Coagulation defects in liver disease and response to transfusion during surgery

Coagulation studies were performed in twentyone patients with liver disease, one patient with obstructive jaundice and three patients with extrahepatic portal hypertension. The coagulation defect in liver disease was found to be a multiple one involving platelets, accelerator globulin, prothrombin, proconvertin, PTC and possibly other unidentified serum and plasma thromboplastic factors. The degree of impairment roughly paralleled the severity of the liver disease. Fibrinolysis of variable degree was observed in 20 per cent of the patients, usually in the presence of normal fibrinogen levels, and in an additional 25 per cent fibrinolytic activity developed during surgery. The prothrombin time was found to be the best screening test available for the evaluation of the plasma coagulation mechanism of these patients. The platelet depression did not necessarily parallel the depression of the other coagulation factors. Severe plasma coagulation abnormalities were corrected partially for twenty-four to forty-eight hours by the combined use of fresh and stored blood. The superiority of fresh blood over stored bank blood was concluded to be, to a large degree, the result of the greater concentration of accelerator globulin and the viability of the platelets in fresh blood. Abnormal oozing was noted during surgery, but uncontrollable hemorrhage was not encountered in the patients studied. Postoperative hemorrhage occurred in two patients, one a spontaneous hemorrhage from a hepatoma and the other associated with hypofibrinogenemia and fibrinolysis.