Identification of injury and shock driven effects on ex vivo platelet aggregometry: A cautionary tale of phenotyping
| Autor: | Lucy Z. Kornblith, Mitchell J. Cohen, Rachael A. Callcut, Alexander T. Fields, Nichole Starr, Zachary A. Matthay, Brenda Nunez-Garcia |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Male
Platelet Aggregation Cardiorespiratory Medicine and Haematology Cardiovascular Critical Care and Intensive Care Medicine 0302 clinical medicine Electric Impedance 2.1 Biological and endogenous factors Platelet Aetiology Shock Hematology Blood Coagulation Disorders Thrombelastography Thromboelastometry trauma Phenotype Shock (circulatory) Cardiology Female medicine.symptom medicine.drug Platelets Adult medicine.medical_specialty Physical Injury - Accidents and Adverse Effects Platelet Function Tests Clinical Sciences Nursing Article 03 medical and health sciences Thrombin Clinical Research Internal medicine platelet activation medicine Coagulopathy Humans Platelet activation business.industry Impaired platelet aggregation 030208 emergency & critical care medicine Platelet Activation medicine.disease Emergency & Critical Care Medicine Case-Control Studies Wounds and Injuries Surgery business Ex vivo |
| Zdroj: | J Trauma Acute Care Surg The journal of trauma and acute care surgery, vol 89, iss 1 |
| ISSN: | 2163-0763 2163-0755 |
| Popis: | 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 that platelets are inactivated before ex vivo stimulated aggregation, which may be altered by injury. We hypothesized that following trauma, platelet aggregation (area under the curve) 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 with 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 with 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 10 Ω increase in baseline electrical impedance, there was an 8% decrease in units of blood transfused in the first 24 h (-0.08; confidence interval, -0.14 to -0.02; p = 0.015). Conclusion 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 postinjury platelet behavior for platelet-based therapeutics. Level of evidence Prognostic, level IV. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|