Abnormalities of hemostasis frequently can be demonstrated in patients with liver disease. However, no pattern of hemostatic dysfunction typical of liver disease has emerged. Published reports, recently reviewed by Ratnoff,1 describe a remarkable variety of defects in blood vessels, in platelets, in many of the components of coagulation, and in clot stability.
Although it is commonly assumed that failure of normal hemostasis contributes to the high incidence of hemorrhage in patients with liver disease, there is scant evidence actually correlating clinical bleeding with degree of hemostatic disturbance. In a recent issue of the Archives of Internal Medicine, Spector and Corn2 reviewed hemostatic-function studies in 59 patients admitted to a medical ward because of cirrhosis. Patients with bleeding, defined as hemorrhage sufficiently severe to require replacement transfusion, were compared with nonbleeding patients. Depression of the "prothrombin complex" and of factor IX (Christmas factor) was clearly more marked in the