrombosis

• Cirrhosis
• portal vein diameter
• thrombosis

• CT
• Cirrhosis
• Imaging features
• MRI
• Ultrasound

• cirrhosis
• liver transplantation
• portal vein thrombus
• protein S

Portal vein thrombosis (PVT) is a common complication of cirrhosis. However, in patients with PVT and cirrhosis, there is no clear evidence supporting effective treatment modalities. In this study, we examined the effectiveness and safety of anticoagulation therapy using danaparoid sodium for PVT in patients with cirrhosis.

This retrospective study assessed 52 cirrhotic patients with PVT treated with danaparoid sodium for 2 weeks between November 2008 and September 2018. The primary outcome measure was the post-treatment status of PVT assessed by reduction in thrombus volume and safety of the therapeutic intervention. PVT status was evaluated with contrast-enhanced computed tomography (CECT). All patients received 1250 units of danaparoid sodium twice daily by intravenous injection for 14 days. Patients on antithrombin III (AT-III) combination therapy were additionally administered 1500 units of AT-III on days 1–5 and days 8–12. Effectiveness was evaluated by CECT from between days 13 and 18. The secondary outcome measure was the prognosis of PVT.

All patients showed reduction in PVT volume without complications. Return of plasma AT-III level to > 70% during the treatment period contributes to ≥75% reduction of PVT volume. The prognosis in PVT patients depends on hepatic reserve capacity. When limited to Child-Pugh B and C liver cirrhosis patients, a ≥ 75% reduction of PVT volume improved the prognosis.

Danaparoid sodium-based anticoagulation therapy was effective and safe for PVT in patients with cirrhosis. Return of plasma AT-III level to the normal range during the treatment period contributes to reduction of PVT volume. A reduction of ≥75% in PVT volume may improve the prognosis of Child-Pugh B and C decompensated cirrhosis patients with PVT.

• Antithrombin III
• Danaparoid sodium
• Liver cirrhosis
• Portal vein thrombosis

We evaluated the risk factors for posthepatectomy thrombosis including portal vein thrombosis (PVT) and clinical outcomes.

We retrospectively analyzed 563 patients who had undergone hepatectomy from February 2009 to December 2014. Twenty-nine patients with preoperatively confirmed thrombosis and tumor recurrence-related thrombosis were excluded. We identified the location of the thrombosis as main portal vein (MPV), peripheral portal vein (PPV) and other site such as hepatic vein or inferior vena cava. Patients with MPV thrombosis and PPV thrombosis with main portal flow disturbance were treated with anticoagulation therapy. We performed operative thrombectomy before anticoagulation therapy who did combined portal vein (PV) segmental resection.

Of the 534 patients, 22 (4.1%) developed posthepatectomy thrombosis after hepatectomy. Among them, 19 (86.4%) had PVT. The mean duration of Pringle's maneuver was significant longer in the PVT group than the no-thrombosis group (P = 0.020). Patients who underwent combined PV segmental resection during hepatectomy were more likely to develop posthepatectomy PVT (P = 0.001). Thirteen patients who had MPV thrombosis and PPV thrombosis with main portal flow disturbance received anticoagulation therapy immediately after diagnosis and all of them were improved. Among them, 2 patients who developed PVT at the PV anastomosis site after PV segmental resection, underwent operative thrombectomy before anticoagulation therapy and both were improved. There were no patients who developed complications related to anticoagulation therapy.

Long duration of Pringle's maneuver and PV segmental resection were risk factors. Anticoagulation therapy or operative thrombectomy should be considered for PVT without contraindications.

• Hepatectomy
• Portal vein
• Risk factors
• Thrombosis
• Treatment outcome

Portal vein thrombosis (PVT) after liver transplantation (LT) is an uncommon complication with potential for significant morbidity and mortality that transplant providers should be cognizant of. Recognizing subtle changes in post-operative ultrasounds that could herald but do not definitively diagnose PVT is paramount.

