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Portal vein thrombosis

Twenty-five percent ofthrombophilic patients develop thrombosis at unusual sites resulting in cerebral venous thrombosis, mesenteric vein thrombosis, hepatic venous thrombosis, retinal vein thrombosis, purpura fulminans, splenic vein thrombosis, portal vein thrombosis, renal vein thrombosis, or axillary vein thrombosis. The thrombotic disorders may involve inflammatory factors that contribute to the vascular deficit. In addition, embolic events also play a role in the development of these thrombotic complications. [Pg.17]

Primary graft non-function Primary graft dysfunction Haemorrhage Vascular complications Hepatic artery thrombosis Portal vein thrombosis... [Pg.104]

Portal hypertension is a consequence of increased resistance to blood flow through the portal vein. Increased resistance is usually due to restructuring of intrahepatic tissue (sinusoidal damage) but may also be caused by presinusoidal damage such as portal vein occlusion from trauma, malignancy, or thrombosis. A third (and the least common) mechanism is outflow obstruction of the hepatic vein. This latter damage is posthepatic, and normal liver structure is maintained. This chapter will focus on portal hypertension caused by intrahepatic damage from cirrhosis. [Pg.324]

Hepatic venous thrombosis, also known as Budd-Chiari syndrome, is caused by hypercoagulable disorders precipitated by pregnancy, infection, and birth control medication. An acute painful abdomen, sudden enlargement of the liver, and the presence of ascites make up a triad of clinical symptoms that are important in the diagnosis of this syndrome. Myeloproliferative disorders such as polycythemia vera and paroxysmal nocturnal dyspnea were previously thought to be responsible. Factor V Leiden and prothrombin 20210 mutations are also known to be responsible, Other intraabdominal thromboses include portal vein thrombosis, mesenteric vein thrombosis and renal vein thrombosis. [Pg.17]

Amitrano L, Brancacio V Guardascione MA, et al. Inherited coagulation disorder in cirrhotic patients with portal vein thrombosis. Hepatology 2000 3 I (2) 345-348. [Pg.551]

A review of 253 cases of Budd-Chiari syndrome found COC use to be the presumed cause in 9% of patients [29]. There appears to be a correlation between the development of BCS and the oestrogenic component of COCs [12]. Obstruction of the hepatic and portal veins has been documented and has been attributed to the thrombotic effects of the COCs however, the affected women may have had an underlying coagulation defect [16]. Budd-Chiari patients should be advised not to use COCs, as such patients have a demonstrated haematological tendency to form thrombi, and oestrogen-containing contraceptives may increase the risk of recurrent thrombosis [2]. [Pg.285]

Collateral hepatic circulation (cirrhosis, portal vein thrombosis, occlusion of hepatic vein, etc)... [Pg.100]

Portal vein thrombosis (see chapter 39.3.3) with gradual or incomplete obstruction merely produces anastomoses and develops asymptomatically. After complete obstruction, ultrasonography will showparaportal, angiomatous anastomoses, predominantly in the porta hepatis (= cavernous transformation). (95) Splenomegaly is evidenced with a normal-sized liver. The portal vein is not detectable. Colour Doppler sonography has become of paramount importance in portal vein system diagnostics. [Pg.130]

Fig. 8.10 DifTuse metastazation in pancreatic carcinoma ( ) numerous focus-Uke signs of aerobilia (f) thrombosis of the left portal vein (A)... Fig. 8.10 DifTuse metastazation in pancreatic carcinoma ( ) numerous focus-Uke signs of aerobilia (f) thrombosis of the left portal vein (A)...
Percutaneous transhepatic hepatophlebography involves a typical puncture of the liver with a needle from the right midaxillary line to enter a hepatic vein. Pressure measurement and CM injection ensure that the position of the needle or the catheter is correct. Thrombosis of the portal vein is an absolute contraindication, which is why indirect splenoportography must be carried out prior to percutaneous hepatophlebography. Serious complications occur in 1.5-4.0% of cases. [Pg.183]

