Approach to thromboelastography-based transfusion in cirrhosis: An alternative perspective on coagulation disorders

Table 1 Three phases of coagulation in liver disease

Hemostasis stage	Hypocoagulable state	Hypercoagulable state
Primary hemostasis: Platelet activation and interaction with injured endothelium	Thrombocytopenia: (1) Decreased amount: Splenic sequestration, decreased thrombopoietin levels, bone marrow suppression, autoantibody destruction; and (2) Poor function: Uremia, changes to the vessel wall phospholipid composition, anemia (Hgb < 7 g/dL), decreased margination	Low levels of ADAMTS-13; Increased levels of vWF; Increased number of activated platelets
Secondary hemostasis: Fibrin clot formation	Low levels of factors II, V, VII, IX, X, and XI; Low levels of fibrinogen; Vitamin K deficiency (malabsorption in cholestatic disorders)	Elevated levels of factor VIII; Decreased levels of proteins C and S; Decreased levels of antithrombin, and heparin cofactor II
Fibrinolysis	Accelerated intravascular coagulation and fibrinolysis: (1) Low levels of factor XIII and thrombin-activated fibrinolysis inhibitor; (2) Elevated levels of tPA; (3) Decreased level of α2-antiplasmin; and (4) Dysfibrinogenemia	Low plasminogen levels; Dysfibrinogenemia; High plasminogen activator inhibitor

Hgb: Hemoglobin; tPA: Tissue plasminogen activator; vWF: von Willebrand factor.