Review article: portal vein thrombosis - new insights into aetiology and management (original) (raw)
Related papers
Portal vein thrombosis: A concise review (Review)
Experimental and Therapeutic Medicine, 2021
Portal vein thrombosis (PVT) is a frequent complication in cirrhotic patients, but it may also exist as a basic vascular condition even without any liver damage. Local and systemic factors play a significant role in the pathogenesis of PVT; yet, in practice, more than one factor may be identified. PVT can be considered a result of liver fibrosis and hepatic insufficiency. The JAK2 mutation has been accepted as a factor producing PVT. In general, the anticoagulants are recommended but this therapy should be used carefully in treating patients that associate coagulopathy or thrombocytopenia and esophageal varices. Acute PVT without bowel infarction has a good prognosis. In liver cirrhosis, the mortality due to hemorrhage is higher than in chronic PVT. Therefore, for the patients with PVT, the survival rate is decreased by 55% in two years, due to hepatic insufficiency. Regarding the treatment, LMWH (low molecular weight heparine) is the most utilized in patients with cirrhosis, non-malignancies, infections, or those who are awaiting a liver transplant. DOACs (direct-acting oral anticoagulants) may be used in the rest of the medical conditions, being safe and equal to LMWH.
Acute portal vein thrombosis unrelated to cirrhosis: A prospective multicenter follow-up study
Hepatology, 2010
Current recommendations for early anticoagulation in acute portal vein thrombosis unrelated to cirrhosis or malignancy are based on limited evidence. The aim of this study was to prospectively assess the risk factors, outcome, and prognosis in patients managed according to these recommendations. We enrolled 102 patients with acute thrombosis of the portal vein, or its left or right branch. Laboratory investigations for prothrombotic factors were centralized. Thrombus extension and recanalization were assessed by expert radiologists. A local risk factor was identified in 21% of patients, and one or several general prothrombotic conditions in 52%. Anticoagulation was given to 95 patients. After a median of 234 days, the portal vein and its left or right branch were patent in 39% of anticoagulated patients (versus 13% initially), the splenic vein in 80% (versus 57% initially), and the superior mesenteric vein in 73% (versus 42% initially). Failure to recanalize the portal vein was independently related to the presence of ascites (hazard ratio 3.8, 95% confidence interval 1.3-11.1) and an occluded splenic vein (hazard ratio 3.5, 95% confidence interval 1.
Portal vein thrombosis; risk factors, clinical presentation and treatment
BMC Gastroenterology, 2007
Background: Portal vein thrombosis (PVT) is increasingly frequently being diagnosed, but systematic descriptions of the natural history and clinical handling of the condition are sparse. The aim of this retrospective study was to describe risk factors, clinical presentation, complications and treatment of portal vein thrombosis in a single-centre.
Portal vein thrombosis: Insight into physiopathology, diagnosis, and treatment
World Journal of Gastroenterology, 2010
Portal vein thrombosis (PVT) is a relatively common complication in patients with liver cirrhosis, but might also occur in absence of an overt liver disease. Several causes, either local or systemic, might play an important role in PVT pathogenesis. Frequently, more than one risk factor could be identified; however, occasionally no single factor is discernable. Clinical examination, laboratory investigations, and imaging are helpful to provide a quick diagnosis, as prompt treatment might greatly affect a patient's outcome. In this review, we analyze the physiopathological mechanisms of PVT development, together with the hemodynamic and functional alterations related to this condition. Moreover, we describe the principal factors most frequently involved in PVT development and the recent knowledge concerning diagnostic and therapeutic procedures. Finally, we analyze the implications of PVT in the setting of liver transplantation and its possible influence on patients' future prognoses.
