Catheter-directed Thrombolysis Combined with Anticoagulation for Acute Extensive Portal Vein Thrombosis: Our Experience (original) (raw)
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1. PORTAL VEIN THROMBOSIS ETIOLOGY, DIAGNOSIS AND MANAGEMENT
Portal Vein Thrombosis (PVT) is a common clinical problem often found in Gastroenterology Clinics. It may occur with or without a pre-existing chronic liver disease. Clinical course may be acute or chronic. Clinical features vary in acute and chronic Portal Vein Thrombosis. Acute PVT usually presents with pain abdomen while as chronic PVT presents with features of Portal Hypertension. Management also differs-acute PVT is managed with anticoagulants while as chronic PVT is managed as portal hypertension.
Portal vein thrombosis (PVT): A study of 20 non-irrhotic cases
Swiss medical weekly: official journal of the Swiss Society of Infectious Diseases, the Swiss Society of Internal Medicine, the Swiss Society of Pneumology
Portal and mesenteric venous thrombosis (PVT) is an uncommon disease with serious consequences if not discovered early in order to prevent complications such as variceal bleeding and intestinal ischaemia. The objective of this study was to describe the clinical presentation and outcome of patients with PVT with a view to early diagnosis and treatment of this disease. The study was restricted to patients with PVT not caused by underlying liver cirrhosis. To analyse important clinical characteristics of this entity we performed a retrospective study of 20 non-cirrhotic patients seen in our hospital from February 1998 to March 2003. The main clinical symptom was abdominal pain (13 patients, 86%), sometimes in combination with diarrhoea and vomiting (5 patients, 33%), nausea and anorexia (3 patients). Laboratory signs were non-specific and diagnosis was usually by computed tomography (19 patients, 95%). Causative factors included prothrombotic states (9 patients, 45%) and/or local facto...
Portal vein thrombosis: A concise review (Review)
Experimental and Therapeutic Medicine, 2021
Portal vein thrombosis (PVT) is a frequent complication in cirrhotic patients, but it may also exist as a basic vascular condition even without any liver damage. Local and systemic factors play a significant role in the pathogenesis of PVT; yet, in practice, more than one factor may be identified. PVT can be considered a result of liver fibrosis and hepatic insufficiency. The JAK2 mutation has been accepted as a factor producing PVT. In general, the anticoagulants are recommended but this therapy should be used carefully in treating patients that associate coagulopathy or thrombocytopenia and esophageal varices. Acute PVT without bowel infarction has a good prognosis. In liver cirrhosis, the mortality due to hemorrhage is higher than in chronic PVT. Therefore, for the patients with PVT, the survival rate is decreased by 55% in two years, due to hepatic insufficiency. Regarding the treatment, LMWH (low molecular weight heparine) is the most utilized in patients with cirrhosis, non-malignancies, infections, or those who are awaiting a liver transplant. DOACs (direct-acting oral anticoagulants) may be used in the rest of the medical conditions, being safe and equal to LMWH.
Journal of International Medical Research, 2011
This observational cohort study reports the short-and long-term clinical outcomes of 31 patients admitted for acute nonmalignant, non-cirrhotic portal vein thrombosis (PVT) over a 10-year period. Patients had a mean age of 43 years at admission and a mean duration of followup of 84 months. All patients were initially treated with anticoagulants. Complete recanalization occurred within 30 days after admission in 18 patients (58%), partially in nine patients (29%), and failed in four patients (13%). During follow-up, 10 patients (32%) had at least one episode of gastrointestinal bleeding. The probability of remaining bleed-free was 0.93 at 24 months and 0.61 at 48 months. Fundal varices were not controlled by endoscopic sclerotherapy, so all four patients underwent portosystemic shunt construction. To date, there has been no mortality. In conclusion, using a combination of different treatment options reduces the risk of death and late complications in patients with nonmalignant, non-cirrhotic PVT.
Review article: portal vein thrombosis - new insights into aetiology and management
Alimentary Pharmacology and Therapeutics, 2005
Portal vein thrombosis may occur in the presence or absence of underlying liver disease, and a combination of local and systemic factors are increasingly recognized to be important in its development. Acute and chronic portal vein thrombosis have traditionally been considered separately, although a clear clinical distinction may be difficult. Gastrooesophageal varices are an important complication of portal vein thrombosis, but they follow a different natural history to those with portal hypertension related to cirrhosis. Consensus on optimal treatment continues to be hampered by a lack of randomized trials, but recent studies demonstrate the efficacy of thrombolytic therapy in acute thrombosis, and the apparent safety and benefit of anticoagulation in patients with chronic portal vein thrombosis.
Diagnosis and management of portal vein thrombosis in patients with cirrhosis of liver
The Southwest Respiratory and Critical Care Chronicles, 2018
Portal vein thrombosis (PVT) is an occlusion of the portal venous system and is a common complication of liver cirrhosis. It can present as either an acute or chronic complication. Acute PVT can present with abdominal pain, diarrhea, ileus, and bleeding. Chronic PVT is often asymptomatic; however, it can be discovered in cases of worsening portal hypertension. Portal vein thrombosis is diagnosed by imaging modalities, such as ultrasound and computed tomography. Contrast-enhanced imaging can be used in cases with difficult visualization. Despite the hemostatic imbalance in cirrhosis, anticoagulants can be safely used to recanalize the vein. Transjugular intrahepatic portosystemic shunt procedures are also an effective method for recanalization.
