The wide use of anticoagulants in the management of thromboembolic disease, and the likelihood of continuation as this disorder becomes increasingly prominent as a major cause of crippling and death, makes reexamination of adequate guiding principles necessary. The therapeutic objective is to block coagulation to prevent in vivo clotting without at the same time endangering hemostasis. To attain this by anticoagulants, the physician must recognize that he is thereby tampering with one of the most important and complicated homeostatic mechanisms of the body.
Despite notable recent advances in this area, many vexatious problems continue to beset the physician. First, let us examine the goal posts—on the one hand the so-called therapeutic range, and on the other, the safe level, of clotting factors. The former term is used rather loosely in the conviction (as yet unproved) that evidence of interference with in vitro clotting truly reflects prevention of in vivo coagulation.