Chronic Portal Vein Thrombosis Research Articles

Management of portal vein thrombosis in liver transplant candidates.

Portal vein thrombosis (PVT) is a frequent event among patients with advanced liver disease, with a prevalence reaching up to 26% in those awaiting liver transplantation (LT). Extensive thrombosis affecting the mesenteric vein confluence correlates with increased morbidity and mortality post-LT, particularly when it impedes physiological anastomosis or contraindicates the LT. Current guidelines advocate for routine PVT screening in all potential liver transplant candidates and prompt treatment upon detection. The main objective in LT candidates is to facilitate physiological portal-to-portal anastomosis. Anticoagulation serves as the first-line therapy, achieving recanalization rates between 33 and 75%. Discontinuation of anticoagulation significantly heightens the risk of rethrombosis in a substantial proportion of patients and therefore, it is recommended to continue anticoagulation until LT for those awaiting LT or potential LT candidates. Nevertheless, 30-60% of patients fail to respond to anticoagulation, with PVT progression occurring in up to 14% despite anticoagulation. In such cases, TIPS placement emerges as a viable alternative to maintain portal vein patency. While the feasibility of TIPS placement diminished with the presence of portal cavernoma or chronic portal vein thrombosis, the introduction of novel interventional radiological techniques to recanalize the portal venous axis through transplenic, transmesenteric and/or transhepatic routes is revolutionizing this landscape. These advancements achieve TIPS placement and recanalization in 90-100% of patients, warranting consideration in cirrhotic patients with chronic PVT for whom LT would otherwise be contraindicated or when physiological anastomosis is not feasible.

Unilateral Abdominoscrotal Hydrocele in a 38-year-old Adult with Chronic Portal Vein Thrombosis from Addis Ababa, Ethiopia

Ascites with a communicating scrotal hydrocele is a rare clinical encounter. It occurs due to communication with the abdominal cavity through the inguinal canal. We report a case of a 38-year-old male with chronic portal vein thrombosis and portal hypertension, who presented with left abdominoscrotal hydrocele, at Adera Medical and Surgical Center (AMSC) in Addis Ababa, Ethiopia.

Cognitive Dysfunction in Children with Chronic Liver Diseases and Portal Vein Thrombosis

Cognitive Dysfunction in Children with Chronic Liver Diseases and Portal Vein Thrombosis

Quantifying Residual Rivaroxaban Plasma Concentration after Antagonization with Andexanet Alfa: A Difficult Task in Routine Clinical Practice.

We describe the case of a 38-year-old man with a history of chronic portal vein thrombosis who presented with abdominal pain after a transjugular intrahepatic portosystemic shunt procedure. Under anticoagulation therapy with rivaroxaban, he experienced active splenic bleeding, leading to hemodynamic instability. Emergency interventions, including andexanet alfa and nanoparticle administration, successfully stopped the bleeding. However, routine tests showed persistently high rivaroxaban levels despite reversal with andexanet alfa. This case report shows that next to standard anti-Xa activity assay, high-performance liquid chromatography is as well unreliable in this regard. In contrast, viscoelastic tests might better serve as indicators of the efficacy of the reversal. The availability of modified anti-Xa tests is urgently needed, to monitor the effects of andexanet alfa reversal.

First report of chronic portal vein thrombosis successfully managed with splenectomy and long-term direct oral anticoagulants

First report of chronic portal vein thrombosis successfully managed with splenectomy and long-term direct oral anticoagulants

