Chronic Portal Vein Thrombosis Research Articles

Natural history of patients with non cirrhotic portal hypertension: Comparison with patients with compensated cirrhosis

BackgroundThe knowledge of natural history of patients with portal hypertension (PH) not due to cirrhosis is less well known than that of cirrhotic patients. AimTo describe the clinical presentation and the outcomes of 89 patients with non-cirrhotic PH (25 with non-cirrhotic portal hypertension, INCPH, and 64 with chronic portal vein thrombosis, PVT) in comparison with 77 patients with Child A cirrhosis. MethodsThe patients were submitted to a standardized clinical, laboratory, ultrasonographic and endoscopic follow-up. Variceal progression, incidence of variceal bleeding, portal vein thrombosis, ascites and survival were recorded. ResultsAt presentation, the prevalence of varices, variceal bleeding and ascites was similar in the 3 groups. During follow-up, the rate of progression to varices at risk of bleeding (p < 0.0001) and the incidence of first variceal bleeding (p = 0.02) were significantly higher in non-cirrhotic then in cirrhotic patients. A PVT developed in 32% of INCPH patients and in 18% of cirrhotics (p = 0.02). ConclusionsIn the patients with non-cirrhotic PH variceal progression is more rapid and bleeding more frequent than in cirrhotics. Patients with INCPH are particularly prompt to develop PVT. This observational study suggests that the management of patients with non-cirrhotic PH should take into consideration the natural history of portal hypertension in these patients and cannot be simply derived by the observation of cirrhotic patients.

Evaluation and management of acute and chronic portal vein thrombosis in patients with cirrhosis.

Evaluation and management of acute and chronic portal vein thrombosis in patients with cirrhosis.

Transjugular portal vein recanalization with creation of intrahepatic portosystemic shunt (PVR-TIPS) in patients with chronic non-cirrhotic, non-malignant portal vein thrombosis.

To determine safety and efficacy of transjugular portal vein recanalization with creation of intrahepatic portosystemic shunt (PVR-TIPS) in patients with chronic non-cirrhotic, non-malignant portal vein thrombosis (PVT). This retrospective study includes 17 consecutive patients with chronic non-cirrhotic PVT (cavernous transformation n = 15). PVR-TIPS was indicated because of variceal bleeding (n = 13), refractory ascites (n = 2), portal biliopathy with recurrent cholangitis (n = 1), or abdominal pain (n = 1). Treatment consisted of a combination of transjugular balloon angioplasty, mechanical thrombectomy, and-depending on extent of residual thrombosis-transjugular intrahepatic portosystemic shunt and additional stenting of the portal venous system. Recanalization was successful in 76.5 % of patients despite cavernous transformation in 88.2 %. Both 1- and 2-year secondary PV and TIPS patency rates were 69.5 %. Procedure-related bleeding complications occurred in 2 patients (intraperitoneal bleeding due to capsule perforation, n = 1; liver hematoma, n = 1) and resolved spontaneously. However, 1 patient died due to subsequent nosocomial pneumonia. During follow-up, 3 patients with TIPS occlusion and PVT recurrence experienced portal hypertensive complications. PVR-TIPS is safe and effective in selected patients with chronic non-cirrhotic PVT. Due to technical complexity and possible complications, it should be performed only in specialized centers with high experience in TIPS procedures.

Pretransplantation Portal Vein Recanalization and Transjugular Intrahepatic Portosystemic Shunt Creation for Chronic Portal Vein Thrombosis: Final Analysis of a 61-Patient Cohort