Management of Variceal Bleeding in Patients with Noncirrhotic Portal Vein Thrombosis
Annals of Surgery, 1988
Since 1971, 70 patients have been seen at Emory University Hospital with gastroesophageal varices secondary to extrahepatic portal vein thrombosis (PVT). Thirty-seven of these patients had had prior major operative therapy. In only three patients (8%) was shunt surgery successful, and there was a high incidence of rebleeding, other morbidity, and mortality. Of especial note are the serious consequences of simple splenectomy; splenomegaly and thrombycytopenia should rarely, if ever, be used as indication for splenectomy in portal hypertension. In 1977, the use of selective distal splenorenal shunt (DSRS) was begun at Emory in this population and a selective shunt has been possible in 24 of 29 patients (83%) who had had no prior operative therapy. Results have been excellent with a greater than 90% patency rate, long-term portal perfusion in all, no encephalopathy, and late rebleeding in one patient. Quantitative studies at 3-6 years show stability of liver function, significant decrease in spleen size, and rise in platelet count. However, long-term follow-up (>15 years) is required in PVT patients before definitive assessment can be obtained. A specific problem of the PVT patient is late shunt stenosis which requires close observation; dilatation of the shunt was performed in six of the 24 patients with a patent shunt. Poor results with non-shunt operative procedures in PVT were again documented. The proper role of endoscopic variceal sclerotherapy is not yet clear, but appears to be an excellent addition to the therapeutic options. In conclusion, for patients with a patent splenic vein, initial therapy should be a selective shunt; for patients without a patent splenic venous system, endoscopic sclerotherapy is the procedure of choice. E n XTRAHEPATIC PORTAL VEIN THROMBOSIS (PVT) in the noncirrhotic is a relatively uncommon cause of portal hypertension in this country. Effective management of bleeding varices in PVT
Saudi Journal of Gastroenterology, 2015
Noncirrhotic portal hypertension (NCPH), as it generally is termed, is a heterogeneous group of diseases that is due to intrahepatic or extrahepatic etiologies. In general, the lesions in NCPH are vascular in nature and can be classified based on the site of resistance to blood flow as "prehepatic," "hepatic," and "posthepatic." The "hepatic" causes of NCPH can be subdivided into "presinusoidal," "sinusoidal," and "postsinusoidal [Table 1]." Portal vein thrombosis was first seen by Stewart and Balfour in the late 1860s in a patient with splenomegaly, ascites, and variceal dilatation. Kobrich coined the term cavernoma to describe spongy appearance of portal vein (PV). [1] Generally a hypercoagulable state, intra-abdominal infection/peritonitis, and PV anomaly (PV stenosis and atresia) are considered important predisposing factors of EHPVO; however, vast majority of cases are due to primary thrombosis of the PV and often with more than one cause. Accurate epidemiological data on PVT is difficult to obtain. Prevalence of autopsy research in the United States and Japan ranges from 0.05% to 0.5% population prevalence of portal vein thrombosis (PVT) studied by Ogran et al. seen on autopsy series is 1%. [2] Thus PVT is responsible for 5%-10% of all cases of portal hypertension in western countries. Of all cases of portal hypertension (PHT) in developing countries, 40% are attributed to PVT. In children, EHPVO accounts for 80% cases of PHT. [3] Incidence of PVT among liver cirrhotics ranges from 0.6% to 64.1%. [4] After cirrhosis, EHPVO is the most common cause of portal hypertension globally. In the Indian subcontinent, 20%-30% of all variceal bleeds are due to EHPVO. In Japan, 10%-20% of variceal bleeds and in the west, 2%-5% of variceal bleeds are due to EHPVO. Clinical presentation of PVT is different in acute and chronic thrombosis. This depends on development and extent of collateral circulation. Intestinal congestion and ischemia with abdominal pain, fever, diarrhea, rectal bleeding, distension, sepsis, and lactic acidosis with or without splenomegaly are common features of acute PVT.
Acute portal vein thrombosis unrelated to cirrhosis: A prospective multicenter follow-up study
Hepatology, 2010
Current recommendations for early anticoagulation in acute portal vein thrombosis unrelated to cirrhosis or malignancy are based on limited evidence. The aim of this study was to prospectively assess the risk factors, outcome, and prognosis in patients managed according to these recommendations. We enrolled 102 patients with acute thrombosis of the portal vein, or its left or right branch. Laboratory investigations for prothrombotic factors were centralized. Thrombus extension and recanalization were assessed by expert radiologists. A local risk factor was identified in 21% of patients, and one or several general prothrombotic conditions in 52%. Anticoagulation was given to 95 patients. After a median of 234 days, the portal vein and its left or right branch were patent in 39% of anticoagulated patients (versus 13% initially), the splenic vein in 80% (versus 57% initially), and the superior mesenteric vein in 73% (versus 42% initially). Failure to recanalize the portal vein was independently related to the presence of ascites (hazard ratio 3.8, 95% confidence interval 1.3-11.1) and an occluded splenic vein (hazard ratio 3.5, 95% confidence interval 1.