The effect of fluid resuscitation strategy on monocyte and T-cell surface markers

Abstract

BackgroundDespite initial lifesaving benefits, posttraumatic resuscitation strategies have been associated with immunologic complications leading to systemic inflammatory response syndrome, sepsis, multiple organ failure, and late trauma death. Nevertheless, the direct effect on immunologic surface markers remains inadequately described. We hypothesized that changes in monocyte and T-cell surface markers were associated with initial posttraumatic fluid resuscitation. Materials and methodsData were extracted from the inflammation and host response to injury (Glue Grant) study. Blood samples were drawn from 492 patients on days 0, 1, 4, 7, 14, and 28 and analyzed for 31 monocyte and T-cell surface markers. Resuscitation strategies during the initial 48 h were quantified, including transfusion of packed red blood cells (PRBCs), fresh frozen plasma (FFP), platelets, and crystalloids. Longitudinal surface marker concentration changes were quantified by the calculation of a within-patient signal intensity change and were associated with resuscitation strategy while controlling confounders. P-values were post hoc corrected using the false detection rate q-value. ResultsThe monocyte surface marker (CD83) trajectory (as measured by a within-patient signal intensity change) was found to be positively associated with volume of PRBCs transfused (q = 0.002) and negatively associated with the transfused volume of FFP (q = 0.004). T-cell surface marker (CD3) was found to be negatively associated with volume of PRBCs transfused (q = 854 × 10−9) and positively associated with the transfused volume of FFP (q = 0.022). Platelets and crystalloid transfusion volumes were not associated with any surface marker trajectories. ConclusionsPRBC and FFP transfusion was associated with opposing effects on CD3 and CD83 trajectories, which may in part explain some of the protective effects of a high FFP:PRBC ratio in trauma-related resuscitation.