Development Of Portal Vein Thrombosis Research Articles

Clinical Impact and Risk Factors of Portal Vein Thrombosis for Patients on Wait List for Liver Transplant.

The effect of portal vein thrombosis on the progression of liver disease is controversial, with no consensus on optimal treatment. We aimed to assess how portal vein thrombosis affects wait list outcomes, identify risk factors associated with its development while on a wait list, and assess its effects on patient and graft survival. This US-based retrospective cohort study analyzed 134 109 adult patients on wait lists for or undergoing primary orthotopic liver transplant between January 2002 and June 2014. Rate of portal vein thrombosis development, time from entry on wait list to transplant, comparisons of wait list drop-off rates between patients with versus those without portal vein thrombosis, risk factors associated with its development while on a wait list, and its effects on patient and graft survival were analyzed. We found that the rate of portal vein thrombosis at listing increased. Patients with the disease at listing were more likely to be removed from wait lists because of being too sick. Portal vein thrombosis at listing was an independent risk factor for being removed from a wait list. Of 63 265 patients who underwent primary orthotopic liver transplant, those with the disease were more likely to have higher Model for End-Stage Liver Disease scores and incidence of nonalcoholic steatohepatitis and diabetes mellitus. Portal vein thrombosis had a negative effect on patient and graft survival. Nonalcoholic steatohepatitis, body mass index, diabetes, and hepatocellular carcinoma were identified as risk factors for its development. Portal vein thrombosis represents an increasing management and outcome burden in liver transplant. Having this disease at listing and/or at time of transplant is associated with worse patient and graft survival. Nonalcoholic steatohepatitis and hepatocellular carcinoma are among the biggest risk factors for its development while on a wait list.

Reconstruction of Anomalous Portal Venous Branching in Right Lobe Living Donor Liver Transplantation: Malatya Approach.

Reconstruction of anomalous portal vein branching (APVB) during right lobe living donor liver transplantation (LDLT) can be challenging. The goal of this article is to describe our surgical technique, named the Malatya Approach, in case of APVB during right lobe LDLT. The technique unifies the APVB and obtains a funnel-shaped common extension with a circumferential fence by a saphenous vein conduit. In total, 126 (10.6%) of 1192 right lobe grafts had APVB that were divided into 2 groups according to the adopted surgical techniques: the Malatya Approach group (n = 91) and the previously defined other techniques group (n = 35). Both groups were compared regarding portal vein thrombosis (PVT), postoperative 90-day mortality and survival. PVT developed in 3 patients (3.3%) in the Malatya Approach group and developed in 10 (28.6%) patients for the other group (P < 0.001). There were 8 (8.8%) 90-day mortalities in the Malatya Approach group (1 PVT related) and 15 patients (9 PVT related) died in the other techniques group (P < 0.001). Mean follow-up time for both groups was similar (999.1 days for the Malatya Approach group versus 1024.7 days for the other group; P = 0.47), but longterm survival in the Malatya Approach group was better than in the other group (84.6% versus 40%; P < 0.001). Multivariate analysis revealed that the Malatya Approach group showed less PVT development and longer survival (P < 0.001). This technique is promising to avoid PVT and mortalities in cases of APVB during right lobe LDLT. Liver Transplantation 23 751-761 2017 AASLD.

African Americans have a lower prevalence of portal vein thrombosis at the time of liver transplantation

BackgroundPerioperative vascular thrombotic events in patients undergoing liver transplantation (LT) are associated with significant morbidity and mortality. MethodsIn this retrospective UNOS database analysis, we evaluated the prevalence of portal vein thrombosis (PVT) and factors contributing to PVT development in different ethnic groups. ResultsOf the 47 953 LT performed between 2002 and 2015, we identified 3642 cases of PVT. African Americans (AA) had a significantly lower prevalence of PVT compared to other ethnic groups (p = 0.0001). Multivariable regression analysis confirmed that AA were less likely than other ethnicities to have PVT (OR = 0.6). AA cohort was more likely to have infectious or autoimmune causes of liver failure (OR = 1.6, 1.7 respectively) as well as higher creatinine and INR compared to other groups (OR = 1.6, 1.3 respectively). AA's were less likely to have encephalopathy, ascites, or variceal bleeding, which might indicate lower portal pressures. AA's were listed for LT later than other ethnicities and had both a lower functional status and higher MELD score at the time of registration. DiscussionAA's had a significantly lower prevalence of preoperative PVT despite having a greater number of factors predisposing to thrombosis. This predisposition should be considered before instituting perioperative antithrombotic therapy.

