PB1048 - Platelet Dysfunction following Severe Trauma: Temporal Insights from a Microfluidic Assay

Tuesday, June 25, 2024

13:45 – 14:45 ICT

Room: Exhibition Hall

Co-Author(s)

Ronit Kar, BS

Research Fellow
Trauma and Transfusion Medicine Research Center, Department of Surgery, University of Pittsburgh
Pittsburgh, Pennsylvania, United States

Presenting Author(s)

JK

Jack Killinger

Research Technician
Trauma and Transfusion Medicine Research Center, Department of Surgery, University of Pittsburgh
Pittsburgh, Pennsylvania, United States

Co-Author(s)

Devin Dishong

Research Fellow
Trauma and Transfusion Medicine Research Center, Department of Surgery, University of Pittsburgh
Pittsburgh, Pennsylvania, United States
Katelin C. Rahn, BS

PhD Candidate
Trauma and Transfusion Medicine Research Center, Department of Surgery, University of Pittsburgh
Pittsburgh, Pennsylvania, United States
LV

Lisa Vavro

Clinical Research Coordinator
Trauma and Transfusion Medicine Research Center, Department of Surgery, University of Pittsburgh
Pittsburgh, Pennsylvania, United States
PS

Philip Spinella

Co-Director
Trauma and Transfusion Medicine Research Center, Department of Surgery, University of Pittsburgh
Pittsburgh, Pennsylvania, United States
Matthew D. Neal, MD, FACS

Vice Chair of Surgery, Academic Training; Watson Chair and Professor of Surgery
University of Pittsburgh, Pittsburgh, PA, USA
Pittsburgh, Pennsylvania, United States
Susan Shea

Assistant Professor
Trauma and Transfusion Medicine Research Center, Department of Surgery, University of Pittsburgh
Pittsburgh, Pennsylvania, United States

Background: Platelet dysfunction in trauma-induced coagulopathy is incompletely understood. Post-injury platelet function remains poorly characterized, and standard clinical assays fall short in their evaluative capabilities.

Aims: This study aims to investigate temporal changes in platelet function following traumatic injury using a microfluidic assay.

Methods: In this prospective observational study, 22 trauma patients with level one activation were enrolled. Serial whole blood samples were collected up to five days post-arrival. A subset (N=13) of samples were incubated with anti-CD41 fluorescent antibody and perfused through a microfluidic channel functionalized with collagen at high shear (3500/s). Mean fluorescence intensity was calculated over 10 minutes of perfusion. Blood counts and peripheral blood smears were also performed. Clinical data are reported as mean ± SD.

Results: The trauma patient cohort, predominantly male (64%) with an average age of 50 ± 17 years, presented with a Glasgow Coma Scale score of 11.2 ± 5.4 and Injury Severity Score of 10.2 ± 9.9. Platelet count decreased within 24 hours post-injury, followed by a rise over the next four days. Notably, microfluidic assay results revealed a decline in platelet deposition within the first 12 hours, a surge at 24 hours, and a return to baseline over the subsequent four days (Figure 1). Peripheral blood smears revealed echinocytes in the acute post-trauma phase that resolved over 24 hours (Figure 2).

Conclusion(s): The observed transient thrombocytopenia ( < 150×10^3cells/µL) and subsequent resolution are consistent with previous reports. However, the microfluidic assay reveals a pattern of initial decline, followed by marked increase, and eventual normalization of platelet function, underscoring that, despite platelet count normalization, significant functional differences persist. The discovery of echinocytes in non-burn trauma patients is a novel observation that warrants further study. Future analysis with more detailed clinical exploration and ongoing patient enrollment will shed light into the mechanisms and clinical implications of these observations.