Background: A widespread approach today is to transfuse bleeding trauma patients with RBC concentrates and plasma at a 1:1 ratio. This regime is supported by a range of observational studies showing lower mortality in bleeding patients receiving equal volumes of plasma and RBCs. The rationale for this practice is still unclear with several studies failing to show any survival benefits of increased plasma use, perhaps due to a failure to account for the timing of transfused units.
Objective: To study the association between plasma-to-RBC ratios and risk of death in trauma patients, using appropriate methods.
Design, Settings, and Participants: In a retrospective cohort study, we assembled data on 741 transfused trauma patients at a large trauma center. Measures of transfusion therapy were assessed entirely time dependently, and relative risk of death was compared between patients receiving low to high plasma-to-RBC ratio (< 0.85 vs > 0.85).
Measurements and Results: In the time-dependent analyses, we saw no significant association between a low plasma ratio and the risk of death. However, age more than 75 years, injury severity score greater than 33, Glasgow Coma Scale less than 8, and systolic blood pressure lower than 90 mm Hg were all significantly associated with increased risk of death. Conversely, when the analyses were conducted with conventional methods, a strong protective effect of high plasma ratios was seen.
Conclusions: The key finding in our study is the strikingly different results produced by time-dependent analyses and the conventional analyses when studying survival and plasma-to-RBC ratio, supporting recent claims that prior studies showing benefit of high plasma ratios might have suffered from survival bias. There is a great need for further studies on the subject to enable improvements in treatment of massively bleeding trauma patients.
1Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
2Department of Anesthesiology and Intensive Care, Danderyd Hospital, Stockholm, Sweden.
3Department of Clinical Immunology and Transfusion Medicine, Karolinska Institutet, Stockholm, Sweden.
4Department of Anesthesiology and Intensive Care, Karolinska University Hospital, Stockholm, Sweden.
5Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
6Department of Epidemiology, Harvard School of Public Health, Harvard University, Boston, MA.
*See also p. 2041.
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Supported, in part, by Svenska Sällskapet för Medicinsk Forskning (SSMF) to Dr. Edgren and the Swedish Strategic research program at Karolinska Institutet.
Dr. Wikman lectured for Octapharma, CSL Behring. Dr. Edgren received grant support from Svenska Sällskapet för Medicinsk Forskning (unrestricted postdoctoral training grant). The remaining authors have disclosed that they do not have any potential conflicts of interest.
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