A201 AORTO-ESOPHAGEAL FISTULA AS A COMPLICATION OF ESOPHAGEAL VARICEAL BANDING

Abstract Aims This is the first reported case of bleeding from an aorto-esophageal fistula as a consequence of ischemic esophageal ulceration post esophageal variceal banding. Methods A 46-year-old male presented with epigastric pain for one-week, which was not associated with fever, jaundice, or symptoms of GI bleed. He was hemodynamically stable with an unremarkable exam and basic labs. He underwent a CT scan which showed chronic portal vein thrombosis extending from the main portal vein into the superior mesenteric vein and evidence of portal hypertension, along with massive esophageal varices. Anticoagulation was not started due to risk of GI bleed. Upper endoscopy confirmed the presence of three columns of large esophageal varices in the distal and mid esophagus, the largest was 3 cm in size. There was no stigmata of recent bleeding and no gastric varices. Seven bands were applied. CT abdomen was repeated on the seventh day of admission, showing extension of portal vein thrombosis. As such, the thrombosis team started a low dose of anticoagulation. (dalteparin 7500 IU). He tolerated it well and showed no signs of bleeding prior to discharge. The day after discharge, the patient presented again with an episode of melena. Examination was remarkable for tachycardia, hypotension and melena. Hemoglobin was stable. Patient was admitted with impression of upper GI bleed most likely secondary to post banding ulcer. He was started on medical therapy. Anticoagulation was held. Next day, the patient had an episode of hematemesis with large amount of blood and clots. Emergent upper endoscopy showed active bleeding in the distal esophagus. Further examination showed a full-thickness, 7 mm defect in the lower esophagus with fresh red blood emptying from it into the esophagus (Figure 1). Thoracic surgery was consulted and suspected a perforated esophageal ulceration at the site of previous banding, with an aorto-esophageal fistula. Patient deteriorated immediately and passed away. The cause of death was cardiac arrest secondary to acute blood loss anemia. Results AEF is a recognized cause of upper GI bleeding with a high mortality rate. While rare, it can occur secondary to ischemic esophageal ulcer post EV banding. Conclusions This is the first reported case of an aorto-esophageal fistula as a consequence esophageal variceal band ligation. While extremely rare, this complication should be considered as a potentially fatal complication of variceal banding, especially in the setting of a diseased or previously repaired aorta.

Relationship between Neutrophil/Lymphocyte Ratio (NLR), Platelet/Lymphocyte Ratio (PLR) and Thrombosis in Patients with Portal Vein Thrombosis (PVT) without Acquired Risk Factor for Thrombosis.

Inflammation occurring after vascular endothelial damage plays a role in thrombus formation. Changes in various blood parameters that develop after the inflammatory condition can be used as a marker to predict thrombus. This study aimed to investigate the relationship between the neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), and portal vein thrombosis (PVT). After applying the exclusion and inclusion criteria to the patients diagnosed with PVT and followed up in our center between January 2006 and May 2018, a total of 38 patients without acquired risk factors for the development of PVT and 52 healthy controls were included in the study. Clinical features and NLR and PLR at diagnosis were evaluated. NLR and PLR values were detected to be significantly higher in patients diagnosed with PVT compared to the control group (P < 0.001 for NLR, P < 0.001 for PLR). Findings were as follows: In acute PVT patients for NLR = 3.645 (area under the receiver operating characteristic (AUROC) 0.886, sensitivity 69.2%, specificity 96.2%, P < 0.001), for PLR = 196.24 (AUROC 0.754, sensitivity 53.2%, specificity 96.2%, P = 0.005), while in chronic PVT patients, for NLR = 3.645 (AUROC 0.744, sensitivity 40%, specificity 96.2%, P = 0.001), and for PLR = 195.93 (AUROC 0.715, sensitivity 44%, specificity 96.2%, P = 0.002). NLR and PLR were associated with the diagnosis of PVT. In PVT patients, NLR and PLR values were observed to be significantly higher than the control group. In our study, the relationship between NLR and PLR in patients with noncirrhotic, nonmalignant PVT without acquired risk factors for thrombosis was shown for the first time.

Rare Complication of Chronic Pancreatitis: Chronic Portal Vein Thrombosis and Splenic vein thrombosis causing non cirrhotic portal hypertension

Splenic vein thrombosis is a well-established complication of chronic pancreatitis, while portal vein thrombosis is a rare complication. In this case, we present an interesting instance of chronic pancreatitis associated with both portal and splenic vein thrombosis, causing non-cirrhotic portal hypertension. A fortysix-year-old male patient presented to us with clinical features of chronic pancreatitis. He underwent a CECT abdomen, which showed chronic pancreatitis with portal vein and splenic vein thrombosis. Screening for thrombophilic conditions and malignancies were negative. An upper gastrointestinal endoscopy showed fundal varices. Chronic portal vein thrombosis and splenic vein thrombosis are rare complications of chronic pancreatitis, which can cause non-cirrhotic portal hypertension.

Transjugular Intrahepatic Portosystemic Shunt (TIPS) Extension for Transhepatic Mesocaval Shunt Creation: A Case Series for Treating Refractory Upper Gastrointestinal Bleeding in Patients with Chronic Portal Vein Thrombosis.