Background and objectives: Portal vein thrombosis (PVT) is an increasingly recognized complication of liver cirrhosis. It is associated with worsening liver function, ascites and the occurrence of gastroesophageal variceal bleeding. The aim of this work was to clarify the risk factors, clinical presentation and complications of portal vein thrombosis in Egyptian patients with liver cirrhosis and to study the outcome with and without treatment after 6 months follow up period. Methods: Hospitalized cirrhotic patients (N = 80) were segregated into the PVT and non-PVT groups. PVT was detected by Doppler ultrasonography; each group was divided in two sub groups (A and B) according to presence or absence of HCC respectively. The 2 groups were compared as regards risk factors, clinical presentation and complications. The outcome of treatment with anticoagulation in 6 patients was evaluated. Result: PVT developed as result of combination of both local and systemic risk factors. HCC, abdominal infection especially spontaneous bacterial peritonitis and abdominal intervention were the most important local risk factors. Abnormalities of coagulation system were among systemic risk factors. Most of cases were asymptomatic and accidentally discovered, others presented with upper GIT bleeding or other complications of liver cell failure. Anticoagulant administration was associated with increased incidence of partial or complete recanalization and less mortality without increased risk of bleeding. Conclusion and Recommendations: Portal vein thrombosis occurs mostly in cirrhotic patients with advanced liver disease. HCC is the most common local risk factor in our country. Patients with less prolonged coagulation parameters might be at particular risk for developing PVT, so regular monitoring using Doppler-ultrasound should be carried out in these patients. Development of varices is a time dependent phenomenon; it is advisable to screen all PVT patients endoscopically. Owing to decrease complications, early administration of anticoagulation is advised in selected cases.
Portal vein thrombosis in cirrhosis: diagnosis, natural history, and therapeutic challenges
Annals of gastroenterology
Portal vein thrombosis (PVT) is a frequent complication in cirrhosis and its prevalence increases with disease severity. Several factors are involved in the development and progression of PVT. The challenge for the management of PVT is the precise evaluation of the bleeding risk as opposed to life-threatening extension of thrombosis. Nevertheless, the impact on the progression and outcome of liver disease is unclear. A critical evaluation of the available data discloses that treating PVT in cirrhotics is safe and effective. However, there are open issues, such as which anticoagulant could represent a safer therapeutic option, and when and for how long this treatment should be administered to cirrhotic patients with PVT.
Non Cirrhotic Portal Vein Thrombosis: Diagnostic and Therapeutic Challenge
The Indonesian Journal of Gastroenterology, Hepatology, and Digestive Endoscopy
Portal vein thrombosis (PVT), the second most common cause of portal hypertension, can be found in cirrhosis and non-cirrhosis patients. Various factors can cause non-cirrhosis PVT, such as biliary infection. Upper gastrointestinal bleeding without sign of liver failure, must be considered as non-cirrhosis PVT manifestation. Combining physical, laboratory, endoscopic and radiological examination is needed to establish the diagnosis of PVT. The principle of PVT management consists of 3 keypoints. They are prevention and treatment of gastrointestinal bleeding, prevention of recurrent thrombosis and portal cholangiopathy therapy. Many aspect should be considered regarding the administration of anticoagulants in PVT patients, especially chronic PVT with cavernomas.
