Abstract
HEMORRHAGES resulting from deficiency of prothrombin can in most instances be adequately controlled by the judicious use of vitamin K. However, it was noted early 1 that in certain patients with severe hepatic damage the deficiency of prothrombin could not be corrected even with large amounts of vitamin K administered over long periods. It has always been assumed that the ineffectiveness of vitamin K in such patients was the result of an inadequacy of hepatic parenchyma to utilize vitamin K in the production, or activation, of prothrombin. Hemorrhage in these persons is likely, and even repeated transfusions of whole blood often will not prevent a fatal outcome. Various types of treatment have been employed in such cases, but transfusions of whole blood have been by far the most successful. It is well known that even whole blood seldom is capable of maintaining normal levels of prothrombin much longer than
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