Citation

Starr NE, Matthay ZA, Fields AT, Nunez-Garcia B, Callcut RA, Cohen MJ, Kornblith LZ. J. Trauma Acute Care Surg. 2020; ePub(ePub): ePub.

Affiliation

Department of Surgery, Zuckerberg San Francisco General Hospital and the University of California, San Francisco.

Copyright

(Copyright © 2020, Lippincott Williams and Wilkins)

DOI

10.1097/TA.0000000000002707

PMID

32218020

Abstract

BACKGROUND: Platelet behavior in trauma-induced coagulopathy is poorly understood. Injured patients have impaired platelet aggregation ('dysfunction') in ex vivo agonist-stimulated platelet aggregometry (PA). However, PA assumes platelets are inactivated prior to ex vivo stimulated aggregation, which may be altered by injury. We hypothesized that following trauma, platelet aggregation (AUC) is decreased regardless of injury burden, but that 1) minor injury is associated with an increased baseline electrical impedance, characteristic of a 'functional' platelet phenotype (platelets that activate in response to injury), and that 2) severe injury is not associated with an increased baseline electrical impedance, characteristic of a 'dysfunctional' phenotype (platelets that do not activate well in response to injury) compared to healthy controls.

METHODS: Blood from 458 trauma patients and 30 healthy donors was collected for PA. Baseline electrical impedance(Ω), platelet aggregation stimulated by adenosine diphosphate, collagen, thrombin, and arachidonic acid, and rotational thromboelastometry were measured. Multivariate regression was performed to identify associations of PA measures with blood transfusion.

RESULTS: Compared to healthy controls, injured patients had impaired platelet aggregation in response to ex vivo stimulation, regardless of injury burden. However, minorly injured patients had increased endogenous platelet activation (baseline electrical impedance, Ω: with shock p=0.012, without shock p=0.084), but severely injured patients did not have significant increases in endogenous platelet activation (baseline electrical impedance, Ω: with shock p=0.86, without shock p=0.37). For every 10Ω increase in baseline electrical impedance, there was a 8% decrease in units of blood transfused in the first 24h (-0.08, CI -0.14- -0.02, p=0.015).

CONCLUSIONS: Injury and shock confer differential patterns of platelet aggregation in PA. Minor injury overestimates the presence of platelet 'dysfunction', while severe injury induces a truly 'dysfunctional' phenotype: platelets that do not activate nor aggregate appropriately after injury. This is consequential in improving accurate phenotyping of post-injury platelet behavior for platelet-based therapeutics. LEVEL OF EVIDENCE: IVStudy Type: Prognostic, Original Article.

Language: en