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:
22
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.
1
In a retrospective study of 1000 patients, Knottenbelt
13
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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Article Info
Footnotes
Address reprint requests to Dennis F. Landers, MD, PhD, Department of Anesthesiology and Pain Management, Southwestern Medical School, 5323 Harry Hines Blvd., Dallas, TX 75235–9068, e-mail: Dennis.Landers@email.swmed.edu
Identification
Copyright
© 1999 W. B. Saunders Company. Published by Elsevier Inc. All rights reserved.
