Current knowledge and management of portal vein thrombosis in cirrhosis

Abstract

Portal vein thrombosis (PVT) is an increasingly recognised complication of cirrhosis whose incidence increases in parallel with the severity of cirrhosis. Several risk factors have been associated with the occurrence and progression of PVT. Although the negative effect of complete PVT on the surgical outcome of liver transplant recipients is clear, its impact on cirrhosis progression remains uncertain. Treatment options include anticoagulants and interventional thrombolytic therapies, which are chosen almost on a case-by-case basis depending on the characteristics of the patient and the thrombus. In this manuscript, we review current knowledge regarding the epidemiology, risk factors, diagnosis and classification, natural history, clinical consequences and treatment of non-neoplastic PVT in cirrhosis.

More Pronounced Hypercoagulable State and Hypofibrinolysis in Patients With Cirrhosis With Versus Without HCC

“…( 21 ) In patients without liver disease, increased activation of coagulation is one of the main factors responsible for the increased thrombotic tendency in patients with cancers. ( 20 , 36 ) While awaiting large prospective trials to establish whether alterations of hemostasis are truly implicated in the pathogenesis of PVT in patients with cirrhosis, ( 5 , 6 ) and to further confirm the association between HCC and increased thrombotic tendency in these patients, we performed a case‐control study to investigate alterations of coagulation in this patient population. Because hemostasis in cirrhosis is complex, ( 1 , 3 ) and altered fibrinolysis may also be responsible for the thrombotic tendency in digestive cancers, ( 19 , 37 ) we included determination not only of coagulation but also of fibrinolysis.…”

“…(6) On the other hand, the pathogenesis of PVT in cirrhosis is multifactorial and likely results from alterations in one or more components of the Virchow's triad (i.e., decreased portal vein inflow, hypercoagulability, and local damage of the portal vein wall). (5) Therefore, it is plausible that a more profound hypercoagulable state, at least in some patients, could contribute to the development of this thrombotic complication. (5) Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer occurring in patients with cirrhosis, (7) and is associated with a purported increased risk of thrombosis, particularly PVT.…”

“…(5) Therefore, it is plausible that a more profound hypercoagulable state, at least in some patients, could contribute to the development of this thrombotic complication. (5) Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer occurring in patients with cirrhosis, (7) and is associated with a purported increased risk of thrombosis, particularly PVT. (8)(9)(10)(11) Cancer is a well-known risk factor for venous thromboembolism (VTE).…”

“…In patients with cirrhosis, however, it has yet to be demonstrated whether alterations of hemostasis are truly responsible for the development of thrombotic complications, including portal vein thrombosis (PVT). (5) In a recent study including 310 patients with mostly compensated cirrhosis followed prospectively for a median of 48 months, Turon et al found that portal vein flow <15 cm/s, but not plasmatic hypercoagulability, was predictive of PVT. (6) On the other hand, the pathogenesis of PVT in cirrhosis is multifactorial and likely results from alterations in one or more components of the Virchow's triad (i.e., decreased portal vein inflow, hypercoagulability, and local damage of the portal vein wall).…”

Treatment of direct oral anticoagulants in patients with liver cirrhosis and portal vein thrombosis

“…The pathophysiology of PVT in cirrhosis is multifactorial and results mainly from alterations in the different components of Virchow's triad: reduced portal blood flow, a hypercoagulable state, or vascular endothelial injury (Figure 2). 22 Recent studies have reported that cirrhosis patients with portal blood flow less than 15 cm/s were at increased risk of developing PVT. 23,24 In addition, an increase in portal blood inflow through portosystemic collaterals also seems to influence PVT development.…”