Transjugular intrahepatic portosystemic shunt (TIPS) is known to benefit patients with decompensated liver disease by alleviating portal pressure. However, TIPS creation is technically difficult and challenging to perform in patients with chronic portal vein thrombosis (PVT) (4,5). Multiple endovascular techniques for portal vein recanalization with or without creating portosystemic shunt are available to decompress and alleviate portal hypertension in patients with PVT. In this case series, we represent TIPS extension to create an endovascular mesocaval shunt for the treatment of refractory upper gastrointestinal bleeding.

Thromboelastography characteristics in critically ill patients with liver disease.

The purpose of this study was to determine how thromboelastography (TEG) parameters differ by various clinical conditions that commonly occur in patients with cirrhosis, including sepsis, acute on chronic liver failure (ACLF), alcohol-associated hepatitis (AAH) and portal vein thrombosis (PVT). TEG, a whole blood assay, is used to assess several parameters of coagulation and is becoming increasingly used in clinical practice. This study was a retrospective chart review of 155 patients admitted to the ICU with decompensated cirrhosis from 2017 to 2019. The R time was significantly shorter in patients when they were septic compared to when they were not and longer in patients with vs. without ACLF grade 3. Alpha angle and maximum amplitude was decreased in patients with severe AAH compared to those without severe AAH; and maximum amplitude was increased in patients with acute PVT compared to those with chronic PVT. R time was positively correlated with Chronic Liver Failure Consortium Organ Failure and Chronic Liver Failure Consortium ACLF scores (rho = 0.22, P = 0.020), while alpha angle and maximum amplitude were negatively correlated with MELD-NA. Findings suggest TEG parameters vary in several clinical conditions in patients with decompensated cirrhosis who are admitted to the ICU. Prospective research is needed to confirm our findings and to determine how this knowledge can be used to guide clinical practice, as well as blood product transfusions in the setting of bleeding or prior to invasive procedures.

S3570 Beckwith-Wiedemann Syndrome: A Rare Presentation of Chronic Portal Vein Thrombosis with Cavernous Transformation Extending to the Superior Mesenteric Vein

S3570 Beckwith-Wiedemann Syndrome: A Rare Presentation of Chronic Portal Vein Thrombosis with Cavernous Transformation Extending to the Superior Mesenteric Vein

Recanalization of portal vein thrombosis after pediatric liver transplantation: Efficacy and safety of the transsplenic access.

Endovascular management of portal vein thrombosis (PVT) is challenging. Transsplenic access (TSA) is growing as an access option to the portal system but with higher rates of bleeding complications. The aim of this article is to evaluate the efficacy and safety of transsplenic portal vein recanalization (PVR) using a metallic stent after pediatric liver transplantation. This is a retrospective review of 15 patients with chronic PVT who underwent PVR via TSA between February 2016 and December 2020. Two children who had undergone catheterization of a mesenteric vein tributary by minilaparotomy were excluded from the patency analysis but included in the splenic access analysis. The technical and clinical success of PVR and complications related to the procedure via TSA were evaluated. Thirteen children with PVT were treated primarily using the TSA. The mean age was 4.1 years (range, 1.5-13.7 years), and the most common clinical presentation was hypersplenism (60%). Technically successful PVR was performed in 11/13 (84.6%) children, and clinical success was achieved in 9/11 (81.8%) children. No major complications were observed, and one child presented moderate pain in the TSA (from a total of 17 TSA). The median follow-up was 48.2 months. The median primary patency was 9.9 months. Primary patency in the first 4 years was 75%, and primary assisted patency was 100% in the follow-up period. Transsplenic PVR is a safe and effective method for the treatment of PVT after pediatric liver transplantation.

