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Review
. 2022 Jul 1;58(1):1-13.
doi: 10.1097/SHK.0000000000001948. Epub 2022 Jul 19.

PLATELET FUNCTION IN TRAUMA: IS CURRENT TECHNOLOGY IN FUNCTION TESTING MISSING THE MARK IN INJURED PATIENTS?

Jacob B Schriner  1 , Mitchell J George  2 , Jessica C Cardenas  1 , Scott D Olson  3 , Kimberly A Mankiewicz  1 , Charles S Cox Jr, Brijesh S Gill, Charles E Wade  1
Affiliations
Review

PLATELET FUNCTION IN TRAUMA: IS CURRENT TECHNOLOGY IN FUNCTION TESTING MISSING THE MARK IN INJURED PATIENTS?

Jacob B Schriner et al. Shock. .

Abstract

Platelets are subcellular anucleate components of blood primarily responsible for initiating and maintaining hemostasis. After injury to a blood vessel, platelets can be activated via several pathways, resulting in changed shape, adherence to the injury site, aggregation to form a plug, degranulation to initiate activation in other nearby platelets, and acceleration of thrombin formation to convert fibrinogen to fibrin before contracting to strengthen the clot. Platelet function assays use agonists to induce and measure one or more of these processes to identify alterations in platelet function that increase the likelihood of bleeding or thrombotic events. In severe trauma, these assays have revealed that platelet dysfunction is strongly associated with poor clinical outcomes. However, to date, the mechanism(s) causing clinically significant platelet dysfunction remain poorly understood. We review the pros, cons, and evidence for use of many of the popular assays in trauma, discuss limitations of their use in this patient population, and present approaches that can be taken to develop improved functional assays capable of elucidating mechanisms of trauma-induced platelet dysfunction. Platelet dysfunction in trauma has been associated with need for transfusions and mortality; however, most of the current platelet function assays were not designed for evaluating trauma patients, and there are limited data regarding their use in this population. New or improved functional assays will help define the mechanisms by which platelet dysfunction occurs, as well as help optimize future treatment.

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Conflict of interest statement

C.S.C. has the following relationships to disclose: Coagulex, Inc. sponsored research funding and equity/royalty (interest via The University of Texas Health Science Center at Houston [UTHealth]). B.S.G. has the following relationships to disclose: Coagulex, Inc. sponsored research funding and equity/royalty (interest via UTHealth). UTHealth has an institutional conflict of interest for holding equity in Coagulex. C.E.W. receives funding from the William Stamps Farish Fund, the Howell Family Foundation, and the James H. “Red” Duke Professorship. Unrelated to the present effort, C.E.W. holds a financial interest in Dicisio Health LLC and receives grants from Grifols and Athersys. J.C.C. has funding from the Department of Defense, Aniara, and has received speaker honoraria and research funding from Grifols. S.D.O. is supported by National Institute of Neurological Diseases and Stroke of the National Institutes of Health award number R21NS116302. J.B.S. is supported by a T32 fellowship from the National Institute of General Medical Sciences of the National Institutes of Health under award number T32GM008792.

Figures

Figure 1.
Figure 1.. Schematic overview of platelet functions following vascular injury and associated functional assays.
Platelets play a critical role in mediating the immediate response to vascular injury. These are divided into 4 key processes that are measurable by distinct methods: (1) activation, (2) adhesion and aggregation, (3) support of fibrin formation, and (4) clot contraction/stabilization. Created with BioRender.com.
See this image and copyright information in PMC

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