EFFECT OF TRANSFUSION ON PHYSIOLOGICAL-CHANGES AFTER RESUSCITATED TRAUMA

Background. The purpose of this experimental study was to test whether transfusion potentiated physiologic changes associated with fluid res uscitated trauma in controlled conditions. Methods. Anesthetized and v entilated mongrel pigs were subjected to soft-tissue injury plus 35% h emorrhage and 1 hour shock and then were resuscitated with either auto logous (shed) or heterologous (cross-transfused) fresh whole blood. Le ukocyte differential counts, T-lymphocyte subsets, neutrophil adherenc e molecule (CD18) expression, granulocyte oxidative burst, plasma cort isol, and serum chemistries were monitored in awake animal with indwel ling catheters on 3 consecutive days. Changes were referenced to prein jury baseline values and to a control group that received heterologous transfusion but no shock. To determine whether these changes might ha ve influenced host defense a low-dose challenge with Escherichia coli endotoxin (lipopolysaccharide [LPS]; 1 to 2 mu g/kg for 30 minutes) wa s administered on day 4. Results. During recovery, neutrophil counts, neutrophil CD18 expression, and granulocyte oxidative burst were gener ally increased, but the changes were not potentiated by transfusion. L ymphocyte subpopulations remained relatively constant. Serum enzyme ma rkers were elevated with trauma plus shed blood or trauma plus cross-t ransfusion, but they remained essentially unchanged after heterologous transfusion only. Plasma cortisol, a nonspecific index of stress, pea ked at 3 to 6 times higher than baseline. The increases tended to be h igher and later with heterologous transfusion only, relative to trauma plus shell blood or trauma plus cross-transfusion. The delayed LPS ch allenge evoked profound but transient pulmonary hypertension and leuko penia, followed by subsequent hypoxemia; the time courses and magnitud e of these changes were similar in all groups. Conclusions. If these m easured variables before and after LPS challenge are a valid index of host defense in this species, then a 35% transfusion does not potentia te the risk for posttrauma immune dysfunction when the magnitude of in jury is constant. Thus the predisposition to infection after human tra uma might be due to cold storage of blood, separation of blood into co mponents, or other transfusion-related practices rather than to transf usion per se.