Transfusion · 2026
Platelet clotting defects in severe trauma identified by a whole blood microfluidic assay.
СтатьяНазвание и аннотация: Перевод в очереди
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Crespo Gian Rivera, Killinger Jack, Bresette Christopher, Shea Susan M, Ku David
Аннотация
BACKGROUND: Hemorrhage is the leading cause of preventable death in severe trauma, with primary hemostasis relying on platelet-rich clot formation under high shear flow. This study quantifies the incidence, severity, and heterogeneity of platelet dysfunction in Level I trauma patients.
STUDY DESIGN AND METHODS: A whole blood assay mimicking arterial hemorrhage fluidic conditions was used to measure platelet-rich clot formation in Level I trauma patients. Blood samples from patients were collected at arrival and tested for defects in platelet clotting immediately and after 12, 24, and 48 h. Additional clinical parameters such as injury severity, complete blood counts, and blood product use were collected.
RESULTS: The high shear assays were completed in under 5 min using 3 mL of blood. All trauma patients exhibited severe defects in platelet clotting at various time points compared to control blood from healthy donors (p < .01). Platelet function varied over time, with some patients exhibiting initial hyper-clotting followed by dysfunction at 24 h, while others showed persistent impairment for the entire 48 h.
DISCUSSION: The rapid assay was able to distinguish heterogeneous platelet dysfunction in Level I trauma patients. The assay enabled real-time tracking of a patient's platelet clotting function and response to interventions. By identifying patients with impaired hemostatic function, this assay could potentially inform targeted resuscitation strategies to improve trauma care outcomes.
STUDY DESIGN AND METHODS: A whole blood assay mimicking arterial hemorrhage fluidic conditions was used to measure platelet-rich clot formation in Level I trauma patients. Blood samples from patients were collected at arrival and tested for defects in platelet clotting immediately and after 12, 24, and 48 h. Additional clinical parameters such as injury severity, complete blood counts, and blood product use were collected.
RESULTS: The high shear assays were completed in under 5 min using 3 mL of blood. All trauma patients exhibited severe defects in platelet clotting at various time points compared to control blood from healthy donors (p < .01). Platelet function varied over time, with some patients exhibiting initial hyper-clotting followed by dysfunction at 24 h, while others showed persistent impairment for the entire 48 h.
DISCUSSION: The rapid assay was able to distinguish heterogeneous platelet dysfunction in Level I trauma patients. The assay enabled real-time tracking of a patient's platelet clotting function and response to interventions. By identifying patients with impaired hemostatic function, this assay could potentially inform targeted resuscitation strategies to improve trauma care outcomes.