Management of Portal/Mesenteric Vein Occlusion (original) (raw)
Related papers
Diagnosis and management of portal vein thrombosis in patients with cirrhosis of liver
The Southwest Respiratory and Critical Care Chronicles, 2018
Portal vein thrombosis (PVT) is an occlusion of the portal venous system and is a common complication of liver cirrhosis. It can present as either an acute or chronic complication. Acute PVT can present with abdominal pain, diarrhea, ileus, and bleeding. Chronic PVT is often asymptomatic; however, it can be discovered in cases of worsening portal hypertension. Portal vein thrombosis is diagnosed by imaging modalities, such as ultrasound and computed tomography. Contrast-enhanced imaging can be used in cases with difficult visualization. Despite the hemostatic imbalance in cirrhosis, anticoagulants can be safely used to recanalize the vein. Transjugular intrahepatic portosystemic shunt procedures are also an effective method for recanalization.
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.
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.
Natural course of nonmalignant partial portal vein thrombosis in cirrhotic patients
Saudi Journal of Gastroenterology, 2014
The liver plays a central role in maintaining the critical balance between bleeding and thrombotic events. Liver cirrhosis (LC) is characterized by a complex picture of impaired coagulation, thrombocytopenia, decreased pro-and anticoagulant factors produced by the liver, increased von Willebrand factor, factor VIII, and decreased pro-and antifibrinolytic factors, with a low tendency to hyperfibrinolysis. [1,2] Despite clear evidence of an increased tendency for bleeding in patients with liver cirrhosis, in some circumstances these patients are characterized by a hypercoagulable state. [3] The incidence of portal vein thrombosis (PVT) in compensated LC was reported between 0.6% and 5%, and much higher (15%-25%) in decompensated disease. [4-6] There are no data regarding the difference in the prevalence between partial and total PVT in cirrhotic patients. PVT is a serious complication of cirrhosis due to further increase in portal venous pressure and decreased blood flow to the liver, with the risk of variceal bleeding and worsening of the liver function. [7,8] However, the impact of PVT on the natural history of cirrhosis remains unclear. [9,10] Also, the natural course of PVT in patients with LC is not well known. Moreover, there are many asymptomatic cirrhotic patients in whom PVT is detected incidentally on abdominal ultrasound, and it is not established whether such ABSTRACT Background/Aim: Portal vein thrombosis (PVT) has a high incidence in patients with liver cirrhosis and determines a poor prognosis of hepatic disease. The aim of our study was to define the natural course of partial PVT in cirrhotic patients, including survival and decompensation rates. Patients and Methods: We performed a prospective, cohort study, in a tertiary referral center. There were 22 cirrhotic patients with partial nonmalignant PVT, without anticoagulant treatment, who were followed-up between January 2011 and October 2013. All patients were evaluated by Doppler abdominal ultrasound and computed tomography. Kaplan-Meier method was used to determine the difference in clinical events between the study subgroups. Results: After a mean follow-up period of 20.22 months, partial PVT improved in 5 (22.73%), was stable in 11 (50%), and worsened in 6 (27.27%) patients. Hepatic decompensation rate at 6 and 18 months was higher in patients with worsened PVT than in those with stable/improved PVT (50% vs. 25%, P < 0.0001 and 100% vs. 56.25%, P < 0.0001, respectively). The survival rate at 6 months was 66.66% in worsened PVT group vs. 81.25% (P = 0.005) in stable/improved group, and 16.66% vs. 81.25% (P < 0.0001) at 18 months, respectively. Multivariate analysis showed that Model of End-Life Disease was the independent predictor of hepatic decompensation [hazard ratio (HR) 1.42; 95% confidence interval (CI): 1.08-1.87, P = 0.012] and survival (HR 1.76; 95% CI: 1.06-2.92, P = 0.028). Conclusions: Nonmalignant partial PVT remained stable/ improved in over half of cirrhotic patients and aggravated in more than one fourth in whom it negatively influenced the survival and decompensation rates.
Portal vein thrombosis (PVT): A study of 20 non-irrhotic cases
Swiss medical weekly: official journal of the Swiss Society of Infectious Diseases, the Swiss Society of Internal Medicine, the Swiss Society of Pneumology
Portal and mesenteric venous thrombosis (PVT) is an uncommon disease with serious consequences if not discovered early in order to prevent complications such as variceal bleeding and intestinal ischaemia. The objective of this study was to describe the clinical presentation and outcome of patients with PVT with a view to early diagnosis and treatment of this disease. The study was restricted to patients with PVT not caused by underlying liver cirrhosis. To analyse important clinical characteristics of this entity we performed a retrospective study of 20 non-cirrhotic patients seen in our hospital from February 1998 to March 2003. The main clinical symptom was abdominal pain (13 patients, 86%), sometimes in combination with diarrhoea and vomiting (5 patients, 33%), nausea and anorexia (3 patients). Laboratory signs were non-specific and diagnosis was usually by computed tomography (19 patients, 95%). Causative factors included prothrombotic states (9 patients, 45%) and/or local facto...
