Anticoagulation in Cirrhosis

Abstract

The clinical utility of anticoagulation for patients with cirrhosis and asymptomatic portal vein thrombosis (PVT) is widely debated. Complex hemostatic derangements in cirrhosis that increase risk of both bleeding and thrombosis, as well as a lack of randomized controlled data, limit conclusive assessments regarding optimal management of anticoagulation in this setting. In this review, we summarize the relevant literature pertaining to PVT in cirrhosis, including the effect of untreated PVT on the natural progression of liver disease and the overall impact of anticoagulation on clot burden and other relevant clinical outcomes. Apart from patients who are symptomatic or listed for liver transplantation, data supporting anticoagulation for the treatment of PVT is limited and without clear consensus guidelines. In patients with cirrhosis without PVT, emerging evidence for the role of prophylactic anticoagulation to mitigate the progression of fibrosis suggests an optimal risk-benefit tradeoff with decreased rates of liver decompensation and mortality, without a heightened risk of bleeding. In summation, as our understanding of the role of both prophylactic and therapeutic anticoagulation in cirrhosis continues to evolve, ongoing risk stratification of patients with asymptomatic PVT demands further attention.

Direct oral anticoagulants in the treatment of portal vein thrombosis in patients with portal hypertension

“…[9] Anticoagulation improves the success of complete and partial portal vein recanalization, lowers the risk of thrombus extension, and decreases the risk of hepatic decompensation. [3,7,9,10,18,19] In patients without cirrhosis, treatment is indicated to prevent mesenteric ischemia and the development of chronic PVT with portal hypertension. [2,3] In patients with cirrhosis, treatment is generally indicated in those with PVT that could lead to the progression of portal hypertension and for liver transplant candidates that have significant clot extension that may exclude them from transplant candidacy and worsen post-transplant outcomes.…”

“…Higher rates of PVT recanalization are seen when anticoagulants are started within 6 months of diagnosis. [18] It is common practice to screen for varices and optimize beta-blocker therapy or perform endoscopic variceal ligation before starting anticoagulation in patients with cirrhosis and recent PVT. [9] Anticoagulation improves the success of complete and partial portal vein recanalization, lowers the risk of thrombus extension, and decreases the risk of hepatic decompensation.…”

“…T A B L E 4 Advantages and disadvantages of DOAC, VKA, or LMWH for anticoagulation : DOACs, direct oral anticoagulants; INR, international normalized ratio; LMWH, low-molecular-weight heparin; PT, prothombin time; VKA, vitamin K antagonist. Based on data from Martens et al,[18] Simonetto et al,[17] and Weinberg 2019 [7]. …”

“…It is common practice to screen for varices and optimize beta-blocker therapy or perform endoscopic variceal ligation before starting anticoagulation in patients with cirrhosis and recent PVT 9 . Anticoagulation improves the success of complete and partial portal vein recanalization, lowers the risk of thrombus extension, and decreases the risk of hepatic decompensation 3,7,9,10,18,19 . In patients without cirrhosis, treatment is indicated to prevent mesenteric ischemia and the development of chronic PVT with portal hypertension 2,3 .…”

“… 2 The decision to start anticoagulation should always be individualized with a shared discussion of risks and benefits with every patient. Higher rates of PVT recanalization are seen when anticoagulants are started within 6 months of diagnosis 18 . It is common practice to screen for varices and optimize beta-blocker therapy or perform endoscopic variceal ligation before starting anticoagulation in patients with cirrhosis and recent PVT 9 .…”