Impact of Early Microparticle Release during Isolated Severe Traumatic Brain Injury: Correlation with Coagulopathy and Mortality

Abstract

Background: Microparticles (MPs) have been implicated in thrombosis and endothelial dysfunction. Their involvement in early coagulopathy and in worsening of outcomes in isolated severe traumatic brain injury (sTBI) patients remains ill defined. Objective: We sought to quantify the circulatory MP subtypes derived from platelets (PMPs; CD42), endothelial cells (EMPs; CD62E), and those bearing tissue factor (TFMP; CD142) and analyze their correlation with early coagulopathy, thrombin generation, and in-hospital mortality. Materials and Methods: Prospective screening of sTBI patients was done. Blood samples were collected before blood and fluid transfusion. MP enumeration and characterization were performed using flow cytometry, and thrombin–antithrombin complex (TAT) levels were determined using enzyme-linked immunosorbent assay (ELISA). Circulating levels of procoagulant MPs were compared between isolated sTBI patients and age- and gender-matched healthy controls (HC). Patients were stratified according to their PMP, EMP, and TFMP levels, respectively (high ≥HC median and low < HC median). Results: Isolated sTBI resulted in an increased generation of PMPs (456.6 [228–919] vs. 249.1 [198.9–404.5]; P = 0.01) and EMPs (301.5 [118.8–586.7] vs. 140.9 [124.9–286]; P = 0.09) compared to HCs. Also, 5.3% of MPs expressed TF (380 [301–710]) in HCs, compared to 6.6% MPs (484 [159–484]; P = 0.87) in isolated sTBI patients. Early TBI-associated coagulopathy (TBI-AC) was seen in 50 (41.6%) patients. PMP (380 [139–779] vs. 523.9 [334–927]; P = 0.19) and EMP (242 [86–483] vs. 344 [168–605]; P = 0.81) counts were low in patients with TBI-AC, compared to patients without TBI-AC. Conclusion: Our results suggest that enhanced cellular activation and procoagulant MP generation are predominant after isolated sTBI. TBI-AC was associated with low plasma PMPs count compared to the count in patients without TBI-AC. Low PMPs may be involved with the development of TBI-AC.