Tc-DTPA Arterial perfusion accounts for 20%-40% of the circulation in portal hypertension, cirrhosis causes arterial perfusion to increase to over 60%. In portal vein thrombosis, only an arterial curve is visible. Liver metastasis usually displays relatively high arterial perfusion. In (rare) occlusions of the hepatic artery, only a portal venous curve is visible. When a bolus injection of 400 MBq "Tc-diethylenetriamine pentaacetic acid (DTPA) is applied, scintigraphy is able to reveal a bi-phasic time-activity curve. The initial increase of activity is produced by the arterial influence and the second peak by the portal venous inflow. Both curves can be evaluated quantitatively. (36) Perfusion scintigraphy may be useful in the case of liver trauma, TIPS, hyper-vascularized hepatic tumours and partial liver resection as well as after liver transplantation. [Pg.194]

Liver cirrhosis (37), liver tumours, liver echinococcosis, portal vein thrombosis, thrombosis of the splenic vein, right heart failure, Budd-Chiari syndrome, peliosis hepatis (39), etc. [Pg.213]

Thrombosis of small portal veins due to bacterial cholangitis with pericholangitis or to malignant and subsequently thrombotic processes can cause an increase in presinusoidal resistance. [Pg.247]

N., Mnsha, H., TakasU, M., Suzuki, N., Shinagawa, T., Suzuki, N., Ohtsnki, T., Arakaw 1, Nakashima, T. Incidence of portal vein thrombosis in hver cirrhosis. An angiographic study in 708 patients. Gastroenterology 1985 89 279 - 286... [Pg.261]

Valla, D., Casadevall, N., Huisse, MG., Tulliez, M., Grange, J.D., Midler, O., Binda, T., Varet, B., Rueff, B., Benhamou, J.R Etiology of portal vein thrombosis in adults. A prospective evaluation of primary myeloprohferative disorders. Gastroenterology 1988 94 1063-1069... [Pg.262]

It is not clearly understood why in some cases oedema without ascites and in other cases ascites without oedema as well as ascites together with oedema or even pleural effusion without ascites occur. Ascites develops most frequently during the course of liver disease (= hepatogenic ascites), in particular in chronic liver diseases with portal hypertension (= portal ascites), (s. tab. 16.7) Various mechanical, biochemical and neural disorders overlap in their effects and pathways, depending on the underlying liver disease. Only rarely is ascites found in diseases with presinusoidal localization of portal hypertension (such as portal vein thrombosis) or with minor restrictions in the synthesis of albumin (as in biliary cirrhosis). Formation of ascites occurs in about 50% of all cirrhotic patients within 10 years of... [Pg.296]

Arteriovenous shunts, arterioportal fistula Portal vein thrombosis... [Pg.297]

Korula, J., Yellin, A., Kanel, G.C., Nichols, R Portal vein thrombosis complicating endoscopic variceal sclerotherapy. Convincing further evidence. Dig. Dis. Sci. 1991 36 1164—1167... [Pg.370]

Orozco, H., Takahashi, T., Mercado, M.A., Prado-Orozco, E., Ferral, H., Hernandez-Ortiz, X, Esquivel, E. Colorectal variceal bleeding in patients with extrahepatic portal vein thrombosis and idiopathic portal hypertension. J. Clin. Gastroenterol. 1992 14 139-143... [Pg.372]

Complications The following complications have been reported (i.) cholangitis, (2.) obstructive jaundice, (i.) intrahepatic cholelithiasis, (4.) sepsis, (J.) portal hypertension (oesophageal varices, portal vein thrombosis, chronic Budd-Chiari syndrome, etc.), (6.) thrombosis of the inferior vena cava, (7.) amyloidosis, (8.) immune complex-associated glomerulonephritis, (9.) metastases, (10.) acute on chronic liver insufficiency or acute liver failure, and (11.) bronchobiliary fistula. [Pg.501]

Elefsiniotis, I.S., Diamantis, I.D., Dourakis, S.P., Kafiri, G., Pantazis, K., Mavrogiannis, C. Anticardiolipin antibodies in chronic hepatitis B and chronic hepatitis D infection, and hepatitis B-related hepatocellular carcinoma. Relationship with portal vein thrombosis. Eur. X Gastroenterol. Hepatol. 2003 15 721-726... [Pg.712]


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See also in sourсe #XX -- [ Pg.8 ]




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