PurposeTo report the final analysis of the safety and efficacy of portal vein (PV) recanalization (PVR) and transjugular intrahepatic portosystemic shunt (TIPS) creation (PVR-TIPS) in patients with PV thrombosis (PVT) in need of liver transplantation. Materials and MethodsSixty-one patients with cirrhosis and PVT underwent PVR-TIPS to improve transplantation candidacy. Median patient age was 58 years (range, 22–75 y), and median pre-TIPS Model for End-Stage Liver Disease score was 14 (range, 7–42). The most common etiologies of cirrhosis were nonalcoholic fatty liver disease in 18 patients (30%) and hepatitis C in 13 patients (21%). Twenty-seven patients (44%) had partial PVT, and 34 patients (56%) had complete thrombosis. Forty-nine patients (80%) had Yerdel grade 2 PVT, and 12 (20%) had Yerdel grade 3 PVT. Twenty-nine patients (48%) had cavernous transformation of the PV. ResultsPVR-TIPS was technically successful in 60 of 61 patients (98%). PV/TIPS patency was maintained in 55 patients (92%) at a median follow-up of 19.2 months (range, 0–105.9 mo). Recurrent PV/TIPS thrombosis occurred in 5 patients (8%), all of whom initially presented with complete PVT. The most common adverse events were TIPS stenosis in 13 patients (22%) and transient encephalopathy in 11 patients (18%). Twenty-four patients (39%) underwent transplantation, 23 of whom (96%) received an end-to-end anastomosis. There were no cases of recurrent PVT following transplantation, with a median imaging follow-up of 32.5 months (range, 0.4–75.4 mo). Five-year overall survival rate was 82%. ConclusionsPVR-TIPS is a safe, effective, and durable treatment option for patients with chronic PVT who need liver transplantation.

An Unusual Cause of Hematemesis: Esophageal Varices in a Child

Portal vein thrombosis (PVT) is characterized by the complete or partial obstruction of the portal vein, due to the presence of a thrombus. This condition eventually results in non-cirrhotic portal hypertension (PHT) and is the leading cause of pediatric PHT and gastrointestinal bleeding. Risk factors for PVT in pediatric patients include those with a history of umbilical vein catheterization, neonatal sepsis, abdominal infection, cardiovascular malformation, coagulation disorder, or previous abdominal surgery. We present a unique case of bleeding esophageal varices due to non-cirrhotic PHT in a child. A 15-year-old male presented with a 1-day history of hematemesis. On presentation, the patient was tachycardic and hypotensive. The patient's initial hemoglobin was 8.0g/dL, and was resuscitated with packed red blood cells and intra-venous fluids. An esophagogastroduodenoscopy was performed which revealed large esophageal varices with nipple sign in the distal esophagus and gastric varices throughout the fundus (Figure 1). The patient underwent variceal band ligation, however continued to have hematemesis. Ultrasound and CT scan of the abdomen showed presence of a chronic portal vein occlusion with significant cavernous transformation (Figure 2). Surgery was consulted and the patient underwent exploratory laparotomy with failed attempt of Meso-Rex bypass and subsequent creation of a splenorenal shunt. Liver biopsy did not show any evidence of cirrhosis. The patient was discharged on post-operative day five after tolerating diet and resolution of symptoms. Prior to discharge, a complete hypercoagulability work-up was performed and the patient was found to have elevated anti-b2 glycoprotein levels, consistent with anti-phospholipid syndrome and the likely cause of this patient's portal vein thrombosis. Patients with chronic PVT may remain asymptomatic for many years, with variceal bleeding usually being the first manifestation of PVT in non-cirrhotic patients, which was the case in our patient. When there is a high clinical suspicion for PVT, ultrasonography (US) of the abdomen is the first line imaging modality. In children, creation of a Meso-Rex bypass, a vascular graft between the superior mesenteric vein and the Rex recessus (left portal vein system), helps improve clinical outcomes. Proper diagnosis of patient's' underlying condition predisposing to PVT is important in preventing further recurrence.Figure: Esophagogastroduodenoscopy showing large esophageal varices with nipple sign (A) and large gastric varices throughout the fundus (B).Figure: Ultrasound of the liver showing main portal vein thrombosis (A), and the use of doppler showing cavernous transformation of the portal vein (B), while CT scan of the abdomen and pelvis (venous phase) showing lack of blood flow through portal vein, findings consistent with presence of portal vein thrombosis, and extensive cavernous transformation (C).

