Portal vein thrombosis (PVT) is considered to be a frequent complication of liver cirrhosis. However, unlike PVT in patients without cirrhosis, very few data are available on the natural history and management of PVT in cirrhosis, despite its association with potentially life-threatening conditions, such as gastroesophageal bleeding and acute intestinal ischemia. Moreover, no consensus regarding PVT in cirrhosis exists. Suggested causes of PVT in cirrhosis include reduced portal blood flow velocity, multiple congenital or acquired thrombophilic factors, inherited or acquired conditions, and derangement of liver architecture. However, the understanding of PVT in cirrhosis is incomplete. In addition, information on the management of PVT in cirrhosis is inadequate. The aims of this review are to: (1) assemble data on the physiopathological mechanism, clinical findings, diagnosis and management of PVT in cirrhosis; (2) describe the principal factors most frequently involved in PVT development; and (3) summarize the recent knowledge concerning diagnostic and therapeutic procedures.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved.Key words: Portal vein thrombosis; Liver cirrhosis; Thrombophilic factors; Anticoagulation; Splenectomy Core tip: Portal vein thrombosis (PVT) is considered to be a frequent complication of liver cirrhosis; however, very few data are available on the natural history and management of PVT in cirrhosis, despite its association with potentially life-threatening conditions. The understanding and information on the management of PVT in cirrhosis are incomplete. The aims of this review are to: (1) assemble data on the physiopathological mechanism, clinical findings, diagnosis and management of PVT in cirrhosis; (2) describe the principal factors most frequently involved in PVT development; and (3) summarize the recent knowledge concerning diagnostic and therapeutic procedures.

An elevated HVPG after B-RTO is one aspect of the effect of liver function, and an HVPG increase of ≥ 20% from baseline is a predictive factor for obtaining an improvement of liver function.

Our results showed that splenectomy promoted liver regeneration by increasing serotonin content in liver even under cirrhotic conditions.

A 56-year-old male with alcohol-induced liver cirrhosis developed rectal varices. He had a prior history of treatment for esophageal varices with endoscopic variceal ligation. Despite the repeated treatment for rectal varices with endoscopic variceal ligation, endoscopic injection sclerotherapy, and surgery, the bleeding from the rectal varices could not be controlled. Multidetector-row computed tomography and 3D-angiography revealed the hemodynamic profile of the rectal varices. We next approached the rectal varices through the umbilical vein on the abdominal wall, and successfully embolized the varices continuing from the inferior mesenteric vein using coils and a 5% solution of ethanolamine oleate with iopamidol.

Prothrombin time and total bilirubin improve in approximately half of cirrhotic patients within a year after splenectomy. HVWF type I and splenomegaly may be predictive factors for improvement in prothrombin time after splenectomy in patients with cirrhosis due to hepatitis C.