A 30-year-old female with a history of alcohol-related cirrhosis presented with painless jaundice and received a deceased donor orthotopic liver transplant. On the first two days post-operatively, her liver Doppler ultrasounds showed a patent portal vein, increased hepatic arterial diastolic flows, and reduced hepatic arterial resistive indices. She was asymptomatic with improving labs. On post-operative day three, her resistive indices declined further, and computed tomography of the abdomen revealed a large extra-hepatic PVT. The patient then underwent emergent percutaneous venography with tissue plasminogen activator administration, angioplasty, and stent placement. Aspirin was started to prevent stent thrombosis. Follow-up ultrasounds showed a patent portal vein and improved hepatic arterial resistive indices. Her graft function improved to normal by discharge. Although decreased hepatic artery resistive indices and increased diastolic flows on ultrasound are often associated with hepatic arterial stenosis post-LT, PVT can also cause these findings.

Reduced hepatic arterial resistive indices on ultrasound can signify PVT post-LT, and thrombolysis, angioplasty, and stent placement are efficacious treatments.

• Portal vein thrombosis
• Portal vein stent
• Liver transplant
• Case report

• Cirrhosis
• Contrast-enhanced ultrasound
• Hepatocellular carcinoma
• Liver
• Malignant
• Portal vein thrombosis
• Ultrasound

• Aged
• Contrast Media
• Diagnosis, Differential
• Female
• Humans
• Image Enhancement/methods
• Male
• Middle Aged
• Portal Vein/diagnostic imaging
• Portal Vein/pathology
• Prospective Studies
• Sensitivity and Specificity
• Ultrasonography/methods
• Venous Thrombosis/diagnostic imaging
• Venous Thrombosis/pathology

To evaluate AngioJet-assisted transvenous portal vein (PV) thrombectomy for non-cirrhotic patients with total portal vein and mesenteric vein thrombosis (PVMVT).

From 2015 to 2016 four patients (3 male, mean 43.9 years, range 33-52 years) with acute (3 cases) and acute-on-chronic (1 case) PVMVT underwent transvenous thrombolysis. All patients received initial AngioJet (Boston Scientific, Natick, MA, USA) thrombectomy followed by continuous catheter directed thrombolysis with Urokinase (Medac, Wedel, Germany) for 22-52 hours. Transjugular intrahepatic portosystemic shunts (TIPS), using Viatorr stent grafts (W.L. Gore and Associates, AZ, USA; mean diameter: 10 mm, length: 60-80 mm), were implanted in all patients. Patients were followed clinically and with imaging (mean 646 days, range 392 to 936 days).

Technical success was 100%. Therapeutic success was achieved in 75% of cases. AngioJet-assisted thrombectomy substantially reduced thrombus load in the acute cases, while only slight improvement was achieved in the acute-on-chronic case. Continuous thrombolysis subtotally re-established PV flow in the acute cases, while only minimal improvement was seen in the acute-on-chronic case. Following TIPS implantation complete PV recanalisation could be achieved in all acute cases. In the acute-on-chronic case initial stagnant PV flow was seen; however, PV and TIPS re-occluded 10 days after implantation. During follow-up PV remained patent in acute cases.

AngioJet-assisted thrombectomy was technically feasible and uncomplicated in all of our patients. The initial results suggest that AngioJet-assisted thrombectomy facilitates recanalisation in acute and severe cases of PVMVT.

• portal vein thrombosis
• thrombectomy
• trans jugular portosystemic shunt

Hepatocellular carcinoma (HCC) is common cancer in ASEAN. Variceal bleeding (VB) is considered to be fatal complication of cirrhosis with HCC. However, limited studies were reported in ASEAN. Aim of this study was to evaluate overall survival rate and predictors of VB in HCC patients.

We conducted a retrospective cohort study of HCC patients aged ≥15 years between January 2012-January 2016 and follow up through June 2016 at Thammasat University Hospital, Thailand. Clinical information and radiologic findings were collected from reviewing computer database of medical records.