Anticoagulation of Chronic Portal Vein Thrombosis in a Patient With Esophageal Varices

Anticoagulation of Chronic Portal Vein Thrombosis in a Patient With Esophageal Varices

How to treat non-tumoral portal vein thrombosis in cirrhosis? Towards the use of direct-acting oral anticoagulants

Nagaoki et al . suggest that edoxaban a direct-acting oral anticoagulant (DOAC) may be more effective than warfarin in case of chronic portal vein thrombosis (PVT) complicating cirrhosis (1). Furthermore, the conclusions of the study are that edoxaban following an initial therapy with danaparoid sodium, is effective to reduce the volume of thrombosis, without significantly increasing the risk of bleeding.

Trans-splenic Access for Portal Venous Interventions in Children: Do Benefits Outweigh Risks?

The primary concern of trans-splenic access for portal interventions is the risk of life-threatening intraperitoneal bleeding. To review the clinical indications and efficacy and evaluate the risk factors for intraperitoneal bleeding during trans-splenic portal interventions in children. A retrospective review of consecutive patients who underwent trans-splenic portal interventions at a tertiary care pediatric institution between March 2011 and April 2017 was performed. Forty-four procedures were performed in 30 children with a median age of 5 (0.3-18) years. Clinical indications, technical success, procedural success, and incidence of complications were recorded. Potential risk factors for intraperitoneal bleeding were evaluated using Wilcoxon rank and Fisher's exact tests. Trans-splenic access was 100% successful. In 35/44 (79%) procedures, the subsequent intervention was successful including recanalization of post-transplant portal vein occlusion in 10/13, embolization of bleeding Roux limb varices in 8/8, recanalization of chronic portal vein thrombosis in native liver in 7/13, splenoportography and manometry in 6/6, and occlusion of portosystemic shunts in 4/4 procedures. Intraperitoneal bleeding occurred during 12/44 (27%) procedures and was managed with analgesics, blood transfusion, and peritoneal drainage without the need for splenectomy or splenic artery embolization. Statistically significant correlation of bleeding was found with intraprocedural anticoagulation, but not with patient age, weight, platelet count, INR, ascites, splenic length, splenic venous pressure, vascular sheath size, or tract embolization technique. Trans-splenic access is a useful technique for successful pediatric portal interventions. Although it entails a substantial risk of intraperitoneal bleeding, this can be managed conservatively.

Caesarean section in a patient with chronic portal vein thrombosis and thrombocytopenia: Case report

We report the case of a pregnant woman at term with primary anti-phospholipid syndrome, portal vein thrombosis, massive splenomegaly, oesophageal varices and thrombocytopenia. The patient underwent an elective caesarean section under general anaesthesia to minimise the risk of spleen and variceal rupture, with a favourable outcome for both the mother and the newborn.Chronic portal vein thrombosis is a rare condition, caused by various reasons, mainly thrombotic diathesis. It leads to increased portal pressure, with development of collateral circulation, splenomegaly and thrombocytopenia. Pregnancy in these conditions is considered high risk, but is not contraindicated if the underlying disorder is stabilised. The management of these patients should be multidisciplinary, under close monitoring; diagnosis and treatment of possible oesophageal varices is essential. The decision about mode of delivery and anaesthetic management must be individualised, depending on obstetric factors, the presence or absence of varices and thrombocytopenia, and associated comorbidities.

Platelet count, spleen length, and platelet count-to-spleen length ratio for the diagnosis of oesophageal varices in people with chronic liver disease or portal vein thrombosis.

Platelet count, spleen length, and platelet count-to-spleen length ratio for the diagnosis of oesophageal varices in people with chronic liver disease or portal vein thrombosis.