Advanced non-alcoholic steatohepatitis cirrhosis: A high-risk population for pre-liver transplant portal vein thrombosis

AIMTo examine if liver transplant recipients with high-risk non-alcoholic steatohepatitis (NASH) are at increased risk for pre-transplant portal venous thrombosis.METHODSData on all liver transplants in the United States from February 2002 through September 2014 were analyzed. Recipients were sorted into three distinct groups: High-risk (age > 60, body mass index > 30 kg/m2, hypertension and diabetes), low-risk and non-NASH cirrhosis. Multivariable logistic regression models were constructed.RESULTSThirty-five thousand and seventy-two candidates underwent liver transplantation and of those organ recipients, 465 were transplanted for high-risk and 2775 for low-risk NASH. Two thousand six hundred and twenty-six (7.5%) recipients had pre-transplant portal vein thrombosis; 66 (14.2%) of the high-risk NASH group had portal vein thrombosis vs 328 (11.8%) of the low-risk NASH group. In general, all NASH recipients were less likely to be male or African American and more likely to be obese. In adjusted multivariable regression analyses, high-risk recipients had the greatest risk of pre-transplant portal vein thrombosis with OR = 2.11 (95%CI: 1.60-2.76, P < 0.001) when referenced to the non-NASH group.CONCLUSIONLiver transplant candidates with high-risk NASH are at the greatest risk for portal vein thrombosis development prior to transplantation. These candidates may benefit from interventions to decrease their likelihood of clot formation and resultant downstream hepatic decompensating events. Prospective study is needed.

Incidence and clinical presentation of portal vein thrombosis in cirrhotic patients

Portal vein thrombosis (PVT) is due to many risk factors, but its pathogenesis is still not clearly understood. To identify the risk factors for PVT, we analyzed the clinical characteristics and complications associated with PVT in cirrhotic patients. We studied patients with liver cirrhosis who were admitted to our unit from April 2009 to December 2014. The patients were divided into the PVT and non-PVT groups, and were compared by variables including gender, age, the etiology of cirrhosis, stage of cirrhosis, complications, imaging, and treatment. PVT was found in 45 (9.8%) of 461 cirrhotic patients admitted to our hospital. Most patients (45.9%) had hepatitis B virus (HBV)-related cirrhosis, with a similar distribution of etiologies between the groups. However, there was no positive relationship between PVT and etiologies of cirrhosis. Most patients (71.5%) were in the stage of hepatic decompensation. No statistically significant differences were found in complications including esophageal varices, ascites, and hepatic encephalopathy between the groups. However, there was a significant positive correlation between hepatocellular carcinoma (HCC) and PVT (P<0.01). In 30 patients with PVT, thrombosis occurred in the portal vein and/or portal branches, 37.8% were diagnosed on ultrasound. The incidence of PVT was 9.8%, mainly in patients with HBV-related cirrhosis. The development of PVT was associated with the severity of liver disease and HCC.

Portal Vein Thrombosis (PVT) Is Associated with Poor Clinical Outcomes in Acute Pancreatitis: Results from a Propensity-Matched Study on a Nationwide Cohort

