Hemostasis is a dynamic process that is the product of interaction between coagulation, platelets, and fibrinolysis, resulting in the formation and revision of clot. Liver disease affects all three of these components, both quantitatively and qualitatively.
- The liver is the site of synthesis for all procoagulant and anticoagulant factors, with the exception of tissue thromboplastin (III), calcium (IV), and von Willebrand factor (VIII). It is also the site for clearance of activated factors.
- Cirrhotic patients are customarily considered to have a bleeding diathesis on the basis of abnormalities in conventional tests of coagulation such as prothrombin time (PT) and partial thromboplastin time (PTT) (yet PT and PTT abnormalities correlate poorly with bleeding complications).
- Platelets provide primary hemostasis by interaction with the vessel wall at the site of injury and forming a physical plug. (Thrombocytopenia is a well-known feature of cirrhosis.)
- A second function of platelets is to promote thrombin generation.
- Platelet counts below a threshold of 100,000/mm3 negatively correlate with thrombin production. Platelet transfusions are not indicated in the absence of bleeding.
- The fibrinolytic system limits and revises clot formation (accelerated fibrinolysis common in patients with cirrhosis).
- Disseminated intravascular coagulation (DIC) is primarily a thrombotic diathesis followed by widespread secondary fibrinolysis. As factors are consumed, DIC becomes a bleeding diathesis of factor and platelet deficiency. It is generally agreed on the basis of examination of these special assays that overt DIC is probably not a feature of stable chronic liver disease.