THE SURGEON'S PERSPECTIVE ON PORTAL VEIN THROMBOSIS IN PATIENTS WITH LIVER CIRRHOSIS

The article discusses the key aspects of the etiology, diagnosis, and treatment of portal vein thrombosis in patients with liver cirrhosis. The prevalence of portal vein thrombosis in individuals with liver cirrhosis ranges from 0.6 % to 26 %, with a higher incidence observed in those with decompensated cirrhosis. Symptoms of portal vein thrombosis are often nonspecific. Approximately one-third of patients with this condition experience no symptoms, and the detection of a thrombus is usually an incidental finding during computed tomography or ultrasound examinations.&#x0D; Acute portal vein thrombosis is characterized by abdominal pain in the right upper quadrant, non-bloody diarrhea, or acute intestinal obstruction when there is symptomatic dilatation of the superior mesenteric vein. On the other hand, chronic portal vein thrombosis manifests through signs of portal hypertension, such as esophageal and gastric bleeding, deterioration of portal gastropathy, splenomegaly, pancytopenia, and significant ascites.&#x0D; The first-line treatment for portal vein thrombosis involves the use of direct and indirect anticoagulants. However, their administration necessitates careful consideration of the risk of intraluminal bleeding, the severity of cirrhosis, and the potential benefits of portal vein recanalization. Mechanical thrombectomy can serve as an alternative to long-term anticoagulant therapy for portal vein thrombosis. In cases of portal vein thrombosis in patients with cirrhosis, after mechanical thrombectomy and thrombolysis, the placement of transjugular intrahepatic portosystemic shunt (TIPS) is often performed.&#x0D; To conclude, portal vein thrombosis frequently occurs in patients with liver cirrhosis, and its appearance is challenging to predict due to its multifactorial nature. The preferred initial treatment for acute portal vein thrombosis, in the absence of intraluminal bleeding or intestinal ischemia, involves the use of direct and indirect anticoagulants. Minimally invasive surgical options, such as mechanical thrombectomy, chemical thrombolysis, and TIPS placement (with or without variceal embolization), are currently available. However, due to the heterogeneous nature of the existing data and the lack of randomized controlled trials, definitive recommendations regarding the optimal treatment strategy are not yet available.&#x0D; Keywords: cirrhosis, coagulopathy, portal hypertension, portal vein thrombosis, anticoagulants.

Application of ultrasonography-elastography score to suspect porto-sinusoidal vascular disease in patients with portal vein thrombosis

BackgroundPorto-sinusoidal vascular disease (PSVD) and portal vein thrombosis (PVT) are causes of portal hypertension characterized respectively by an intrahepatic and a pre-hepatic obstacle to the flow in the portal system. As PVT may be a consequence of PSVD, in PVT patients at presentation, a pre-existing PSVD should be suspected. In these patients the identification of an underlying PSVD would have relevant implication regarding follow-up and therapeutic management, but it could be challenging. In this setting ultrasonography may be valuable in differential diagnosis. The aim of the study was to use ultrasonography to identify parameters to discriminate between PSVD and “pure” PVT and then to suspect PVT secondary to a pre-existing PSVD. MethodsFifty-three patients with histologically proven PSVD and forty-eight patients affected by chronic PVT were enrolled and submitted to abdominal ultrasonography with elastography by acoustic radiation force impulse (ARFI). ResultsARFI was higher and superior mesenteric vein (SMV) diameter was wider in PSVD patients than in PVT patients. Thus, a prognostic score was obtained as linear combinations of the two parameters with a good discrimination capacity between PSVD and PVT (the area under the curve = 0.780; 95% confidence interval: 0.690-0.869). ConclusionsA score based on ARFI and SMV diameter may be useful to suspect an underlying PSVD in patients with PVT and to identify a subgroup of patients to be submitted to liver biopsy.

Clinical outcomes and prognostic factors in non-cirrhotic non-neoplastic patients with portal vein thrombosis: A single-centre experience

IntroductionThe knowledge of natural history and prognostic factors of portal vein thrombosis (PVT) is still based on a limited number of studies. AimTo describe our single-center experience with 79 consecutive non-neoplastic non-cirrhotic patients with PVT (15 recent/64 chronic PVT). ResultsAmong patients with recent PVT, 7 received anticoagulation alone, 4 systemic thrombolysis, 3 direct thrombolysis through a TIPS and 1 TIPS alone. Portal recanalization was achieved in 11 patients. In patients with chronic PVT, the rate of variceal progression was high (20% at one year and 50% at two years). The thrombotic involvement of splenic and superior mesenteric veins was the only risk factor for variceal enlargement. The cumulative bleeding rates were 10% at one year and 20% at two years. A multisegmental thrombosis and large varices at entry and a previous variceal bleeding were the independent predictors for variceal bleeding. The cumulative rate of new thrombotic events was 14% at one year and 18% at two years. Eight patients died, 2 because of thrombotic events. There were no bleeding-related deaths. Two-year cumulative survival rate was 90%. ConclusionsOur study supports the importance of anticoagulation especially when a more extended thrombosis is present. Moreover, in patients with chronic PVT, the timing of follow-up endoscopy should be based on the extension of thrombosis and not, as in cirrhosis, on the size of varices at first endoscopy.