Introduction: In acute pancreatitis (AP), the inflammatory process may involve the portal vein, this together with action of proteolytic enzymes, weakens the vessel wall and causes stasis of blood flow, which serves as a milieu for the development of portal vein thrombosis (PVT). PVT may adversely influence the clinical course of AP; however there are no inpatient, population-based studies assessing the impact of PVT in AP. We evaluated the prevalence and clinical outcomes of PVT in AP patients in a propensity matched analysis. Methods: The national inpatient sample (1998-2012) was reviewed to identify all patients hospitalized with AP with a concomitant diagnosis of PVT. The primary clinical outcome (mortality, renal failure, respiratory failure and pseudocyst) and secondary resources outcomes (length of stay and total hospital cost) were analyzed using univariate and multivariate comparisons. Propensity score-matched analysis (matched for patient demographics, hospital characteristics, etiology, and AHRQ-Elixhauser comorbidities) was performed to compare the outcomes in patients with and without PVT. Results: PVT is associated with 0.2% (5681/ 3454400) of all AP admissions. There is trend for increased PVT during the study period (47.5/100,000 in 1998 to 347.8/100,000; Cochran Armitage Trend test p < 0.001). Multivariate analysis showed PVT is associated with increased mortality [odds ratio (OR): 1.3, 95% confidence interval (CI) 1.0, 1.7; p=0.023], renal failure (OR 1.5, 95% CI 1.3, 1.6; p < 0.001), respiratory failure (OR: 3.1, 95% CI 2.7, 3.5; p < 0.001), severe AP (OR: 2.5, 95% CI 2.3, 2.8; p < 0.001), prolonged stay (median 5.4 days, p < 0.001) and higher hospital cost (median: $36,509, p < 0.001). Propensity matched analysis confirmed PVT is associated with increased renal failure (OR 1.8; p=0.002), respiratory failure (OR: 2.9; p=0.002), respiratory failure (OR: 2.9; p < 0.001), pseudocyst complication (OR: 4.5; p < 0.001) prolonged stay (median: 5.5 days, p < 0.001) and higher hospital cost (median: $38,123, p < 0.001). Conclusion: PVT is associated with adverse clinical outcomes like organ failure, severe AP, prolonged hospital stay and increased hospital charges which negatively impacts inpatients healthcare utilization. Further studies are needed to determine the optimal strategy for its detection and to reduce disease burden on AP patients.

Nontumoral portal vein thrombosis in patients awaiting liver transplantation.

Portal vein thrombosis (PVT) occurs in approximately 2%-26% of the patients awaiting liver transplantation (LT) and is no longer an absolute contraindication for LT. Nearly half of PVT cases are accidentally found during the LT procedure. The most important risk factor for PVT development in cirrhosis may be the severity of liver disease and reduced portal blood flow. Whether other inherited or acquired coagulation disorders also play a role is not yet clear. The development of PVT may have no effect on the liver disease progression, especially when it is nonocclusive. PVT may not increase the risk of wait-list mortality, but it is a risk factor for poor early post-LT mortality. Anticoagulation and transjugular intrahepatic portosystemic shunt (TIPS) are 2 major treatment strategies for patients with PVT on the waiting list. The complete recanalization rate after anticoagulation is approximately 40%. The role of TIPS to maintain PV patency for LT as the primary indication has been reported, but the safety and efficacy should be further evaluated. PVT extension and degree may determine the surgical technique to be used during LT. If a "conventional" end-to-end portal anastomotic technique is used, there is not a major impact on post-LT survival. Post-LT PVT can significantly reduce both graft and patient survival after LT and can preclude future options for re-LT.

Intra-abdominal hypertension triggered by portal vein thrombosis postoperatively: an ignored, but potential, cause of acute kidney failure in patients with cirrhosis

Intra-abdominal hypertension (IAH), even abdominal compartment syndrome, resulting from major stem portal venous thrombosis (MSPVT) postoperatively can lead to acute kidney failure (AKF). However, few physicians consider this clinical presentation, which is rarely reported in the literature. IAH often induces a few obvious clinical presentations, such as oliguria, anuria, and abdominal distension, etc., even in cases with normal liver function. Many doctors consider that AKF is due to hepatorenal syndrome (HRS), while postoperative development of portal vein thrombosis (PVT) may be another important factor inducing AKF, which appears to have been ignored in recent years. In fact, devascularization surgery and/or shunt placement for treatment of portal hypertension are known to easily induce PVT, especially during devascularization procedures because of the rapid accumulation of platelets. In addition, the risk of hypercoagulability increases because of the use of hemostatic agents. Also, PVT may lead to gastro-intestinal congestion and tissue edema, which can contribute to the development of IAH. Abdominal distension became very obvious because collateral circulation could not be restored in time due to MSPVT after ligamentectomy surrounding the liver. Thus, it was difficult to arrive at a diagnosis of PVT at an earlier stage by B-type ultrasound and/or measurement of D-dimer levels. To achieve an early diagnosis, it is very important to actively incorporate the methods mentioned above. However, these methods are not recommended unless the diagnosis of HRS is definitive. The effective treatment is to administer anticoagulants, such as low-molecular-weight heparin, and to discontinue hemostatic agents in time. AKF will not benefit from Terlipressin if HRS was not considered as the major cause of AKF, especially in cases of IAH. It is well known that peritoneal dialysis and/or hemodialysis should be adopted to sustain kidney function postoperatively .