333 patients had completely retrievable information. Of which, 27 patients (8.1%) had documented with VB. Clinical presentations with weight loss and jaundice were higher in VB than non-VB groups (40.74% vs. 34.64%, p=0.525 and 7.41% vs. 2.29%, p=0.116) but the differences were not significant. The most common causes of cirrhosis in HCC patients with VB were chronic HBV infection (55.56%). In multivariate analysis; presence of ascites, Child-Pugh score>6, presence of varices were independent risk factors of having VB in HCC patients (OR=7.59, 95%CI=1.13-50.88, p=0.037; OR=5.07, 95%CI=1.08-23.76, p=0.039; OR=23.51, 95%CI=4.71-117.35, p<0.001, respectively). In HCC patients with VB, 1-year and 2.5-year survival rates were 56.6% and 28.3%.

HCC patients with ascites, Child-Pugh score>6 and presence of varices might be important predictive factors of VB. Having VB were greatly impact to the survival rate of HCC patients. Clinical suspicion and regular surveillance of VB in HCC patients at risk could improve treatment outcomes.

• Hepatocellular carcinoma
• variceal bleeding
• Thailand

The oral thrombopoietin (TPO) receptor agonist lusutrombopag (Mulpleta®) was developed to improve thrombocytopenia in patients with chronic liver disease prior to elective invasive medical procedures. Mulpleta® was first approved for use in Japan in 2015 and in the USA in 2018. In the present report, we discuss a case in which pain management was performed during left renal artery embolization via continuous epidural anesthesia following oral administration of lusutrombopag. To our knowledge, this is the first report to discuss the use of lusutrombopag prior to epidural anesthesia.

The patient was a 78-year-old woman scheduled to undergo renal artery embolization to address a 3-cm aneurysm of the left renal artery. Fourteen days prior to the scheduled embolization procedure, the urologist was asked to insert an epidural catheter for perioperative and postoperative analgesia. Type C chronic cirrhosis was observed, and platelet count was 5.6 × 10⁴/μL. Eleven days prior to embolization, oral lusutrombopag was initiated at a dosage of 3 mg/day (day 1). Oral lusutrombopag therapy was continued for 5 days, and platelet count on day 11 (i.e., the day prior to surgery) was 12.6 × 10⁴/μL. An epidural catheter was inserted on day 12, following which embolization was performed. Platelet count on day 13 was 11.0 × 10⁴/μL, and the catheter was removed on day 14. No symptoms of epidural hematoma or thrombosis were observed during the patient’s disease course.

As lusutrombopag is a relatively safe platelet-increasing agent, we believe that this drug can serve as a potential treatment option when performing elective epidural anesthesia in patients with chronic liver disease complicated by thrombocytopenia.

• Epidural anesthesia
• Liver cirrhosis
• Lusutrombopag
• Pain management
• Thrombocytopenia
• Thrombopoietin

• anticoagulation
• coagulation disorder
• hypercoagulable
• venous thrombosis

• D-dimer
• coagulation
• complications
• liver transplant
• thrombosis

• Animals
• Biomedical Research/methods
• Blood Coagulation Tests
• Hemorrhage/blood
• Hemorrhage/diagnosis
• Hemorrhage/epidemiology
• Hemorrhage/therapy
• Hemostasis
• Humans
• Liver/metabolism
• Liver Diseases/blood
• Liver Diseases/diagnosis
• Liver Diseases/epidemiology
• Liver Diseases/therapy
• Prognosis
• Risk Factors
• Thrombosis/blood
• Thrombosis/diagnosis
• Thrombosis/epidemiology
• Thrombosis/therapy

• Contrast-enhanced
• Dynamic contrast-enhanced ultrasound (DCE-US)
• Liver
• Malignant liver lesions
• Microbubbles
• Molecular imaging
• Ultrasound

• Liver Cirrhosis
• Portal Hypertension
• Portal Vein

• Doppler
• Ultrasound
• hepatic artery
• hepatic vein
• liver cirrhosis
• portal vein

To investigate wall shear stress (WSS) magnitude and distribution in cirrhotic patients with portal hypertension using computational fluid dynamics.

