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In this review, we discuss the features of PVT, pointing out new insights into clinical, diagnostic, and therapeutic issues, making an overview of current beliefs regarding portaa outcome and, finally, reporting controversies about the correct management of PVT in the setting of liver transplantation.

The latter effect is well known, and is employed therapeutically in resective liver surgery. Eur J Gastroenterol Hepatol. As a consequence of portal vein obstruction, systemic and splanchnic hemodynamics undergo specific and important modifications[ 4 ].

Successful recanalization of portal vein thrombosis before liver transplantation using transjugular intrahepatic portosystemic shunt. Transcatheter thrombolytic therapy for acute mesenteric and portal vein thrombosis.

Malformación cavernomatosa de la vena porta

Acute thrombosis of the splanchnic veins. In addition, collateral circulation develops rapidly from pre-existing veins in the porta hepatis within 2 to 3 d after the onset of acute thrombosis, particularly in the gallbladder wall[ 619495 ]. Portal hypertension due to portal venous thrombosis: However, the number of bleeding episodes in PVT patients receiving anticoagulant therapy didnot increased, and in long-term follow-up studies, anticoagulants seem to be effective in preventing new thrombotic events with a low mortality[ 66].

Intraoperatory grading of PVT extension[ 17 ]. The principal diagnostic criteria are usually incompletely met in these patients, probably because of the atypical manifestation of the disease[ 50 ].

Several studies[ – lx showed that surgical thrombectomy, thromboendovenectomy with venous reconstruction, interposition of vein graft, porto-caval hemitransposition, and radiological endovascular interventions, can resolve venous obstruction in liver transplant recipients[ ].


Evolving consensus in portal hypertension. Catheter-directed thrombolysis with transjugular access in portal vein thrombosis secondary to pancreatitis. GA prothrombin gene mutation and other trombophilic polymorphisms in patients with portal or hepatic venous thrombosis. MR, CT, and ultrasonography of splanchnic venous thrombosis.

Hemodynamics during liver transplantation: MRI might porfa confirm the vascular occlusion; at spin-echo MR, the clot appears isointense on T1- weighted images, or hyperintense if recent, and usually has a more intense signal on T2 images.

A retrospective analysis of cases and associated clinical implications.

Portal vein thrombosis: Insight into physiopathology, diagnosis, and treatment

Protean manifestations of pylethrombosis. However, in the general population, its role in PVT development seems less clear, as it is considered a weak prothrombotic risk factor.

Extrahepatic portal vein obstruction. Percutaneous transhepatic treatment of symptomatic mesenteric venous thrombosis. The history of PVT has been characterized by difficulties in diagnosis and treatment, which, today, have almost been overcome. This mild, transient, ascites is due to intestinal venous congestion in the absence of the mechanisms activated in liver cirrhosis[ 6364 ].

Portal hypertension-related complications after acute portal vein thrombosis: PVT is considered a milestone in the natural history of liver cirrhosis and it is related to serious complications, morbidity, and mortality, as previously discussed[ 87 ]. Portal vein thrombosis in adults: Chronic mesenteric venous thrombosis: Single center experience of 39 patients with preoperative portal vein thrombosis among adult living donor liver transplantations.

Cause of portal or hepatic venous thrombosis in adults: Etiology of portal vein thrombosis in adults.

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In the presence of sporadic local or systemic promoting events, an underlying intrinsic predisposition might be the access key to thrombosis development[ 113 ]. Male sex, previous treatment for PVT, Child-Pugh class C, and alcoholic liver disease might be associated with recurrence[ 85]. Am J Clin Caverhoma. However, levels of prothrombin and other coagulation factors could be laa decreased, while D-dimer is usually increased[ 822 ].


A prospective multicentric follow-up study on patients with acute portal vein thrombosis PVT: Management of portal vein thrombosis in liver vna Prevalence of thrombotic risk factors in series of routinely investigated, consecutive adult patients with non tumorous and non cirrhotic, acute or chronic, PVT[ ].

Finally, shunt surgery distal splenorenal shunt or Rex shunt, in children might be applied as the last choice, and only in absence of splenic or superior mesenteric vein thrombosis[ ].

laa Transhepatic thrombolysis in acute portal vein thrombosis after laparoscopic splenectomy. Table 2 Most frequent systemic risk factors for PVT[ 38917186479 ]. Cavernous transformation of the portal vein: The use of EUS to diagnose malignant portal venous system invasion by pancreatic cancer.

J Am Coll Surg.

In contrast, chronic PVT can be completely asymptomatic, or characterized by splenomegaly, pancytopenia, varices, and, rarely, dde 3 ]. Transjugular intrahepatic portosystemic shunt placement in patients with cirrhosis and concomitant portal vein thrombosis.

In addition, in hypoperfused areas, hepatic enhancement appears increased during the arterial phase and decreased during the portal phase.

The goal of treatment is similar in acute and chronic PVT, and consists in correction of causal factors, prevention of thrombosis extension, and achievement of portal vein patency. A gain-of-function mutation of JAK2 in myeloproliferative disorders.

Portal vein thrombosis: Insight into physiopathology, diagnosis, and treatment

Thrombophilic gene mutations in cirrhotic patients with portal vein thrombosis. This vsna an arbitrary distinction, which is sometimes difficult to apply in clinical practice; patients who develop symptoms, such as abdominal pain, nausea, and fever, within sixty days prior to hospital admission, might have an acute PVT development[ 5859 ]. Biliary changes in extrahepatic portal venous obstruction: