RESUMEN
BACKGROUND: Acute traumatic coagulopathy (ATC) has many phenotypes and varying morbidity and mortality. The MA-R ratio, calculated from the admission thromboelastogram, serves as a biomarker to identify 1 phenotype of ATC and has previously been associated with significant derangements in the inflammatory response. This study evaluates outcomes related to abnormal MA-R ratios, including inflammatory responses, in a heterogeneous patient population. STUDY DESIGN: Patients from the Pragmatic, Randomized Optimal Platelet and Plasma Ratios (PROPPR) dataset were included. The MA-R ratio was calculated from admission thromboelastography, with a CRITICAL ratio defined as 11 or less. Key inflammatory mediators were identified as a priori. Cytokine expression was assessed during 24 hours using multivariable logistic regression. RESULTS: Significant elevations in the proinflammatory cytokines IL-1b, IL-6, and IL-8, as well as in the chemokines eotaxin, IFN-γ-induced protein 10, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1ß, persisted during the first 24 hours. CRITICAL patients had significantly lower survival at 1, 3, 6, 12, and 18 hours and demonstrated significantly increased ARDS (odds ratio [OR] 1.817, 95% CI 1.082 to 3.051, p = 0.0239). CRITICAL patients had fewer ICU-free days (CRITICAL, 10 days, interquartile range [IQR] 0 to 25; vs NORMAL, 22 days, IQR 4 to 26, p < 0.0001) and fewer ventilator-free days (CRITICAL, 15 days, IQR 0 to 28; vs NORMAL, 26 days, IQR 9 to 28, p < 0.0001). CRITICAL patients were protected against systemic inflammatory response (OR 0.521, 95% CI 0.322 to 0.816, p = 0.0044). CONCLUSIONS: The subtype of ATC identified by the low MA-R ratio is associated with significant elevations in multiple proinflammatory cytokines at admission. Early mortality remains elevated in the CRITICAL group, in part due to coagulopathy. The MA-R ratio at admission is associated with a particularly morbid type of coagulopathy, associated with significant alterations in the inflammatory response after severe injury in heterogeneous patient populations.