Hepatic Encephalopathy in Patients With Non-Cirrhotic Portal Hypertension: Description, Prevalence and Risk Factors

Background: Hepatic encephalopathy (HE) is a common complication of cirrhosis but it's less studied in patients with non-cirrhotic portal hypertension (NCPH). Aims: To describe the prevalence of cognitive impairment (overt and covert HE) in NCPH patients and to identify the risk factors for its development. Methods: 51 patients with NCPH, 35 with chronic portal vein thrombosis (PVT) and 16 with idiopathic non-cirrhotic portal hypertension (INCPH), were evaluated for the presence of previous or present overt HE (OHE). The psychometric hepatic encephalopathy score and the SCAN battery were used to detect the presence of covert HE (CHE). 34 compensated cirrhotic patients were used as control. In NCPH patients, abdominal scans were performed to detect the presence of shunts. Results: None of the patients experienced OHE at evaluation while 5.7% of PVT and 12.5% of INCPH patients referred at least one documented episode of previous OHE, similarly to patients with cirrhosis (14.7%). Even if lower than in patients with cirrhosis (64.7%), a considerable proportion of patients with chronic PVT (34.3%) and INCPH (25%) had CHE (P = 0.008). The presence of a large portal-systemic shunt was the only factor significantly correlated to cognitive impairment in NCPH patients (Figure 1). Conclusion: HE is a tangible complication of NCPH and is mainly related to the presence of portal-systemic shunts (Table 1).Table 1Prevalence of MetabolitesMinimal, Previous, Overt HE and of Global Cognitive Impairments in the Patients Included in the Study.Cirrhosis (n = 34)Chronic PVT (n = 35)INCPH (n = 16)PMinimal HE (Phes and/or Scan)22 (64.7%)*12 (34.3%)4 (25.0%)0.008Overt HE0 (0.0%)0 (0.0%)0 (0.0%)NSPrevious HE5 (14.7%)2 (5.7%)2 (12.5%)NSCognitive impairment23 (67.6%)*13 (37.1%)5 (31.3%)0.012 Open table in a new tab The authors have none to declare.

Hemodynamic Changes in Portal Vein and Frequencies of Acute and Chronic Portal Vein Thrombosis in Pediatric Patients Presenting with Hematemesis

&lt;p&gt;&lt;strong&gt;Objective:&lt;/strong&gt; The objective of the study is to calculate the frequency of portal vein thrombosis in pediatric patients presenting with hematemesis and to estimate the frequency of acute and chronic portal vein thrombosis in these cases.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Patients and Methods:&lt;/strong&gt;&lt;strong&gt; &lt;/strong&gt;Pediatric patients of 1 – 15 years of age of either sex, presenting to emergency or gastroenterology department with complaint of hematemesis were included. Informed consent was taken from parents/guardians. This is a Descriptive cross sectional study conducted in department of pediatric radiology, Children Hospital and Institute of child Health Lahore from 11-12-2012 to 10-6-2013. Doppler ultrasound of these patients was performed at Core Vision pro SSA 350-A Doppler machine (Toshiba, Japan) using standard imaging protocols. The data was analyzed using SPSS version 17.0 (SPSS Inc., IL, Chicago, USA)&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results:&lt;/strong&gt;&lt;strong&gt; &lt;/strong&gt;In this study, 41% (n = 41) between 1 – 5 years, 38% (n = 38) between 6 – 10 years and only 21% (n = 21) between 11 – 15 years of age, 64%( n = 64) were male and remaining 36% (n = 36) were females, frequency of portal vein thrombosis in pediatric patients presenting with hematemesis reveals in 37% (n = 37) while 63% (n = 63) had no findings of PVT, frequency of acute and chronic forms in patients positive for portal vein thrombosis was 40.54% (n = 15) had acute and 59.46% (n = 22) had chronic portal vein thrombosis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion:&lt;/strong&gt;&lt;strong&gt; &lt;/strong&gt;We concluded that the frequency of portal vein thrombosis in pediatric patients presenting with hematemesis and frequency of acute and chronic forms in patients positive for portal vein thrombosis is in accordance with other studies while color Doppler ultrasound is a useful diagnostic modality being noninvasive and cost effective.&lt;/p&gt;