Portal vein thrombosis in cirrhosis with variceal hemorrhage
Journal of Gastrointestinal Surgery, 1997
Organized thrombus in the main tnmk of the portal vein was encountered in 85 (6.5%) of 1300 patients with cirrhosis and variceal hemorrhage who underwent direct portacaval shunt (PCS). The thrombus was successfully removed with restoration of portal blood flow in all patients by phlebothrombectomy and balloon catheter extraction. Of the 85 patients, 65 were among 400 unselected patients who underwent emergency PCS (16%), and 20 were among 900 selected patients who underwent elective PCS (2%). All patients were closely followed for at least 5 years. Patients with portal vein thrombosis (PVT) had more advanced liver disease than those without PVT, reflected preoperatively in significantly higher (P <0.01) incidences of ascites (75%), severe muscle wasting (52 %), varices of very large size (94%), the hyperdynamic state (94%), severe hypersplenism with a platelet count of less than 50,000/mm 3 (92%), and placement in Child's class C (52%). Side-to-side PCS reduced the portal vein-inferior vena cava pressure gradient to a mean of 23 mm saline solution in patients with PVT, similar to the marked pressure reduction obtained in patients without PVT. PCS promptly stopped variceal bleeding in all patients in the emergency PCS group. Permanent prevention of recurrent variceal bleeding was successful in 95% of patients with PVT and more than 99% of patients without PVT. Survival rates were similar in patients with and without PV-E In patients with PVT, survival rates at 30 days and 1, 5, 10, and 15 years following emergency PCS were 69%, 66%, 65%, 55 %, and 51%, respectively, and following elective PCS were 95%, 90%, 70%, 65%, and 60%, respectively. Quality of life was similar in patients with and without PVT. Long-term PCS patency was demonstrated yearly in 93% of patients in the group with PVT and in 99.7% of patients without PVT. Other similarities after 5 years between patients with and without PVT, respectively, were the incidences of recurrent encephalopathy (9% vs. 8%), alcohol abstinence (61% vs. 64%), improved liver function (68% vs. 62% to 75%), and return to work (52% vs. 56% to 64%). It was concluded that in patients with cirrhosis and variceal hemorrhage it is almost always possible to remove portal vein thrombus by means of phlebothrombectomy and then perform a direct PCS with results similar to those achieved in the absence of PVT.
Systemic thrombolysis of portal vein thrombosis in cirrhotic patients: A pilot study
Digestive and Liver Disease, 2010
Background: Portal vein thrombosis is a frequent complication in liver cirrhosis. Encouraging reports of systemic thrombolysis in non-cirrhotic patients suffering from acute portal vein thrombosis led us to start a pilot study on the efficacy and safety of systemic low dose recombinant tissue plasminogen activator (Actilyse ® , Boheringer Ingelheim, Florence, Italy). Patients: Nine cirrhotic patients (6 males and 3 females) with recent portal vein thrombosis were enrolled. Exclusion criteria were portal cavernomatosis, recent (30 days) surgery, active bleeding, hepatocellular carcinoma and cancer in other sites. Methods: All cases were treated for a maximum of 7 days by continuous i.v. infusion of 0.25 mg/kg/die of r-tPA plus subcutaneous low molecular weight heparin. Efficacy was evaluated by colour doppler sonography monitoring and confirmed by contrast enhanced computerized tomography. Results: The combined r-tPA/LMWH treatment was well tolerated without clinically significant side effects. Complete resolution of thrombosis occurred in 4 cases, partial regression in 4 and none in 1. Retreatment of a complete recurrence in 1 patient was successful. Variceal pressure dropped from 30.7 ± 4.5 mmHg to 21.2 ± 6.6 mmHg (p = 0.012). Conclusions: Our preliminary data demonstrate that thrombolytic treatment of recent portal vein thrombosis with i.v. r-tPA and LMWH in patients with cirrhosis appears to be safe and effective and can significantly reduce pressure in oesophageal varices.
Hepatology, 2016
In patients with chronic noncirrhotic, nontumoral portal vein thrombosis (PVT), the usually recommended strategy for endoscopic screening and management of varices is the same as in cirrhosis. However, the efficacy of this policy in patients with PVT is unknown. We assessed the course of gastroesophageal varices in a large cohort of patients with chronic PVT. Patients prospectively registered in two referral centers for vascular liver disorders were eligible for the study. Endpoints were development and growth of varices and the incidence and outcome of portal hypertension‐related bleeding. Included were 178 patients with chronic PVT. Median follow‐up was 49 (1‐598) months. Variceal bleeding was the initial manifestation in 27 (15%) patients. Initial endoscopy in the remaining 151 patients showed no varices in 52 (34%), small esophageal varices in 28 (19%), large esophageal varices (LEVs) in 60 (40%), and gastric varices without LEVs in 11 (7%). Ascites and splenomegaly were indepen...