Idealized portal vein (PV) system models were reconstructed with different angles of the PV-splenic vein (SV) and superior mesenteric vein (SMV)-SV. Patient-specific models were created according to enhanced computed tomography images. WSS was simulated by using a finite-element analyzer, regarding the blood as a Newtonian fluid and the vessel as a rigid wall. Analysis was carried out to compare the WSS in the portal hypertension group with that in healthy controls.

For the idealized models, WSS in the portal hypertension group (0-10 dyn/cm²) was significantly lower than that in the healthy controls (10-20 dyn/cm²), and low WSS area (0-1 dyn/cm²) only occurred in the left wall of the PV in the portal hypertension group. Different angles of PV-SV and SMV-SV had different effects on the magnitude and distribution of WSS, and low WSS area often occurred in smaller PV-SV angle and larger SMV-SV angle. In the patient-specific models, WSS in the cirrhotic patients with portal hypertension (10.13 ± 1.34 dyn/cm²) was also significantly lower than that in the healthy controls (P < 0.05). Low WSS area often occurred in the junction area of SV and SMV into the PV, in the area of the division of PV into left and right PV, and in the outer wall of the curving SV in the control group. In the cirrhotic patients with portal hypertension, the low WSS area extended to wider levels and the magnitude of WSS reached lower levels, thereby being more prone to disturbed flow occurrence.

Cirrhotic patients with portal hypertension show dramatic hemodynamic changes with lower WSS and greater potential for disturbed flow, representing a possible causative factor of PV thrombosis.

• Portal hypertension
• Wall shear stress
• Portal vein system
• Distribution
• Disturbed flow

• Adult
• Case-Control Studies
• Computer Simulation
• Female
• Finite Element Analysis
• Hemodynamics
• Humans
• Hydrodynamics
• Hypertension, Portal/physiopathology
• Liver Cirrhosis/complications
• Male
• Mesenteric Veins/physiopathology
• Middle Aged
• Portal Vein/physiopathology
• Shear Strength
• Splenic Vein/physiopathology
• Stress, Mechanical
• Tomography, X-Ray Computed
• Venous Thrombosis/complications

AIM: To evaluate the clinical efficacy of agitation thrombolysis via transjugular access for the treatment of acute portal vein thrombosis.

METHODS: Thirteen patients with acute portal vein thrombosis treated from October 2012 to March 2015 at our hospital were analyzed retrospectively. The portal vein was approached via the transjugular intrahepatic portosystemic route, followed by agitation thrombolysis to resolve the thrombi. The need for transjugular intrahepatic portosystemic shunt (TIPS) was based on the presence of portal hypertension, and then a catheter was indwelled into the thrombi. The success rate, thrombolytic therapeutic time and effect, and complications were observed. Computed tomography and Doppler ultrasound were performed to follow the patency of the portal vein and TIPS stent.

RESULTS: Agitation thrombolysis were successfully created in 12 patients. Of 8 patients who underwent TIPS, 1 underwent wide resection due to confirmed extensive intestinal necrosis on postoperative day 2; however, the patient died 9 d later. In the remaining 11 patients, the portal vein was recanalized > 90% as revealed by CT findings. There was a significant difference in lumen occupancy between pre- and post-operation (P < 0.01). The clinical symptoms such as abdominal pain, ascites, and gastrointestinal bleeding were all relieved or disappeared. The complications were mainly as follows: intraoperative subcapsular bleeding in one patient; death due to intestinal necrosis in one patient; hepatic encephalopathy at 3 mo in one patient with TIPS; and hematuria during thrombolysis in one patient. During follow-up, TIPS stent stenosis was noted in one patient at 7 mo and treated by balloon angioplasty.

CONCLUSION: Agitation thrombolysis via transjugular access for the treatment of acute portal vein thrombosis is safe and effective.