Safety and Efficacy of Transjugular Intrahepatic Portosystemic Shunt for Non-tumoral Cirrhotic Portal Vein Thrombosis Not Responding to Anticoagulation Therapy.

To evaluate the feasibility, safety, and efficacy of add-on transjugular-intrahepatic-portosystemic shunt (TIPS) for portal vein recanalization (PVR) in cirrhotic patients with non-tumoral chronic portal vein thrombosis (PVT) after 6months of monitored anticoagulation therapy (ACT). We conducted a retrospective search of the hospital database for patients who underwent TIPS for persistent PVT despite 6months of ACT (January 2011 to August 2021). These patients were compared to control group (ACT group; no TIPS but continued on ACT). Post-TIPS periodic assessment was done to look for clinical outcome, PVR (using contrast-enhanced CT scan), and complications. A total of 90 patients were analyzed. Thirty-six patients in TIPS group and 54 patients in ACT group. TIPS was successfully performed in all patients. TIPS group showed complete recanalization of portal vein in 77.8%, partial recanalization in 16.7%, and stable thrombus in 5.5% of the patients. TIPS thrombosis was seen in 3 patients, all underwent successful endovascular thrombolysis. Seven patients developed post-TIPS hepatic encephalopathy and were managed conservatively. In contrast, no patient in ACT group achieved PVR on 12-month follow-up. After propensity score matching, patients in TIPS group showed significantly lower incidence of variceal re-bleeding (22.2% vs. 77.8%, p = 0.03) and refractory ascites (11.1% vs. 51.9%, p < 0.01) with significantly better 12-month survival as compared to ACT group (88.9% vs. 69.4%, p = 0.04). TIPS in cirrhotic patients with PVT result in superior recanalization rates, better control of ascites, and variceal re-bleeding resulting in better survival. TIPS may be considered a preferred therapy after anticoagulation failure. TIPS is associated with good technical and clinical success in patients of cirrhosis with PVT and should be considered in patients not responding to ACT.

Prevalence of portal vein and splanchnic venous thrombosis in dogs with chronic hepatitis.

Alterations in haemostasis have been described in dogs and humans with chronic hepatitis. Portal vein thrombosis is a recognised complication of chronic hepatitis in humans; however, its prevalence in dogs with chronic hepatitis has not been reported. We aimed to estimate the prevalence of, and describe clinical and laboratory data of dogs with chronic hepatitis and portal vein thrombosis and splanchnic venous thrombosis. Retrospective cross-sectional study. Medical records of dogs admitted to a veterinary teaching hospital between 2009 and 2019 were reviewed. Dogs were included if chronic hepatitis was histopathologically confirmed, and if diagnostic imaging or necropsy indicated the presence of thrombosis. Clinical and laboratory data (i.e. haematology, biochemistry, coagulation panels) were recorded. Descriptive statistics were used to characterise dogs with and without thrombosis. Records from 136 dogs with chronic hepatitis were identified. Three of these dogs, 2.2% (95% confidence interval: 0.8 to 6.3%) all females, were diagnosed with portal vein thrombosis. Five dogs in total, (3.7%; 95% confidence interval: 1.6 to 8.3%), including three with portal vein thrombosis, all females, were diagnosed with splanchnic venous thrombosis. Dogs with portal vein and splanchnic venous thrombosis often had hyperbilirubinaemia, increased serum gamma-glutamyl transferase activity, and decreased plasma antithrombin 3 activity. They also had relatively high alternative Child-Pugh scores for dogs (median 6 out of 13). Portal vein and splanchnic venous thrombosis are potentially serious complications that were identified in a relatively low proportion of dogs with chronic hepatitis.

