PB0368 - Platelet flux in trauma-associated venous thromboembolism: a secondary analysis of the Consortium of Leaders in the Study of Traumatic Thromboembolism (CLOTT)-1 & 2 studies

Sunday, June 23, 2024

13:45 – 14:45 ICT

Room: Exhibition Hall

Co-Author(s)

Elizabeth Z. Andraska

Resident in Vascular Surgery
UPMC
Pittsburgh, Pennsylvania, United States

Co-Author(s)

AF

Alexander Fields

Physician
UCSF
San Francisco, California, United States
BN

Brenda Nunez-Garcia

Research Program Manager
UCSF
San Francisco, California, United States
Ernest E. Moore, MD

Director of Research
Ernest E Moore Shock Trauma Center ay Denver Health
Denver, Colorado, United States
CW

Charles Wade

Physician
University of Texas
Houston, Texas, United States
MK

M. Margaret Knudson

Physcian
UCSF
San Francisco, California, 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

Presenting Author(s)

Lucy Z. Kornblith, MD

Associate Professor of Surgery
UCSF
San Francisco, California, United States

Background: Trauma patients are at significant risk for venous thromboembolism (VTE). Platelet-based prevention of VTE has been reported, but associations between platelet count and function with trauma-associated VTE are unknown.

Aims: To evaluate platelet count and function in association with the development of trauma-associated VTE.

Methods: This study was a secondary analysis of the CLOTT studies which enrolled patients at 17 US level-I trauma centers (2018-2020) with at least one trauma-associated VTE risk factor. Those who developed trauma-associated VTE were compared to those who did not. Thromboelastography (TEG) and platelet aggregometry were prospectively performed in a subset of patients at three centers. Platelet count and function were examined by univariate and multivariable analyses, and were time-ordered prior to VTE development.

Results: 7,912 patients (mean [SD] age, 29 [6.4] years; 75.4% male) were included in the analysis, and 425 (5.4%) developed trauma-associated VTE. The median injury severity score (ISS) was 16, and 458 (5.8%) patients presented in shock (systolic blood pressure < 90mmHg). Admission platelet counts were similar between groups (no VTE 254.2±80.8 vs. VTE 242.8±86.9; p= < 0.01), but dropped significantly more on day 1 (no VTE 196.6±66.2 vs. VTE 156.8±68.7; p= < 0.01), day 2 (no VTE 173.1±62.8 vs. VTE 136.2±57.2; p= < 0.01), and day 3 (no VTE 175.3±67.1 vs. VTE 139.9±61.42; p= < 0.01) in those who developed VTE (Fig 1A). Each 10-count drop in platelets was independently associated with a 10% increase in odds of VTE (OR [95% CI] 1.10 [1.05-1.14]) (Fig 1B). Platelet function did not significantly differ between groups (Fig 2A-F).

Conclusion(s): In a large population of injured patients, reduction in platelet count early after injury was independently associated with development of VTE. A drop in platelet count in the first 72 hours after injury may be a useful marker of risk of VTE, and should be considered in VTE-screening protocols.