Overlap Syndrome of Autoimmune Hepatitis, Primary Biliary Cholangitis, and Primary Sclerosing Cholangitis in a Patient with Systemic Lupus Erythematosus: A Case Report of Complex Autoimmune Liver Disease

Introduction: Overlap syndrome is a spectrum of clinical manifestations between Autoimmune hepatitis (AIH), Primary Biliary Cholangitis (PBC), and Primary Sclerosing Cholangitis (PSC). Overlap syndromes between AIH-PBC and AIH-PSC are well recognized. Overlap between PBC-PSC has only been reported in a few patients. To our knowledge, it is extremely rare for PBC, PSC and probable AIH overlap syndrome to occur in the same patient.Figure 1Figure 2Case report: The patient is a 48-year old Hispanic male with liver cirrhosis and SLE. His cirrhosis was complicated by esophageal varices, thrombocytopenia, coagulopathy, hypoalbuminemia, and chronic portal vein thrombosis. His biochemical profile revealed elevated ALT (2X upper limit of normal (ULN)) and AST (4X ULN), persistently elevated alkaline phosphatase (3X ULN) and elevated bilirubin (2X ULN). Investigations for etiology of cirrhosis included a detailed social history were done. Viral hepatitis serology, iron studies, celiac panel, ceruloplasmin and alpha-1 antitrypsin level were unremarkable. Anti-nuclear antibody (ANA) was positive with a titer of 1:320, anti-smooth muscle antibody (ASMA) was positive with a serum level of 20 (Normally < 20) and P-ANCA was positive. Anti-Soluble liver antigen (anti-SLA) and anti-liver kidney microsomal 1 antigen (Anti-LKM1) were negative. Gamma globulin level was elevated at 2501 mg/dL (normal range 694-1617). Anti-mitochondrial antibody (AMA) was positive with a level of 71.9 units (Normally < 20). The more specific antibody for PBC, AMA-M2, was also positive as well. He also had a positive anti-dsDNA. The patient met criteria for AIH-PBC overlap syndrome based on Paris Criteria. He was on prednisone for autoimmune thrombocytopenia and was started on oral Ursodeoxycholic acid. We also performed an ERCP with cholangiography which showed segmental irregularities of intrahepatic bile ducts with beaded appearance suggestive of sclerosing cholangitis. Based on patient's liver enzymes profile, autoimmune markers, and ERCP findings; he was diagnosed with AIH-PBC-PSC overlap syndrome. We wanted to obtain a liver biopsy, however it could not be done as patient deceased due to septic shock. Conclusion: We are presenting a case with complex clinical spectrum of autoimmune liver diseases which include AIH, PBC, and PSC. To our knowledge, this is only the second reported case of all these diseases overlapping in the same patient; and the first reported case in a patient with SLE.

An Uncommon Cause of Chronic Portal Vein Thrombosis, Large Varices, and Massive Splenomegaly

A 68-year-old female presents to hepatology for further management of chronic portal vein thrombosis (PVT). She was diagnosed with mesenteric vein thrombosis in 1995 after she developed acute onset of severe abdominal pain. She required exploratory laparotomy at which time the diagnosis was made and was treated with warfarin for six months. She underwent hypercoagulable workup which was negative. In 2003, she was noted to have extension of the superior mesenteric vein (SMV) thrombus into the portal vein. She was restarted on warfarin which she remains on. She has a history of esophageal and fundal varices on propranolol 600 mg daily. The varices were never treated endoscopically and she denies history of gastrointestinal bleeding. She has not had prior liver biopsy. Family history is negative for venous thromboembolism. Social history is negative for alcohol use. She has two healthy children and no history of miscarriage. Review of systems is negative for jaundice, icterus, pruritus, encephalopathy, ascites, or peripheral edema. On exam, abdomen is distended but soft and nontender. Splenomegaly is present and there is no obvious ascites. There are no chronic liver disease stigmata. Labs are significant for a platelet count of 80, normal liver function tests, normal albumin, and elevated INR in the setting of warfarin. MRI of liver with elastography reveals cavernous transformation of the intra- and extrahepatic portal veins with a prominent system of pericholecystic collaterals. Massive splenomegaly of 25 cm length is noted and the SMV is patent. There are no suspicious liver lesions. Stage III to IV liver fibrosis is noted. Transjugular liver biopsy shows extramedullary hematopoiesis without evidence of cirrhosis. Upper endoscopy with endoscopic ultrasound reveals grade III esophageal varices and type 1 gastroesophageal varices without stigmata of recent bleeding. No further intervention is recommended by surgery or interventional radiology and her beta blockade and anticoagulation are continued. Patient is referred to hematology due to liver biopsy finding of extramedullary hematopoiesis. Bone marrow biopsy reveals hypocellular bone marrow with marked myelofibrosis and molecular analysis is positive for JAK2 V617F mutation, consistent with a diagnosis of primary myelofibrosis. This case illustrates the importance of keeping in mind myeloproliferative neoplasms as a potential etiology of PVT, noncirrhotic portal hypertension, and massive splenomegaly.

