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The ponderous literature on the subject of hemostasis could perhaps be considered a classical example of the infinite ability of the human mind for abstract speculation. For several years, the number of working theories of the hemostatic mechanism greatly exceeded and not always respected the confirmed experimental facts. In recent years, however, the revived interest in this field has led to an accumulation of new findings which has been almost too rapid for their orderly incorporation into a logical working pattern. As a result, we have rapidly gone from a state of “orderly ignorance” to one of “confused enlightenment,” from which we have not emerged as yet.


Mario Stefanini, April 19541


The first recorded blood product transfusion to a human being occurred in 1667 in France and involved transfusion of approximately three tablespoons of whole blood from a calf to a man who was suffering from insanity.2 The physician performing the transfusion postulated that the calm temperament of the calf would transfer to the patient via its blood. The procedure was well tolerated, although the patient developed severe flank pain and tar-colored urine following the subsequent three transfusions: the first recorded evidence of immune-mediated hemolysis, albeit unbeknownst to the physician at the time.


Although transfusion medicine has undergone enormous development since this sentinel event, as summarized by Stefanini, important gaps in scientific knowledge persist, and several fundamental issues involving hemotherapy following major trauma remain controversial. There has been an explosion in the science of hemostasis, with a resultant revolution in all aspects of the care of the coagulopathic trauma patient. Our understanding of the mechanisms of coagulation has shifted from that of a simple enzymatic cascade to a cell-based paradigm, in which endothelium, erythrocytes, leukocytes, and platelets interact to coordinate a delicate balance between thrombosis and fibrinolysis. Furthermore, both an early postinjury endogenous coagulopathy associated with traumatic shock and a myriad of secondary factors that exacerbate this condition have been elucidated. Diagnosis of coagulopathy is shifting from the routine use of laboratory tests designed to monitor anticoagulation therapy toward point-of-care testing, which provides essential real-time clinical correlates. Treatment algorithms of traumatic coagulopathy have emphasized early replacement of both clotting factors and platelets with concomitant restraint of crystalloid administration (termed damage control resuscitation), as well as pharmacologic adjuncts that exploit the endogenous coagulation system. On the other hand, documentation of the deleterious effects of overzealous blood component replacement has led to a reevaluation of this strategy, in an attempt to reach a balance between abatement of coagulopathy and minimization of subsequent organ dysfunction. This chapter will attempt to synthesize recent developments in the complex management of the bleeding, coagulopathic trauma patient.


Red blood cell (RBC) transfusion is lifesaving in the face of critical anemia associated with hemorrhagic shock. However, the optimal target hematocrit during resuscitation remains unknown. Shock is defined broadly as the development of an oxygen debt due to impaired delivery, ...

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