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Packed red blood cell transfusion increases local cerebral oxygenation.Smith MJ, Stiefel MF, Magge S, et al. Crit Care Med 2005; 33: 1104-1108. Reviewer: Michael H. Wall, MD Abstract: This single center retrospective study evaluated the effect of red blood cell transfusion (RBCT) on brain tissue oxygen partial pressure (Pbto2) in hemodynamically stable patients with traumatic brain injury (TBI) or subarachnoid hemorrhage (SAH). Thirty-five patients with severe TBI or SAH, all with Glasgow Coma scores ≤ 8 who were volume resuscitated and stabilized for ≥ 12 hours were studied. Patients who showed evidence of coronary artery disease, congestive heart failure, prior cerebrovascular disease or who received a RBCT within 12 hours of injury were excluded. Patients were treated aggressively to maintain systolic blood pressure ≥ 100 mmHg and intracranial pressure (ICP) < 20 mmHg utilizing mechanical ventilation, sedation, analgesia, muscle paralysis, CSF drainage, surgical decompression and pentobarbital coma. All patients had an intraparenchymal ICP, temperature and Pbto2 probe placed in normal, uninjured white matter. PRBT was not based on Pbto2 values, but was given for anemia (hemoglobin ≤ 10 g/dL) in 86% of patients, preoperatively in 11% of patients and post-operatively in 3% of patients. Data from one hour before PRBT was compared to one hour after PRBT. There was no change in CPP, SaO2 or FiO2. Hb increased significantly (8.7 ± 0.9 to 10.2 ± 1.2 g/dL) following PRBT. Pbto2 significantly increased by 15% (29.1 ± 15.7 to 32.2 ± 17.3 mmHg, p < 0.05). Pbto2 increased (by 49%) in 26 of 35 patients and decreased in nine of 35 patients. The authors were not able to identify any variables that predicted an increase or decrease in Pbto2. Further, there was no difference in the age of the red blood cells given to patients whose Pbto2 increased (19 + 10 days) or decreased (24 ± 10 days). The authors conclude that in volume resuscitated hemodynamically stable patients transfusion from a Hb of 8 to 10 was associated with a significant increase in Ptbo2 in 75% of patients. Comments: Previous multi-center prospective randomized trials1 have shown no improvement in outcome comparing transfusion triggers of Hb < 7 g/dL vs Hb < 9 g/dL in hemodynamically stable ICU patients, however, questions remain regarding transfusion triggers in patients with neurologic disease (and coronary disease). This excellent study showed that transfusion (from Hb 8 g/dL to 10 g/dL) was associated with a significant increase in normal brain tissue oxygen partial pressure in 75% of patients with severe TBI or SAH. But PRBT decreased Pbto2 in 25% of patients and unfortunately there is no way to predict which patients Pbto2 was going to go up or down. This study raises many important questions: Does Pbto2 in a normal brain predict changes in an injured brain? Does Pbto2 accurately measure cellular oxygenation? Should the transfusion trigger be based on the Ptbo2 (vs anemia)? Since this group has previously seen an association with PRBT and vasospasm following SAH,2 prospective randomized studies are desperately needed to evaluate the effect of transfusion on clinical outcomes of patients with TBI and SAH. Until these trials are completed decisions on when to transfuse brain injured patients will be controversial. References:
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