Complicated Portal Cavernoma Cholangiopathy (PCC) in a Patient with Pre-existing TIPS Managed Successfully by Endoscopic Biliary Stenting

PCC is the presence of typical cholangiographic changes in patients with a portal cavernoma due to chronic portal vein thrombosis (PVT), in the absence of other biliary tract diseases. Symptomatic PCC is rare; estimates range between 5-38% of patients with PVT. A 41 year old black woman with a PMH of Hodgkin's lymphoma s/p chemotherapy, isolated factor VII deficiency, complicated cirrhosis s/p TIPS and PVT presented to GI clinic with RUQ pain, dark urine, and acholic stool. Physical examination revealed scleral icterus and RUQ tenderness. The total bilirubin was 3.3 MG/DL, AST 111 U/L, ALT 29 U/L, ALP 603, and INR 1.4. After hospitalization, MRCP and MRI pancreas revealed cavernous portal vein transformation and chronic intrahepatic biliary dilation compatible with PCC. There was narrowing of the biliary system at the confluence secondary to extrinsic compression from cavernous transformation. No CBD dilation or filling defects, pancreatic mass, or PD dilation was noted. ERCP with an occlusion cholangiogram revealed a normal CBD. Unexpected vigorous hemobilia was encountered. Cholangioscopy was limited by fresh blood and clots up to the confluence - a bleeding source could not be identified. Interventional Radiology was consulted. CT angiogram revealed no active bleeding. TIPS was patent. Overnight the patient developed fever, leukocytosis, increasing RUQ abdominal pain, and worsening bilirubin consistent with ascending cholangitis. Antibiotics were initiated. Emergent ERCP was performed. Balloon sweeps of the CBD extracted clots and re-precipitated hemobilia. Cholangiogram revealed turbulence and dilution of contrast at the confluence, suggesting a bleeding source in the vicinity. A fully covered metallic stent was deployed at the confluence. Cholangioscopy was performed through the stent. No active bleeding was noted. The patient did well post procedure with resolution of bleeding, pain, and fever. Treatment of complicated PCC is multi faceted. It involves endoscopic biliary decompression followed by portal decompression (proximal splenorenal shunt or TIPS). Patients who remain symptomatic may undergo biliary drainage surgeries (hepaticojejunostomy or choledochojejunostomy). Hemobilia has been reported rarely after balloon sweeps, attributed to suspected intracholedochal varices and managed successfully by covered metal stents.Figure 1Figure 2Figure 3

A case report of simultaneous orthotopic liver transplantation and jejunectomy.

BackgroundLiver transplantation (LT) accompanied by jejunectomy to treat patients with acute or chronic hepatic cirrhosis with thrombosis in the portal system is extremely rare.Case presentationA 47-year-old man presented with hematemesis and melena, and a diagnosis of decompensated cirrhosis, chronic portal vein thrombosis (PVT) and secondary gastro-esophageal variceal hemorrhage was made. Coagulants were administered, but portal vein thrombi occurred rapidly, and gastrointestinal bleeding recurred shortly thereafter. The patient underwent LT, phlebothrombectomy and a partial jejunectomy. His recovery from a fistula was uneventful, and follow-up visits over 70 months were unremarkable.ConclusionLiver transplantation and partial jejunectomy is a feasible and effective surgical option for select patients with end-stage liver disease accompanied by acute portal venous thrombosis.