Idiopathic non-cirrhotic portal hypertension: a review.

Idiopathic non-cirrhotic portal hypertension (INCPH) is a rare disease characterized of intrahepatic portal hypertension in the absence of cirrhosis or other causes of liver disease and splanchnic venous thrombosis. The etiology of INCPH can be classified in five categories: 1) immunological disorders (i.e. association with common variable immunodeficiency syndrome, connective tissue diseases, Crohn’s disease, etc.), 2) chronic infections, 3) exposure to medications or toxins (e.g. azathioprine, 6- thioguanine, arsenic), 4) genetic predisposition (i.e. familial aggregation and association with Adams-Oliver syndrome and Turner disease) and 5) prothrombotic conditions (e.g. inherited thrombophilias myeloproliferative neoplasm antiphospholipid syndrome). Roughly, INCPH diagnosis is based on clinical criteria and the formal exclusion of any other causes of portal hypertension. A formal diagnosis is based on the following criteria: 1) presence of unequivocal signs of portal hypertension, 2) absence of cirrhosis, advanced fibrosis or other causes of chronic liver diseases, and 3) absence of thrombosis of the hepatic veins or of the portal vein at imaging. Patients with INCPH usually present with signs or symptoms of portal hypertension such as gastro-esophageal varices, variceal bleeding or splenomegaly. Ascites and/or liver failure can occur in the context of precipitating factors. The development of portal vein thrombosis is common. Survival is manly limited by concomitant disorders. Currently, treatment of INCPH relies on the prevention of complications related to portal hypertension, following current guidelines of cirrhotic portal hypertension. No treatment has been studied aimed to modify the natural history of the disease. Anticoagulation therapy can be considered in patients who develop portal vein thrombosis.

De-novo portal vein thrombosis in liver cirrhosis: risk factors and correlation with the Model for End-stage Liver Disease scoring system.

Portal vein thrombosis (PVT) is a potential lethal complication in late liver cirrhosis. There is a lack of knowledge of the clinical features and risk factors of PVT. We aimed to investigate the clinical and radiological characteristics, and biochemical markers of cirrhotic patients to determine the high-risk individuals for PVT attending our center. Of 426 cirrhotic patients, only 120 consecutive patients were included. Clinical, biochemical, immunological, Model for End-stage Liver Disease (MELD) score, portal vein patency, and flow velocity were measured in all patients at baseline and every 6 months thereafter. Variables that could predict the development of PVT within 1 year were identified by multiple logistic regression. Only 95 patients completed the study; PVT was found in 17 (17.9%) patients. PVT was observed mainly in the portal trunk, superior mesenteric vein, and splenic vein. Univariate analysis showed that diabetes mellitus, lower levels of hemoglobin, platelet counts, and portal vein flow velocity as well as increased MELD scores, platelet indices, portal vein diameter, and splenic thickness were associated with PVT patients than in non-PVT patients (all P<0.01). The incidence of PVT was 17.9%. PVT occurred mainly in the portal vein trunk, superior mesenteric vein, and splenic vein. Diabetes mellitus, lower levels of hemoglobin, platelet count and portal vein flow velocity as well as increased MELD score, platelet indices, portal vein diameter, and splenic thickening were associated with PVT. Splenic thickening, marked reduced of mean portal flow velocity, and diabetes mellitus may be risk factors for PVT.

