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VASCULAR ACCESS AND FLUID RESUSCITATION IN TRAUMA

Issues of Blood and Blood Products
      For the past 2 decades, resuscitation after major trauma has included intravenous (IV) infusions of isotonic fluids. The hemodynamic response to the initial fluid bolus provides information on the amount and type of additional fluid needed. Patients who become hemodynamically stable and do not seem to have ongoing blood loss may continue to be treated with crystalloid IV infusions, together with close monitoring of urine output and hemodynamic parameters. Patients who are not hemodynamically stable or who seem to have ongoing blood loss may require transfusion of erythrocytes and other blood products. The decision to transfuse homologous blood or blood components requires consideration of the complications associated with transfusion therapy, including transfusion reactions, transfusion-transmitted disease, and transfusion-induced immunomodulation.
      The solitary use of a specific hemoglobin level as a transfusion trigger should be avoided. Before transfusing blood or blood products to trauma patients, consideration should be given to the patients' oxygen delivery and oxygen consumption. Oxygen delivery is a function of both cardiac output and arterial oxygen content. Arterial oxygen content is a function of hemoglobin oxygen saturation, hemoglobin concentration, and the amount of oxygen physically dissolved in arterial blood:
      • Stehling L.C.
      • Doherty D.C.
      • Faust R.J.
      • et al.
      Practice guidelines on blood component therapy: A report by the American Society of Anesthesiologists Task Force on blood component therapy.
      CaO2 = (SaO2/100) × (1.39 + Hgb) + (0.03 + PaO2)
      where CaO2 is the arterial oxygen content, SaO2 is the hemoglobin oxygen saturation, Hgb is the hemoglobin concentration, and PaO2 is the arterial oxygen pressure.
      The effects of hypovolemia must be separated from those of anemia and oxygen transport. The effect of the initial fluid bolus and the need for subsequent fluid therapy helps to identify hypovolemic patients. Table 1 shows the four classes of shock as defined by the American College of Surgeons Committee on Trauma. Experience has shown that patients who lose up to 30% of their blood volume (class I or II) can usually be treated adequately with crystalloid infusion. A loss of more than 30% total blood volume (class III or IV) generally requires the addition of blood to the replacement fluid.
      • American College of Surgeons Committee on Trauma
      In a retrospective study of 1000 patients, Knottenbelt
      • Knottenbelt J.D.
      Low initial hemoglobin levels in trauma patients: An important indicator of ongoing hemorrhage.
      demonstrated a correlation between low initial hemoglobin levels and mortality in trauma patients. Although it is traditionally taught that it takes hours for the body to respond to blood loss by moving fluid into the capillary circulation from interstitial spaces, Knottenbelt's data suggest that patients who present with low initial hemoglobin may have suffered significant hemorrhage that has resulted in autotransfusion. Extracellular fluid is drawn into a capillary (autotransfusion) when the plasma oncotic pressure exceeds the capillary hydrostatic pressure. This readily occurs in trauma patients with excessive blood loss and severe hypotension. Knottenbelt's study also concluded that finding low hemoglobin on presentation after injury indicates severe and ongoing blood loss, and the anemia is not caused by the dilutional effect of the initial fluid bolus. Therefore, the effect of autotransfusion has important implications in clinically assessing blood loss.
      This article reviews the use of blood and blood components in trauma patients, the appropriate use of blood component therapy, complications of transfusion therapy, and complications of massive transfusion. Blood component therapy is supportive rather than primarily therapeutic, even with regard to hemostasis. Thus, four major reasons exist for transfusion blood or its components into the hemorrhaging patient: (1) improvement of systemic oxygen transport; (2) restoration of critical red cell mass; (3) correction of bleeding caused by dilutional thrombocytopenia, platelet dysfunction, or pathologic platelet consumption; and (4) correction of bleeding caused by a factor deficiency or pathologic consumption of coagulation proteins.
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