Hepatic encephalopathy in patients with non-cirrhotic portal hypertension: Description, prevalence and risk factors

BackgroundHepatic encephalopathy (HE) is a common complication of cirrhosis but it is less studied in patients with non-cirrhotic portal hypertension (NCPH). AimsTo describe the prevalence of cognitive impairment (overt and covert HE) in NCPH patients and to identify the risk factors for its development. Methods51 patients with NCPH, 35 with chronic portal vein thrombosis (PVT) and 16 with idiopathic non-cirrhotic portal hypertension (INCPH), were evaluated for the presence of previous or present overt HE (OHE). The psychometric hepatic encephalopathy score and the SCAN battery were used to detect the presence of covert HE (CHE). 34 compensated cirrhotic patients were used as control. In NCPH patients, abdominal scans were performed to detect the presence of shunts. ResultsNone of the patients experienced OHE at evaluation while 5.7% of PVT and 12.5% of INCPH patients referred at least one documented episode of previous OHE, similarly to patients with cirrhosis (14.7%). Even if lower than in patients with cirrhosis (64.7%), a considerable proportion of patients with chronic PVT (34.3%) and INCPH (25%) had CHE (p=0.008). The presence of a large portal-systemic shunt was the only factor significantly correlated to cognitive impairment in NCPH patients. ConclusionHE is a tangible complication of NCPH and is mainly related to the presence of portal-systemic shunts.

Portal vein thrombosis in liver cirrhosis - the added value of contrast enhanced ultrasonography.

Portal vein thrombosis (PVT) is a frequent complication of liver cirrhosis and its prevalence increases with the severity of liver disease. Patients with liver cirrhosis and hepatocellular carcinoma may have either malignant or blunt (benign) PVT. In these patients, the diagnosis and characterization of PVT is important for the prognosis and further treatment. Ultrasound (US) is the modality of choice for the diagnosis of PVT. The features of PVT on B-mode (gray-scale) US include: dilatation of the portal vein, visualization of the thrombus and, in chronic PVT- cavernous transformation. Sensitivity of US in the diagnosis of PVT is improved by the use of Doppler US and of ultrasound contrast agents. In the latter years, contrast enhanced ultrasound (CEUS) showed high sensitivity in the differential diagnosis between benign and malignant PVT and could be the diagnostic method of choice for the characterization of PVT. Blunt thrombi are avascular and will not enhance during CEUS examination, while a hyperenhancement pattern of the portal thrombus in the arterial phase, with "wash out" in the portal or late phase is typical for malignant PVT.

Portal Vein Stent Placement in Five Patients with Chronic Portal Vein Thrombosis Prior to Pancreatic Surgery

Five patients with pancreatic tumors and chronic portal vein (PV) thrombosis underwent PV stent placement before surgery. The patients either had resectable tumors or locally advanced tumors with stable, partial, or complete response to neoadjuvant therapy. PV stent placement removed periportal collaterals in all cases, with no complications, in a mean time of 150 minutes. Patients received a daily dose of subcutaneous low-molecular-weight heparin until 12 hours before surgery, and low-molecular-weight heparin was resumed for 30 days after surgery. Surgery was performed 1 day to 3 months after PV stent placement, with no complications related to periportal collaterals.

3:00 PMAbstract No. 426 - Portal vein recanalization and transjugular intrahepatic portosystemic shunt to improve transplant candidacy of patients with chronic portal vein thrombosis

3:00 PMAbstract No. 426 - Portal vein recanalization and transjugular intrahepatic portosystemic shunt to improve transplant candidacy of patients with chronic portal vein thrombosis