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.
Hepatology, 2015
on behalf of Groupe d'Etude et de Traitement du Carcinome H epatocellulaire In cirrhosis, portal vein thrombosis (PVT) could be a cause or a consequence of the progression of liver disease. We analyzed data from a prospective trial of ultrasound screening for hepatocellular carcinoma in order to identify risk factors for and the impact of PVT in patients with cirrhosis. In all, 1,243 adults with cirrhosis without PVT were enrolled from 43 liver units in France and Belgium between June 2000 and March 2006. The mean follow-up was 47 months. Doppler ultrasonography was used to check the portal vein. Progression of liver disease was defined by the development of: ascites, hepatic encephalopathy, variceal bleeding, prothrombin <45%, serum bilirubin >45 lmol/L, albumin <28 g/L, and/or creatinine >115 lmol/L. G20210A prothrombin and factor V gene mutations were assessed in sera stored at three large centers. The 5year cumulative incidence of PVT was 10.7%. PVT was mostly partial and varied over time. The development of PVT was independently associated with baseline esophageal varices (P 5 0.01) and prothrombin time (P 5 0.002), but not with disease progression before PVT, or prothrombotic mutations. Disease progression was independently associated with baseline age (hazard ratio [HR] 1.55; 95% confidence interval [CI]: 1.11-2.17), body mass index (HR 1.40; 95% CI: 1.01-1.95), prothrombin time (HR 0.79; 95% CI: 0.70-0.90), serum albumin (HR 0.97; 95% CI: 0.94-0.99), and esophageal varices (HR 1.70; 95% CI: 1.21-2.38) but not with the prior development of PVT (HR 1.32; 95% CI: 0.68-2.65). Conclusion: In patients with cirrhosis, the development of PVT is associated with the severity of liver disease at baseline, but does not follow a recent progression of liver disease. There is no evidence that the development of PVT is responsible for further progression of liver disease. (HEPATOLOGY 2015;61:660-667) W ith the increased frequency of liver imaging thanks to accurate, noninvasive techniques, portal vein thrombosis in the absence of malignancy (so-called nonmalignant portal vein thrombosis and thereafter referred to as PVT) is increasingly identified in patients with cirrhosis. The estimated prevalence of PVT in these patients ranges from 0.6 to 26%. 1-3 Although several risk factors have been proposed
Splanchnic and Extrasplanchnic Thrombosis in Cirrhosis: Prophylaxis vs Treatment
Current Hepatology Reports, 2014
Venous thromboembolism (deep vein thrombosis and pulmonary embolism) and portal vein thrombosis (PVT) occur in up to 6.3 % and 15.9 % of patients with cirrhosis, respectively. There is recent evidence that a procoagulable prothrombotic state is related to cirrhosis despite the reduced levels of many coagulation factors, and decreased platelet counts. Indeed, (i) the combination of high levels of factor VIII, with low levels of protein C and antithrombin induces a procoagulant state in vitro; while (ii) increased levels of von Willebrand factor and decreased ADAMTS 13 activity can compensate for decreased platelet counts.
Risk factors and clinical presentation of portal vein thrombosis in patients with liver cirrhosis
Journal of Hepatology, 2004
Portal vein thrombosis in patients with liver cirrhosis is usually associated to hepatocellular carcinoma. Clinical presentation of non-neoplastic portal vein thrombosis (PVT) in cirrhotic patients has not been specifically studied and risk factors of PVT in this group of patients are still poorly understood.We studied all patients with PVT and liver cirrhosis admitted to our Unit from January 1998 to December 2002. They were paired (by gender, age and Child-Pugh score) to a group of cirrhotic patients without PVT and screened for acquired and inherited thrombophilic risk factors. These factors together with the site of thrombosis and the severity of the liver disease were correlated to the clinical presentation of PVT.Out of a total of 701 cirrhotic patients admitted to our hospital and routinely screened with Doppler ultrasound, 79 (11.2%) were found to have PVT. Of these, 34 (43%) were asymptomatic and 45 (57%) were symptomatic (31 presented with portal hypertensive bleed and 14 with abdominal pain, 10 of whom had intestinal infarction). Mesenteric vein involvement was never asymptomatic and lead to intestinal ischemia or infarction. Most patients were in class Child-Pugh B and C. Among thrombophilic risk factors studied only the mutation 20210 of the prothrombin gene resulted independently associated to PVT.Portal vein thrombosis may be completely asymptomatic in patients with liver cirrhosis; however in more than half of cases presents with life-threatening complications such as gastrointestinal haemorrhage and intestinal infarction. Cirrhotic patients with PVT usually have an advanced liver disease and the presence of the mutation 20210 of the prothrombin gene increases more than fivefold the risk of PVT.