In this retrospective study, we evaluated the association between blood type O and the mortality in 901 patients with severe trauma. Findings indicated that blood type O was the independent risk factor for all-cause in-hospital mortality and death due to exsanguination, TBI, and other causes after adjusting for potential confounders. The number of units of RBC transfusions administered within 24 h upon admission to the ED tended to be more in patients with blood type O; however, there was no significant difference between blood type O and other blood types. To the best of our knowledge, this is the first study to report the association between ABO blood type and mortality in patients with severe trauma. Although we cannot alter the risk of blood type O itself, an adequate recognition of the risk enables us to control for the intensity of trauma critical care. Recognizing those patients requiring damage-control resuscitation is a crucial issue since damage-control resuscitation, including strategic multiple operation, sufficient amounts of available transfusions with adequate ratios, and perioperative critical care, requires a large amount of human and healthcare resources. Therefore, recognizing the additional risk of the difference in blood type would imply the potential to optimize the implementation or damage-control resuscitation and indirectly improve the outcome of patients with severe trauma.

Several studies have reported that patients with blood type O had 25–30% lower plasma von Willebrand factor (vWF) levels than the those with non-O blood, increasing their risk of hemorrhage [14, 15]. vWF plays a decisive role in primary hemostasis by mediating the adhesion of blood platelets to the subendothelium of the damaged vessel walls and promoting the aggregation of activated platelets. In addition, vWF acts as a carrier of factor VIII clotting activity and protects it from premature proteolysis [16,17,18]. Therefore, a lower vWF level is a possible explanation for the increase in mortality in patients with blood type O, as observed in this study. However, many of the differences in the mechanisms of hemostasis according to blood type remain unknown. Further basic study is warranted to reveal the role of blood type in maintaining hemostasis during critical situations.

Although the results of the multivariate analysis showed that blood type O was an independent risk factor for all-cause trauma-related mortality and death due to exsanguination, there was no significant difference in the number of units of RBC transfusions administered within 24 h of admission in patients with blood type O compared with those with other blood types. One possible explanation for this discrepancy is the issue of survivor bias. Patients who died shortly after ED arrival or who did not have a surgical indication due to too severe an injury were less likely to receive large amounts of transfusion. Another possible explanation was beta error. The number of patients who received a RBC transfusion was only 20% of the total patients included, and it prevented us from detecting the significant difference between the two groups.

In this study, although ISS was similar between the two groups, RTS observed in patients with blood type O was lower than that in patients with other blood types. The physiological status of patients with blood type O may deteriorate even if these patients suffered injuries of the same intensity. Because this was a retrospective cohort study with a limited sample size, patient background could not be similarly distributed, and it was uncertain whether the statistically significant difference observed in RTS was a clinically meaningful result. Although completely adjusting the difference using a statistical approach was generally insufficient, in this study the RTS value was incorporated into the model and the difference was accounted for. Our results demonstrated that the impact of blood type O on trauma death was extremely high. The impact of blood type O on all-cause mortality was comparable to 12 increases in ISS, 1.5 decrease in RTS, and 26 increases in age. Furthermore, the impact of blood type O seemed to be higher for the outcome of death due to exsanguination than the all-cause trauma-related mortality. It would be of great significance for clinicians to recognize the potential risk of blood type O.