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Recently, a panel of experts recommended the application of anticoagulant therapy only in PVT patients with a proven thrombophilic disorder or familial history of venous thrombosis[], thereby obtaining an improvement in survival and reduction in risk of gastrointestinal bleeding[].

Transjugular intrahepatic portosystemic shunt approach and local thrombolysis for treatment of early posttransplant portal vein thrombosis. Portal vein thrombosis PVT is a relatively common complication in patients with liver cirrhosis, but might also occur in absence of an overt liver disease. The history of PVT has been characterized by difficulties in diagnosis and treatment, which, today, have almost been overcome.

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Vascular complications after orthotopic liver transplantation. Inflammatory abdominal foci such as appendicitis, diverticulitis, inflammatory bowel diseases, pancreatitis, cholecystitis, hepatic abscesses, and cholangitisliver cirrhosis or tumors, represent the most common local thrombotic risk factors[ 81218 ]. It has been demonstrated in rats, that the progressive obliteration of the portal vein stimulates apoptosis of hepatocytes in the hypoperfused lobe[ 10 ], while increasing the mitotic activity in the normal perfused one.

Single-center experience of portal vein thrombosis patients undergoing liver transplantation in China.

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

Moreover, PVT might have indirect effects on other abdominal organs, causing intestinal ischemia and infarction, or predisposition to vascular neoformation and gastrointestinal bleeding. Portal vein thrombosis after variceal endoscopic sclerotherapy in cirrhotic patients: If CT scan is not rapidly available, obtain Doppler-sonography Obtain Doppler-sonography, then either CT scan or MRI, before and after a vascular contrast agent, to make a diagnosis of chronic PVT In patients with acute PVT and high fever, septic pylephlebitis should be considered, whether or not an abdominal source of infection has been identified, and blood cultures should be routinely obtained Base the diagnosis on the absence of a visible normal portal vein and its replacement with serpiginous veins In acute PVT, the possibility of intestinal infarction should be considered from presentation until resolution of pain.


After liver transplantation, PVT development is a rare but possible event, especially in the early postoperative period[ 60 ]. Otherwise, prognosis depends on the underlying liver disease[ 1122279 ].

In patients with acute PVT and high fever, septic pylephlebitis should be considered, whether or not an abdominal source of infection has been identified, and blood cultures should be routinely obtained. Deficiency of natural anticoagulant proteins C, S, and antithrombin in portal vein thrombosis: Biliary changes in extrahepatic portal venous obstruction: Hemodynamic changes in patients with portal venous obstruction. PVT can be classified into four categories, depending on the extension: In fact, when thrombosis is extended to both portal and mesenteric veins, the risk of bowel ischemia is considerable and mortality high, despite a lower risk portw variceal bleeding[ 61 ].

Unfortunately, in practice, this policy is not applicable without difficulty. Wolff M, Hirner A. J Cardiovasc Surg Torino ; Transjugular intrahepatic portosystemic shunt placement in patients with cirrhosis and concomitant portal vein thrombosis. Finally, shunt surgery distal splenorenal shunt or Rex shunt, in children might be caveroma as pprta last choice, and only in absence of splenic or superior mesenteric vein porat ]. Hypercoagulation and thrombophilia in liver disease.

However, the relatively low prevalence of genetic, in respect to acquired, thrombophilic disorders, might represent a potential diagnostic matter in PVT patients, and should be considered carefully in clinical practice[ 30 ].

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

In PVT patients, liver function is typically conserved. Sobhonslidsuk A, Reddy KR.

As a consequence of cavsrnoma vein obstruction, systemic and splanchnic hemodynamics undergo specific and important modifications[ 4 ]. 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]. Table 1 Most frequent local risk factors for PVT[ 38917186479 ].

Moreover, we describe the principal factors most frequently involved in PVT development and the recent knowledge concerning diagnostic and therapeutic procedures. If thrombosis is recent and there is no underlying thrombophilic condition, anticoagulation should be administered for mo, as a complete portal vein recanalization can occasionally be delayed[ 79,- ]. Instead, a rapid and complete obstruction of the portal or mesenteric vein, without the involvement of the mesenteric venous arches, induces only intestinal congestion; the main feature is a diffuse thickening of the intestinal wall, visible even without alterations in contrast enhancement.


Factor V Leiden mutation, prothrombin gene mutation, and deficiencies in coagulation inhibitors associated with Budd-Chiari dde and portal vein thrombosis: Although in the general population PVT is considered a rare event, its prevalence among cirrhotic patients ranges between 4.

Malformación cavernomatosa de la vena porta

Usually, the original portal vein becomes a thin, fibrotic cord, which is difficult to visualize[ 89 ]. In the future, due to innovations in imaging and pharmaceuticals, clinical attention must be focused on the realization of a scheduled, preemptive, therapeutic approach to the patient, to better define the profile of toxicity and reduce side effects, especially in cirrhotic patients.

A review of thirty-four patients. The incidence among cirrhotic patients is still unknown, but recent data suggest a prevalence of about 0. Portal vein thrombosis following splenectomy.

MR, CT, and ultrasonography of splanchnic venous thrombosis. A partial thrombosis is often associated with few symptoms. Portal vein thrombosis, Portal hypertension, Thrombophilic factors, Liver cirrhosis, Liver transplantation, Anticoagulants.

CT scanning is able to demonstrate hyperattenuating material in the portal vein lumen and the absence of enhancement after contrast injection. The principal diagnostic criteria are usually incompletely met in these patients, probably because of the atypical manifestation of the disease[ 50 ]. Typically, patients with an advanced thrombosis do not always remember any previous trigger event or disease[ 226364 ].

Intestinal congestion and ischemia are typical manifestations of acute PVT; abdominal pain or distention, diarrhea, rectal bleeding, nausea, vomiting, anorexia, fever, lactacidosis, splenomegaly and sepsis might be variably cavegnoma 6364 ]. Risk factors of thrombosis in abdominal veins.

Webb LJ, Sherlock S.