• Portal vein thrombosis
• Agitation thrombolysis
• Transjugular access

• Bleeding
• Cirrhosis
• Hemostasis
• Thrombosis

• Anticoagulants/therapeutic use
• Blood Coagulation Tests
• Coagulants/therapeutic use
• Drug Monitoring
• Esophageal and Gastric Varices/etiology
• Gastrointestinal Hemorrhage/prevention & control
• Hemostasis
• Humans
• Liver Cirrhosis/complications
• Liver Cirrhosis/physiopathology
• Postoperative Hemorrhage/prevention & control
• Thrombosis/prevention & control

• Hepatocellular carcinoma
• Homocysteine
• MTHFR status
• Portal vein thrombosis
• Thrombophilia

• Endoscopic Treatment
• Esophageal Varices
• Iran
• Liver Cirrhosis
• Liver Transplantation
• Portal Vein Thrombosis
• Risk Factors

AIM: To determine the clinical impact of portal vein thrombosis in terms of both mortality and hepatic decompensations (variceal hemorrhage, ascites, portosystemic encephalopathy) in adult patients with cirrhosis.

METHODS: We identified original articles reported through February 2015 in MEDLINE, Scopus, Science Citation Index, AMED, the Cochrane Library, and relevant examples available in the grey literature. Two independent reviewers screened all citations for inclusion criteria and extracted summary data. Random effects odds ratios were calculated to obtain aggregate estimates of effect size across included studies, with 95%CI.

RESULTS: A total of 226 citations were identified and reviewed, and 3 studies with 2436 participants were included in the meta-analysis of summary effect. Patients with portal vein thrombosis had an increased risk of mortality (OR = 1.62, 95%CI: 1.11-2.36, P = 0.01). Portal vein thrombosis was associated with an increased risk of ascites (OR = 2.52, 95%CI: 1.63-3.89, P < 0.001). There was insufficient data available to determine the pooled effect on other markers of decompensation including gastroesophageal variceal bleeding or hepatic encephalopathy.

CONCLUSION: Portal vein thrombosis appears to increase mortality and ascites, however, the relatively small number of included studies limits more generalizable conclusions. More trials with a direct comparison group are needed.

• Hepatology
• Coagulopathy
• Liver
• Ascites
• Hepatic encephalopathy
• Portal hypertension

• T32 CA163177 NCI NIH HHS
• T32 DK007769 NIDDK NIH HHS

• Algorithm
• Anticoagulation
• Cirrhosis
• Portal vein thrombosis
• Therapy
• Transjugular shunt

Acute thrombosis of the portal vein (PV) and/or the mesenteric vein (MV) is a rare but potentially life-threatening disease. A multitude of risk factors for acute portal vein thrombosis (PVT)/mesenteric vein thrombosis (MVT) have been identified, including liver cirrhosis, malignancy, coagulation disorders, intra-abdominal infection/inflammation, and postoperative condition.

This article analyses the treatment options for acute PVT/MVT.

Initially, the clinical management should identify patients with an intra-abdominal focus requiring immediate surgical intervention (e.g. bowel ischaemia). Subsequently, emphasis is placed on the recanalization of the PV/MV or at least the prevention of thrombus extension to avoid long-term complications of portal hypertension. Several therapeutic options are currently available, including anticoagulation therapy, local/systemic thrombolysis, interventional or surgical thrombectomy, and a combination of these procedures. Due to the lack of prospective randomized studies, a comparison between these therapeutic approaches regarding the efficacy of PV/MV recanalization is difficult, if not impossible.

In patients with acute PVT/MVT, an individualized treatment based on the clinical presentation, the underlying disease, the extent of the thrombosis, and the patients' comorbidities is mandatory. Therefore, these patients should be considered for an interdisciplinary therapy in specialized centres with the option to utilise all therapeutic approaches currently available.

