Numerous examples may be found in clinical literature demonstrating that an impaired activity of one organ or tissue may produce an abnormal performance of another, often one having an entirely different physiologic function. The tendency to hemorrhage in obstructive jaundice is a typical example. The distinct susceptibility of jaundiced patients to bleeding introduces a grave complicating factor in the treatment of this malady, as surgical intervention, the only satisfactory remedial procedure, may lead to fatal hemorrhage. The observations of Walters1 several years ago, that the death of more than half of a series of jaundiced patients subsequent to abdominal operation was the result of large intraperitoneal hemorrhage, emphasizes the importance of this complicating feature.
Several theories postulating a deficiency of one of the clotting elements have been advanced to explain the abnormal mechanism of coagulation in obstructive jaundice, and each in turn has been largely abandoned. The calcium theory