Effects of surgical procedures on the occurrence and development of postoperative portal vein thrombosis in patients with cirrhosis complicated by portal hypertension

ObjectiveWe have compared the influences of three surgical strategies on the occurrence and development of portal vein thrombosis (PVT) in patients with liver cirrhosis complicated by portal hypertension (PHT) in this study. MethodsTotal 116 patients who respectively underwent pericardial devascularization (PCDV) with splenectomy (PDS group: n = 50), selective PCDV (SPD group: n = 28) and splenorenal shunt (SRS) combined with PCDV (combined group: n = 38) were investigated in this study. The incidence of PVT before and after operation was monitored. The incidence of Grade II-IV PVT was used to assess the severity of PVT. The liver function was assessed according to the Child-Pugh classification. ResultsThe incidence and severity of PVT and live function were similar among the three groups before operation (P > 0.05). The incidence of PVT was significantly increased after surgery in each group (P < 0.001), but recovered to the baseline level at six months in combined group (P = 0.629). Besides, the severity of PVT was significantly aggravated in PDS (P < 0.001) and SPD (P = 0.026) groups after operation, but not in combined group (P = 0.525). Patients in combined group showed significantly lower incidence and severity of PVT than those in the other two groups at each follow-up time point (P < 0.05). In addition, the liver function in the combined group was significantly improved compared with the other two groups. ConclusionsSRS combined with PCDV is superior to PCDV with splenectomy and selective PCDV for PHT in liver cirrhotic patients in inhibiting the occurrence and development of postoperative PVT and improving liver function.

Causes and consequences of portal vein thrombosis in 1,243 patients with cirrhosis: results of a longitudinal study.

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 μmol/L, albumin <28 g/L, and/or creatinine >115 μmol/L. G20210A prothrombin and factor V gene mutations were assessed in sera stored at three large centers. The 5-year 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 = 0.01) and prothrombin time (P = 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). 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.

Role of D-dimer in the Development of Portal Vein Thrombosis in Liver Cirrhosis: A Meta-analysis.

Background and Aims:A meta-analysis was performed to explore the role of the D-dimer in the development of portal vein thrombosis (PVT) in liver cirrhosis.Methods:All papers were searched via PubMed, EMBASE, China National Knowledge Infrastructure, Wan Fang, and VIP databases. A standardized mean difference (SMD) with 95% confidence interval (CI) was pooled.Results:Overall, 284 studies were initially identified, of which 21 were included. Cirrhotic patients with PVT had a significantly higher D-dimer concentration than those without PVT (pooled SMD = 1.249, 95%CI = 0.740–1.758). After the portal hypertension-related surgery, cirrhotic patients with PVT had a similar preoperative D-dimer concentration to those without PVT (pooled SMD = 0.820, 95%CI = −0.122–0.286), but a higher postoperative value of D-dimer concentration than those without PVT (pooled SMD = 2.505, 95%CI = 0.975–4.036). Notably, the D-dimer concentration at the 1st postoperative day was similar between cirrhotic patients with and without PVT (pooled SMD = 0.137, 95%CI = −0.827–1.101), but that at the 7th post-operative day was higher in cirrhotic patients with PVT than in those without PVT (pooled SMD = 1.224, 95%CI = 0.277–2.171).Conclusion:D-dimer might be regarded as a diagnostic marker for PVT in liver cirrhosis. In addition, postoperative D-dimer testing is worthwhile for the diagnosis of PVT after portal hypertension-related surgery.

Associations of antiphospholipid antibodies with splanchnic vein thrombosis: a systematic review with meta-analysis.

Splanchnic vein thrombosis (SVT) refers to Budd-Chiari syndrome (BCS) and portal vein system thrombosis (PVST). Current practice guidelines have recommended the routine screening for antiphospholipid antibodies (APAs) in patients with SVT. A systematic review and meta-analysis of observational studies was performed to explore the association between APAs and SVT. The PubMed, EMBASE, and ScienceDirect databases were searched for all relevant papers, in which the prevalence of positive APAs or levels of APAs should be compared between BCS or noncirrhotic PVST patients versus healthy controls, or between cirrhotic patients with portal vein thrombosis (PVT) versus those without PVT. Fourteen studies were eligible. Only 1 study evaluated the role of APAs in BCS patients and found that positive immunoglobulin (Ig) G anticardiolipin antibody (aCL) was more frequently observed in BCS patients than in healthy controls; however, the associations of other APAs with BCS were not evaluated. Positive IgG aCL was more frequently observed in noncirrhotic patients with PVST than in healthy controls; however, other APAs, such as IgM aCL, lupus anticoagulants (LAs), anti-β2-glycoprotein-I antibody (aβ2GPI), and aβ2GPI-oxidized low-density lipoprotein antibody (ox-LDL) were not associated with noncirrhotic PVST. Positive unclassified aCL was more frequently observed in cirrhotic patients with PVT than in those without PVT; however, the association of IgG aCL and IgM aCL with the development of PVT in liver cirrhosis remained inconsistent among studies. The risk of BCS and noncirrhotic PVST might be increased by positive IgG aCL but not IgM aCL, LA, aβ2GPI, or aβ2GPI ox-LDL. However, the evidence regarding APAs in BCS originated from only 1 study. The association between APAs and PVT in liver cirrhosis was unclear.