Recurrent Portal Vein Thrombosis In Liver Transplantation With Renoportal Anastomosis Caused by Spontaneous Reno-Caval Shunts: A Case Report

Orthotopic liver transplantation (OLT) in patients with cirrhosis complicated by portal hypertension, portosystemic shunts, and chronic portal vein thrombosis (PVT) has long been challenging. Spontaneous spleno-renal shunts (SRS) allow new surgical techniques to restore portal vein patency and hepatopetal flow. Renoportal anastomosis (RPA) has emerged as an accepted method for transplanting these patients, with good long-term patient and graft survival. Orthotopic liver transplantation with RPA is known to be complicated by recurrent PVT, with few details discussed in the literature. We present a case of a 56-year-old woman with decompensated cirrhosis who underwent deceased donor whole graft OLT using RPA with iliac vein conduit. The postoperative course was complicated by occlusive thrombosis in the portal vein and iliac vein conduit. Venography revealed enlarged left gonadal and lumbar vein varices acting as reno-caval shunts with hepatofugal flow. Embolization of the varices re-established durable venous patency that was confirmed on post-transplant day 68 with no other hemodynamic complications. This showcases an interesting mechanism by which recurrent PVT may occur in patients undergoing OLT with RPA. Because durable portal vein patency can be achieved with Interventional Radiology embolization of reno-caval varices, assessing these communications is an important preoperative consideration for planned OLT with RPA.

Portal Vein Thrombosis in a Woman with a Large Uterine Fibroma

This article presents a case of portal vein thrombosis accompanied by a large uterine fibroma. A 37-year-old virgin woman presented with vaginal bleeding, abdominal mass, fever, dyspnea and lower limbs edema. In past medical history, she did not have any systemic diseases. She had menometrorrhagia from four years ago. She was admitted with diagnosis of a large uterine fibroma and was suspected of COVID 19 pneumonia or thrombophlebitis. The final diagnosis was a large uterine fibroma with chronic portal vein thrombosis. Although uterine fibromas are benign tumors, they may make serious life-threatening complications like thrombosis. The cause of thrombosis is the pressure effect of fibroma and/ or transfusion to treat anemia. Although there may be other unknown etiologies for thrombosis in these patients. We suggest that existence of a large uterine myomas should be known as a risk factor for thrombosis ( like IBS, Covid 19 and etc.) and be given a score in Caprini Score system, to start anticoagulation before and after any surgical intervention.

PORTAL VEIN THROMBOSIS – A STUDY OF RISK FACTORS, CLINICAL PROFILE, COMPLICATIONS AND MANAGEMENT

Background: The portal vein is formed by the conuence of the splenic and superior mesenteric veins. Occlusion of the portal vein by thrombus (portal vein thrombosis [PVT]) typically occurs in patients with cirrhosis and/or prothrombotic disorders/ pancreatitis. Patients with acute PVT have the sudden onset of portal venous occlusion due to thrombus. Patients with acute PVT have not yet developed features of chronic PVT, such as collateral circulation (e.g., cavernous portal transformation) or portal hypertension. Chronic PVT develops when acute doesn't resolve with formation of collaterals. In patients with suspected acute PVT, we typically obtain a contrast-enhanced abdominal computed tomography (CECT) to conrm the diagnosis, evaluate for predisposing conditions (eg, intra-abdominal infection), assess the extent of the thrombosis and the anatomy of collaterals, and detect evidence of intestinal infarction. Doppler and MRI are other alternative imaging modalities. The primary management of acute portal vein thrombosis (PVT) is anticoagulation and, when possible, treatment of predisposing condition. The goal of anticoagulation is to prevent extension of the clot and to allow for recanalization, so that intestinal infarction and portal hypertension do not develop. Unlike chronic PVT, where the role of anticoagulation in patients with cirrhosis is unclear, studies suggest anticoagulation for acute PVT is benecial for patients with cirrhosis. However, because patients with cirrhosis may have esophageal varices, we typically screen for varices prior to initiating anticoagulation. 60 cases of extrahepatic portal vein thrombosis or intrahepatic Methods: portal vein thrombosis were included. All registered diagnoses were based on either ultrasound with Doppler, CT-angiography or MRI. In our study, Ris Results: k factors were established in 24 cases (80%). When including all risk factors, 16 cases (53.3%) had local risk factor, and 8 cases (26.6%) had a systemic risk factor. Anatomical location was in 26 cases (86%)extrahepatic, (14%) intrahepatic. In addition, patients with extrahepatic PVT also had intrahepatic thrombosis (38%) and/or in the splenic vein (23%). 66% had oesophageal varices, 53% gastric varices, 46% portal hypertensive gastropathy, 26% variceal haemorrhage, and 40% ascites. Most patients had a combination of local and systemic risk Conclusion: factors for PVT. Partial/ complete recanalization is more in patients treated with anticoagulation therapy, and that regression of varices was more in patients who were treated with active endoscopy combined with beta blockers.