Authors: Mary A. Williamson Mt(ascp) Phd,L. Michael Snyder Md
Decreased synthesis of plasminogen and protein C, S, antithrombin → tendency to thrombosis.
Decreased synthesis of fibrinolytic inhibitors → excessive fibrinolysis with increased bleeding, but counterbalanced by decreased plasminogen.
Synthesis of abnormal clotting factors → bleeding; occasionally risk of thrombosis.
Hypersplenism → thrombocytopenia that exacerbates bleeding.
The coagulopathy of liver transplantation is extremely complex, with DIC and pathologic fibrinolysis predominating.
Laboratory Findings
PT is prolonged (INR is not recommended to evaluate liver function or the bleeding diathesis of liver disease).
PTT is prolonged, but less consistently than PT.
Factors V, VII, II, IX, and X are decreased.
Antithrombin is decreased.
Fibrinolytic inhibitors: thrombin activatable fibrinolysis inhibitor (TAFI), plasminogen activator inhibitor-1 (PAI-1), and α2-antiplasmin are decreased.
DIC screen may be positive. The differentiation between DIC and excessive fibrinolysis may be difficult. The two conditions may coexist.
Suggested Readings
Lisman T, Porte RJ. Rebalanced hemostasis in patients with liver disease: evidence and clinical consequences.
Blood.
2010;116:878–885.
Tripodi A, Mannucci PM. The coagulopathy of chronic liver disease.
N Engl J Med.
2011;365:147–156.
ANTICOAGULANTS, CIRCULATING
Definition