Widespread portal venous thrombosis in a patient with pancreatic cancer

Pancreatic cancer is a risk factor for the development of portal vein thrombosis because pancreatic lesions sometimes compress and/or directly invade the portal vein. We herein present a case of pancreatic cancer with widespread thrombosis of the portal vein system. A 52-year-old male was admitted to our hospital with epigastralgia. An abdominal contrast-enhanced computed tomography scan demonstrated a non-enhanced low-density tumor in the head of the pancreas and widespread thrombus formation in the superior mesenteric and portal veins. 18F-FDG positron emission tomography showed uptake in the tumor but not in the thrombi. We diagnosed the patient with pancreatic cancer with widespread portal venous thrombosis without tumor thrombi, and pancreaticoduodenectomy with reconstruction of the portal vein was performed. Histological examinations showed that the majority of the emboli consisted of blood thrombi including a few tumor cells. Although the patient ultimately died due to multiple liver metastases, he lived for 19 months after the surgery. The present case indicates that performing radical pancreatic resection in patients with pancreatic cancer is possible, even when widespread portal venous thrombosis is present.

Portal vein thrombosis in liver cirrhosis

Portal vein thrombosis (PVT) is considered to be a frequent complication of liver cirrhosis. However, unlike PVT in patients without cirrhosis, very few data are available on the natural history and management of PVT in cirrhosis, despite its association with potentially life-threatening conditions, such as gastroesophageal bleeding and acute intestinal ischemia. Moreover, no consensus regarding PVT in cirrhosis exists. Suggested causes of PVT in cirrhosis include reduced portal blood flow velocity, multiple congenital or acquired thrombophilic factors, inherited or acquired conditions, and derangement of liver architecture. However, the understanding of PVT in cirrhosis is incomplete. In addition, information on the management of PVT in cirrhosis is inadequate. The aims of this review are to: (1) assemble data on the physiopathological mechanism, clinical findings, diagnosis and management of PVT in cirrhosis; (2) describe the principal factors most frequently involved in PVT development; and (3) summarize the recent knowledge concerning diagnostic and therapeutic procedures.

Risk factors and clinical characteristics of portal vein thrombosis after splenectomy in patients with liver cirrhosis

Portal vein thrombosis (PVT) is a potential lethal complication and may have negative influence on the prognosis after splenectomy in patients with liver cirrhosis. Prevention and timely detection of PVT are quite significant. There is a lack of knowledge about the clinical features and risk factors of PVT. Our study aimed to investigate the risk factors and clinical characteristics of PVT in order to figure out the high-risk individuals. We collected the clinical data of 472 consecutive patients with non-neoplastic liver cirrhosis who had undergone splenectomy from January 2008 to December 2010 in our institution. Clinical and surgical characteristics of patients who developed PVT postoperatively and those who did not develop PVT were compared. Univariate and multivariate analyses of risk factors of PVT were performed. The mortality and rebleeding rate of the patients were also evaluated. Of the 472 patients, 52 were excluded from the study. PVT developed in 71 (71/420, 16.9%) patients. Multivariate analysis revealed that wider preoperative portal vein diameter, postoperative thrombocytosis, prolonged prothrombin time and periesophagogastric devascularization were significantly correlated with PVT development [odds ratio (OR): 5.701, 2.807, 1.850 and 2.090, respectively]. The incidence of PVT in patients who took antiplatelet drugs was not lower than that in those who did not. Follow-up showed that patients in the PVT group had a tendency towards reduced overall survival but it was not statistically significant. Gastrointestinal bleeding occurred more often in the PVT group than that in the non-PVT group (P=0.044). Wider preoperative portal vein diameter, postoperative thrombocytosis, prolonged prothrombin time and periesophagogastric devascularization are independent risk factors of PVT. PVT is related with higher risk of postoperative gastrointestinal hemorrhage but has no significant impact on the overall survival.

