Aims and Objectives Trauma is a leading cause of death for those under 44. Patients with blood group O (bgO) have been reported to have higher mortality. The existing hypothesis (that lower levels of circulating von Willebrand factor/factor VIII in patients with bgO increases mortality through a bleeding tendency) has not been tested. Our study uniquely investigates the association between all ABO Rh groups and 30-day all-cause mortality in a large adult trauma patient cohort. Understanding post-trauma physiological shifts may identify potential therapeutic targets to attenuate risks.

Method and Design All patients ≥16 years old attending the East of England Major Trauma Centre (2016-2019) who met Trauma Audit Research Network (TARN) criteria were included. The primary outcome was 30-day mortality; secondary outcomes included admission clotting profile (PT/aPTT). Data reported as number (percentage), median [interquartile range]. Proportions were compared with a Chi-square test, reported as relative risk (95% confidence interval) (RR (95%CI)). Continuous data were compared with a Kruskal-Wallis test, reported as p-value. Data analyses were performed in Python v.3.8.9. Bonferroni correction was used for multiple comparisons.

Results and Conclusion 4188 patients were included. The median age was 59.3 [39.0-77.9] years, n=2634 (62.9%) were male, the median injury severity score was 19 [10-25], and 30-day mortality was 9.3%. Pairwise comparison demonstrated increased mortality in O Rh negative patients (Oneg) compared to three other groups, table 1. Compared to all other ABO Rh groups combined, Oneg patients had significantly greater 30-day mortality – 15.1% compared to 8.8%; RR 1.72 (95%CI 1.32-2.24), p=0.0002 (significance defined as p<0.0063 (eight comparisons)). There was no difference in admission PT or aPTT between Oneg and all other groups combined, p=0.12 and p=0.26 respectively. Trauma patients with Oneg had significantly greater 30-day mortality compared to other ABO Rh groups, which questions the existing hypothesis of the underlying mechanism.