Which statement about coagulation in cirrhosis is correct?

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In cirrhosis, coagulation is not simply deficient; both procoagulant and anticoagulant pathways are altered, creating a rebalanced hemostasis that carries risks on both sides. The liver’s reduced synthesis lowers many clotting factors, while levels of natural anticoagulants (like protein C, protein S, and antithrombin) also drop. At the same time, increases in von Willebrand factor and often in factor VIII, along with platelet dysfunction and splenic sequestration, shift the balance in ways that can still favor clot formation in certain contexts. Because standard tests such as INR reflect hepatic synthetic function rather than this dynamic balance, they don’t reliably predict bleeding risk. So patients with cirrhosis can both bleed and thrombose, depending on circumstance, making the idea of a single universal bleeding risk or mandatory correction insufficient. Prophylactic corrections should be individualized and guided by functional assessment rather than relying on a single lab value.