Beyond the count: platelet dysfunction profile in pediatric trauma patients

Existing clinical coagulation assays are inadequate to evaluate posttraumatic platelet dysfunction in children.

To elucidate changes in flow-dependent platelet function after injury in children using a microfluidic assay.

We enrolled 18 children who presented with highest-acuity trauma activation and 10 healthy children at an academic pediatric center. For the control cohort, outpatient blood samples were collected, and for the trauma cohort, blood was collected in the trauma bay for conventional coagulation tests, thromboelastography, von Willebrand factor A1 domain activity, and a microfluidic assay using a stenotic channel (shear rate = 3500 s^-1).

The trauma cohort characteristics were 67% male, median (IQR) age 6 years (4-12), median (IQR) injury severity score 17 (9-26), and 78% blunt mechanism. In total, 50% required blood transfusion and 11% (2/18) died. While thromboelastography maximum amplitude (59.9 ± 6.1 mm) and platelet counts (306.3 ± 111.1 × 10³ cells/μL) were within normal limits, the microfluidic assay revealed significantly lower platelet deposition in the trauma cohort versus the control cohort (1.18 ± 0.25 vs 3.06 ± 0.82 mean fluorescence intensity fold change; P < .0001). Lower levels of platelet deposition correlated with receipt of blood transfusion within 6 hours of arrival (r = -0.44, P = .048). von Willebrand factor A1 domain activity was not different between groups and was not correlated with platelet deposition based on mean fluorescence intensity fold change (R ² < 0.0001).

Posttraumatic platelet dysfunction was observed by utilizing a microfluidic assay in a pediatric trauma cohort. Further study is needed to understand the underlying mechanisms and significance of posttraumatic platelet dysfunction in children.