• Intervention
• Portal/mesenteric vein thrombosis
• Recanalization
• Surgery

• diagnosis
• etiology
• predict
• portal hypertension

• Adult
• Aged
• Case-Control Studies
• Cohort Studies
• Female
• Fibrin Fibrinogen Degradation Products/metabolism
• Humans
• Liver Cirrhosis/blood
• Liver Cirrhosis/complications
• Liver Cirrhosis/diagnosis
• Liver Cirrhosis/pathology
• Male
• Middle Aged
• Portal Vein/pathology
• Postoperative Period
• Venous Thrombosis/blood
• Venous Thrombosis/diagnosis
• Venous Thrombosis/etiology
• Venous Thrombosis/pathology

Portal vein thrombosis (PVT) is not uncommon in patients with liver cirrhosis, and it increases the risk of gastroesophageal hemorrhage. At present, pharmacological treatment is the preferred selection of management of PVT. Studies have shown that anticoagulation therapy does not increase the risk of gastrointestinal bleeding. Therefore, patients having indications should be given anticoagulation therapy as early as possible. When patients fail to respond to anticoagulation therapy, interventional therapy or surgery may be considered. This article reviews the recent knowledge about the treatment of PVT and discusses the progress in treatment of nontumoral PVT in liver cirrhosis.

• Portal vein thrombosis
• Cirrhosis
• Anticoagulation treatment
• Interventional therapy

• Cirrhosis
• Malignancy
• Myeloproliferative neoplasm
• Portal vein thrombosis
• Thrombophilia

Hepatic encephalopathy (HE) is a cognitive disturbance characterized by neuropsychiatric alterations. It occurs in acute and chronic hepatic disease and also in patients with portosystemic shunts. The presence of these portosystemic shunts allows the passage of nitrogenous substances from the intestines through systemic veins without liver depuration. Therefore, the embolization of these shunts has been performed to control HE manifestations, but the presence of portal vein thrombosis is considered a contraindication. In this presentation we show a cirrhotic patient with severe HE and portal vein thrombosis who was submitted to embolization of a large portosystemic shunt. Case report: a 57 years-old cirrhotic patient who had been hospitalized many times for persistent HE and hepatic coma, even without precipitant factors. She had a wide portosystemic shunt and also portal vein thrombosis. The abdominal angiography confirmed the splenorenal shunt and showed other shunts. The larger shunt was embolized through placement of microcoils, and the patient had no recurrence of overt HE. There was a little increase of esophageal and gastric varices, but no endoscopic treatment was needed. Since portosystemic shunts are frequent causes of recurrent HE in cirrhotic patients, portal vein thrombosis should be considered a relative contraindication to perform a shunt embolization. However, in particular cases with many shunts and severe HE, we found that one of these shunts can be safely embolized and this procedure can be sufficient to obtain a good HE recovery. In conclusion, we reported a case of persistent HE due to a wide portosystemic shunt associated with portal vein thrombosis. As the patient had other shunts, she was successfully treated by embolization of the larger shunt.

• Recurrent hepatic encephalopathy
• Liver cirrhosis
• Port systemic shunt
• Shunt embolization
• Portal vein thrombosis

• Embolization, Therapeutic/methods
• Female
• Hepatic Encephalopathy/diagnosis
• Hepatic Encephalopathy/etiology
• Hepatic Encephalopathy/physiopathology
• Hepatic Encephalopathy/therapy
• Humans
• Liver Circulation
• Liver Cirrhosis/complications
• Liver Cirrhosis/diagnosis
• Middle Aged
• Phlebography
• Portal Pressure
• Portal Vein/diagnostic imaging
• Portal Vein/physiopathology
• Recurrence
• Splenic Vein/diagnostic imaging
• Splenic Vein/physiopathology
• Treatment Outcome
• Venous Thrombosis/diagnosis
• Venous Thrombosis/etiology
• Venous Thrombosis/physiopathology

• Liver cirrhosis
• Nadolol
• Non-selective β-blockers
• Portal vein thrombosis
• Propranolol

• Adrenergic beta-Antagonists/adverse effects
• Blood Flow Velocity/drug effects
• Humans
• Liver Circulation/drug effects
• Liver Cirrhosis/complications
• Liver Cirrhosis/drug therapy
• Liver Cirrhosis/physiopathology
• Portal Vein/drug effects
• Portal Vein/physiopathology
• Regional Blood Flow/drug effects
• Risk Assessment
• Risk Factors
• Venous Thrombosis/chemically induced
• Venous Thrombosis/physiopathology