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Impact of Early Microparticle Release during Isolated Severe Traumatic Brain Injury: Correlation with Coagulopathy
Venencia Albert1, Arulselvi Subramanian1, Hara Prasad Pati2
1Departments of Laboratory Medicine, Jai Prakash Narayan Apex Trauma Centre, AIIMS, New Delhi, India.
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.
Insights
Severe traumatic brain injury (sTBI) increases platelet-derived microparticles (PMPs) and endothelial cell-derived microparticles (EMPs). Low PMP levels are associated with early coagulopathy in sTBI patients.
Area of Science:
- Trauma research
- Hematology
- Vascular biology
Background:
- Microparticles (MPs) are linked to thrombosis and endothelial dysfunction.
- Their role in early coagulopathy and outcomes in severe traumatic brain injury (sTBI) is unclear.
Purpose of the Study:
- Quantify circulating MP subtypes (platelet-derived, endothelial cell-derived, tissue factor-bearing) in sTBI patients.
- Analyze correlations with early coagulopathy, thrombin generation, and mortality.
Main Methods:
- Prospective study of sTBI patients, collecting blood pre-transfusion.
- Flow cytometry for MP enumeration and characterization.
- ELISA for thrombin-antithrombin complex (TAT) levels.
- Comparison with healthy controls (HC).
Main Results:
- sTBI patients showed increased platelet-derived microparticles (PMPs) and endothelial cell-derived microparticles (EMPs) versus HCs.
- Tissue factor-bearing MPs (TFMPs) showed no significant difference.
- Early TBI-associated coagulopathy (TBI-AC) was observed in 41.6% of patients.
- Patients with TBI-AC had lower PMP and EMP counts compared to those without TBI-AC.
Conclusions:
- Isolated sTBI leads to increased cellular activation and procoagulant MP generation.
- TBI-associated coagulopathy is linked to lower plasma PMP counts.
- Low PMPs may contribute to the development of TBI-AC.
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