PORTAL VEIN THROMBOSIS IN PATIENTS WITH LIVER CIRRHOSIS ;RISK FACTORS,CLINICAL PRESENTATION AND OUTCOME

Introduction: The liver has many haemostatic functions, including the synthesis of most coagulation factors and inhibitors as well as fibrinolytic factors . The balance between procoagulant and anticoagulant factors is essential to avoid excessive thrombin generation under physiological conditions. Therefore, advanced liver disease results in a complex pattern of defects in haemostatic functions in the form of reduced synthesis of coagulation factors, inhibitors, and abnormal clotting factors, abnormalities of fibrinolytic activity, disseminated intravascular coagulation and platelet function defects. Development of portal vein thrombosis (PVT) is asignificant milestone in the natural history of cirrhosis. It is associated with worsening liver function, ascites, and the occurrence of gastroesophageal variceal bleeding. It is clear that PVT increases morbidity and mortality associated with liver transplant and may even contraindicate it and. Thus, taken together, these data suggest that PVT is a major index of poor prognosis in patients with cirrhosis. Although spontaneous resolution of PVT has been reported in the literature specific therapeutic management is mandatory to resolve portal vein obstruction and avoid serious complications. The goal of treatment is similar correction of causal factors, prevention of thrombosis extension, and achievement of portal vein patency Objective: the aim of the work was to clarify the risk factors , clinical presentation and complications of portal vein thrombosis in patients with liver cirrhosis and to study the out come after short term follow up. Subject and methods :- A total number of 80 patients with cirrhosis were included and were classified into two main groups. Group I ( 50 ) cirrhotic patients with portal vein thrombosis. Group II ( 30 ) cirrhotic patients without portal vein thrombosis. Each group was divided in two sub groups A and B a ccording to prescence or absence of HCC respectively.The 2 groups were compared as regard risk factors and clinical presentation and out come. Result: PVT developed as result of combination of both local and systemic risk factors. HCC and abdominal infection specially spontaneous bacterial peritonitis and intervention to the portal system ,were the most important local risk factors . Protein C and S defficincy were amog systemic risk factors. Most of cases were asymptomatic and accidentally discovered , other patients presented with upper GIT bleeding or other complications of liver cell failure .Anticoagulant administration was associated with increased incidence of partial or complete recanalization without increased risk of bleeding. Conclusion and Recommendations:- Portal vein thrombosis occurs mostly in a cirrhotic patient with advanced liver disease. Patients with advanced liver cirrhosis and not so prolonged coagulation parameters might be at particular risk of developing PVT. So regular monitoring using Doppler-ultrasound should be carried out in these patients. Development of varices is a time dependent phenomenon, so it is advisable to screen all PVT patients endoscopically.Early administration of anticoagulation was associated with increased incidence of partial or complete recanalization. Keywords :Portal vein ,Thrombosis, risk factors, cirrhosis

Hyperammonemic Encephalopathy Associated with Portal Vein Thrombosis in a Thoroughbred Foal

Hyperammonemic Encephalopathy Associated with Portal Vein Thrombosis in a Thoroughbred Foal

Portal Vein Thrombosis: Should Anticoagulation Be Used?

Portal vein thrombosis (PVT) can contribute to significant morbidity and mortality; in patients with cirrhosis, this can make transplant more technically challenging. Additionally, the clot may extend further into the mesenteric and splenic veins, and disturbance of the hepatic blood flow may lead to faster progression of the cirrhosis. Development of PVT is associated with local risk factors, and many patients have associated systemic prothrombotic factors. Anticoagulation in noncirrhotic patients should be initiated at diagnosis, using low-molecular-weight heparin overlapping with vitamin K antagonists. Cirrhotic patients with PVT should be screened for varices and then anticoagulated with low-molecular-weight heparin for at least a 6-month period. All patients should be assessed for triggering factors and tumors, as well as systemic prothrombotic factors. Newer evidence suggests that prophylactic anticoagulation in patients with cirrhosis may have a role in clinical management with decreased incidence of PVT and improved survival; further study is needed.