Effect of red blood cell transfusion on cerebral oxygenation and metabolism following severe traumatic brain injury

Introduction

Following severe traumatic brain injury (sTBI), cerebral hypoxia is a common secondary insult that is associated with worsened neurological outcome. Traditionally, red blood cell (RBC) transfusion has been employed in patients with sTBI to improve oxygen delivery to the brain. The objective of this study was to determine the effect of RBC transfusion on cerebral oxygenation and metabolism in patients with sTBI.

Methods

Adult patients with sTBI were randomized to one of three transfusion thresholds: 8, 9, or 10 g/dl. Patients with active hemorrhage or coronary ischemia were excluded. A tissue oxygen monitor and cerebral microdialysis catheter were placed in the nondominant frontal region. When the patient's hemoglobin concentration fell below their assigned threshold, 2 units packed RBCs were transfused, each over 1 hour. Following transfusion, a 1-hour period of stabilization was observed prior to final data collection. The primary outcome was change in brain tissue oxygen (PbO₂). Secondary outcomes included dependence of baseline hemoglobin concentration and baseline PbO₂ on the relationship of transfusion and PbO₂, and the effect of transfusion on lactate/pyruvate ratio and brain pH as markers of cerebral metabolic state. Analysis was performed using a population-averaged panel-data model developed using a generalized estimating equation (GEE) variant of the generalized linear method.

Results

Thirty patients (21 male) with a mean (SD) age of 39 (15) years were studied. The median (IQR) pre-intubation GCS was 7 (6, 10). Transfusion occurred on median (IQR) day 4 (3, 6) after injury. Patients received a mean (SD) of 551 (58) ml packed RBCs. Transfusion resulted in a significant increase in hemoglobin concentration (pre-transfusion mean [SD] 8.4 [0.8], post-transfusion 10.2 [0.9]; P < 0.0001). Multivariable GEE analysis revealed the following variables to be positively associated with an increase in PbO₂: [Hb] 0.10 kPa/(g/dl) (95% CI: 0.03–0.17, P = 0.003); PaO2 0.09 kPa/kPa (95% CI: 0.04–0.13. P < 0.001); and CPP 0.02 kPa/mmHg (95% CI: 0.008–0.031, P = 0.001). Probe location, age, GCS, time of transfusion from injury, pHb, PbCO₂, and temperature were not significantly related to the change in PbO₂. Improvement in PbO₂ was not associated with the baseline Hb, assigned transfusion threshold group or low baseline PbO₂ (<1 kPa). The lactate/pyruvate ratio and pHb did not change during the course of the study.

Conclusion

RBC transfusion improved PbO₂ without an effect on the cerebral metabolism.