Survival of Patients with Portal Vein Thrombosis: Analysis Based on Disease Onset (original) (raw)
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Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver, 2018
The knowledge of natural history of patients with portal hypertension (PH) not due to cirrhosis is less well known than that of cirrhotic patients. To 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. The 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. At 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 cir...
Idiopathic portal hypertension: Natural history and long-term outcome
Hepatology, 2014
Idiopathic portal hypertension (IPH) is a rare cause of intrahepatic portal hypertension. Data on natural history and prognosis of IPH are limited. We sought to describe the complications and long-tem outcome of IPH by retrospectively studying 69 biopsyproven cases of IPH. Mean duration of follow-up was 6.7 6 4.6 years. All patients had evidence of portal hypertension (PH) at diagnosis, and 42% were symptomatic. Variceal bleeding (VB) was the most common manifestation. In those without bleeding at diagnosis, 74% had varices at first endoscopy. In those with large varices, the 1-year probability of first bleeding despite primary prophylaxis was 9%. The 1-year probability of rebleeding was 22%. Ascites and hepatic encephalopathy was documented in 26% and 7% of patients, respectively, at least once during the clinical course. The 1-year probability of developing portal vein thrombosis (PVT) was 9%, and 53% of patients receiving anticoagulation achieved recanalization. Human immunodeficiency virus (HIV) infection and VB at diagnosis were the independent predictors of PVT. Seven patients died (6 as a result of an IPH-related cause) and 2 were transplanted. Probability of liver transplantation-free survival was 82% at 10 years. Presence of a severe associated disorder and ascites as a presenting symptom were associated with poor survival. Conclusion: Variceal bleeding is a major complication of IPH. Using, in IPH patients, the same management approach for PH as in cirrhosis is safe and maintains a low incidence of first bleeding and rebleeding in IPH patients. PVT is a frequent complication, particularly in those with HIV infection. Despite several complications, overall survival of patients with IPH is considerably good. (HEPATOLOGY 2014;59:2276-2285
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.
journal of hepatology, 2015
See Editorial, pages 543-545 Portal hypertension is the haemodynamic abnormality associated with the most severe complications of cirrhosis, including ascites, hepatic encephalopathy and bleeding from gastroesophageal varices. Variceal bleeding is a medical emergency associated with a mortality that, in spite of recent progress, is still in the order of 10-20% at 6 weeks. The evaluation of diagnostic tools and the design and conduct of good clinical trials for the treatment of portal hypertension have always been difficult. Awareness of these difficulties has led to the organisation of a series of consensus meetings. The first one was organised again in Baveno in 2005 (Baveno IV) [9,10], in Atlanta in 2007 [11], and again in Stresa in 2010 (Baveno V) [12,13]. The aims of these meetings were to develop definitions of key events in portal hypertension and variceal bleeding, to review the existing evidence on the natural history, the diagnosis and the therapeutic modalities of portal hypertension, and to issue evidence based recommendations for the conduct of clinical trials and the management of patients. All these meetings were successful and produced consensus statements on some important points, although several issues remained unsettled. To continue the work of the previous meetings, a Baveno VI workshop was held on April 10-11, 2015. The workshop was attended by many of the experts responsible for most of the major achievements of the last years in this field. Many of them had attended the previous meetings as well. A concept that has gained wide acceptance over the past few years is the fact that patients in different stages of cirrhosis have different risks of developing complications and of dying. Accordingly, the Baveno VI workshop was entitled ''Stratifying risk and individualizing care for portal hypertension''. The main fields of discussion were the use of invasive and non-invasive methods for the screening and surveillance of gastroesophageal varices and of portal hypertension, the impact of aetiological therapy for cirrhosis, the primary prevention of decompensation, the management of the acute bleeding episode, the prevention of recurrent haemorrhage and other decompensating events, and vascular diseases of the liver in cirrhotic and non-cirrhotic patients. For each of these topics, a series of consensus statements were discussed and agreed upon. Whenever applicable, the level of existing evidence was evaluated and the recommendations were ranked according to the Oxford System [14] (i.e., level of evidence from 1 = highest to 5 = lowest; grade of recommendation from A = strongest, to D = weakest). The presentations given during the workshop are reported 'in extenso' in the Baveno VI proceedings [15]. A summary of the most important conclusions is reported here. Whenever relevant, the changes from previous consensus statements are outlined. The areas where major new recommendations were made are: screening and surveillance, the importance of obesity, comorbidities and malnutrition, the use of beta blockers in patients with refractory ascites/end-stage liver disease, and anticoagulation and portal vein thrombosis in liver cirrhosis. Definitions of key events regarding the bleeding episode (changed from Baveno V) Six-week mortality should be the primary endpoint for studies for treatment of acute variceal bleeding (5;D). 5 day treatment failure is defined using Baveno IV/V criteria without ABRI (adjusted blood requirement index) and with a clear definition of hypovolemic shock (1b;A). Baveno IV/V criteria correlate with 6-week mortality (1b;A) and should be included in future studies as a secondary endpoint to allow further validation (5;D). Additional endpoints should be reported including: need for salvage therapy (tamponade, additional endoscopic therapy, transjugular intrahepatic portosystemic shunt [TIPS], surgery etc.); blood transfusion requirements and days of ICU/hospital stay (5;D).
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...
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.
Risk Factors Regarding Portal Vein Thrombosis in Chronic Liver Disease
Acta Medica Transilvanica
The portal vein thrombosis (PVT) is one of the most frequent vascular diseases of the liver, with a high rate of morbidity and mortality. The most common causes of the PVT are hepatic cirrhosis, hepatobiliary neoplasms, inflammatory and infectious abdominal diseases, and myeloproliferative syndromes.(1,2) The natural progress of the PVT has as a result portal hypertension which leads to splenomegaly and the formation of portosystemic collateral vessels, as well as gastroesophageal, duodenal and jejunal varices. Ultrasonography, especially Doppler ultrasound, is the most widely used imaging method to asses, supervise and diagnose PVT in patients with hepatopathies. The purpose of acute PVT treatment is to re-permeabilize the obstructed vessels; the endoscopic ligature of the varices in the eventuality of their rupture is safe and extremely efficient in chronic PVT. To conclude, PVT is the most common hepatic vascular disorder, and its prevalence has increased particularly among the p...
Relation between liver pathology and prognosis in patients with portal hypertension
World Journal of Surgery, 1994
The most common causes of variceal bleeding are cirrhosis, schistosomiasis, and extrahepatic portal venous obstruction. The prognosis for an individual patient depends on the severity of the bleeding episode and the underlying liver function. Liver function is determined to a large extent by the underlying liver pathology. Patients with noncirrhotic portal hypertension or cirrhosis with good liver function have good short-and long-term prognoses. In patients with established cirrhosis, the presence of alcoholic hepatitis, hepatocellular carcinoma, or portal venous thrombosis may adversely affect prognosis. In addition to affecting prognosis, the underlying pathology may also influence choice of treatment. This point is particularly true for treatments such as shunt surgery, liver transplantation, or transjugnlar intrahepatic shunts.