Browsing by Author "Thomas, Scott"

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    CRASH-2 Study of Tranexamic Acid to Treat Bleeding in Trauma Patients: A Controversy Fueled by Science and Social Media
    (Hindawi, 2015-09-07) Binz, Sophia; McCollester, McCollester; Thomas, Scott; Miller, Joseph; Pohlm, Timothy; Waxman, Dan; Shariff, Faisal; Tracy, Rebecca; Walsh, Mark; Department of Surgery, IU School of Medicine
    This paper reviews the application of tranexamic acid, an antifibrinolytic, to trauma. CRASH-2, a large randomized controlled trial, was the first to show a reduction in mortality and recommend tranexamic acid use in bleeding trauma patients. However, this paper was not without controversy. Its patient recruitment, methodology, and conductance in moderate-to-low income countries cast doubt on its ability to be applied to trauma protocols in countries with mature trauma networks. In addition to traditional vetting in scientific, peer-reviewed journals, CRASH-2 came about at a time when advances in communication technology allowed debate and influence to be leveraged in new forms, specifically through the use of multimedia campaigns, social media, and Internet blogs. This paper presents a comprehensive view of tranexamic acid utilization in trauma from peer-reviewed evidence to novel multimedia influences.
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    Traumatic brain injury causes platelet adenosine diphosphate and arachidonic acid receptor inhibition independent of hemorrhagic shock in humans and rats
    (Wolters Kluwer, 2014) Castellino, Francis J.; Chapman, Michael P.; Donahue, Deborah L.; Thomas, Scott; Moore, Ernest E.; Wohlauer, Max V.; Fritz, Braxton; Yount, Robert; Ploplis, Victoria; Davis, Patrick; Evans, Edward; Walsh, Mark; Biochemistry and Molecular Biology, School of Medicine
    Background: Coagulopathy in traumatic brain injury (CTBI) is a well-established phenomenon, but its mechanism is poorly understood. Various studies implicate protein C activation related to the global insult of hemorrhagic shock or brain tissue factor release with resultant platelet dysfunction and depletion of coagulation factors. We hypothesized that the platelet dysfunction of CTBI is a distinct phenomenon from the coagulopathy following hemorrhagic shock. Methods: We used thrombelastography with platelet mapping as a measure of platelet function, assessing the degree of inhibition of the adenosine diphosphate (ADP) and arachidonic acid (AA) receptor pathways. First, we studied the early effect of TBI on platelet inhibition by performing thrombelastography with platelet mapping on rats. We then conducted an analysis of admission blood samples from trauma patients with isolated head injury (n = 70). Patients in shock or on clopidogrel or aspirin were excluded. Results: In rats, ADP receptor inhibition at 15 minutes after injury was 77.6% ± 6.7% versus 39.0% ± 5.3% for controls (p < 0.0001). Humans with severe TBI (Glasgow Coma Scale [GCS] score ≤ 8) showed an increase in ADP receptor inhibition at 93.1% (interquartile range [IQR], 44.8-98.3%; n = 29) compared with 56.5% (IQR, 35-79.1%; n = 41) in milder TBI and 15.5% (IQR, 13.2-29.1%) in controls (p = 0.0014 and p < 0.0001, respectively). No patient had significant hypotension or acidosis. Parallel trends were noted in AA receptor inhibition. Conclusion: Platelet ADP and AA receptor inhibition is a prominent early feature of CTBI in humans and rats and is linked to the severity of brain injury in patients with isolated head trauma. This phenomenon is observed in the absence of hemorrhagic shock or multisystem injury. Thus, TBI alone is shown to be sufficient to induce a profound platelet dysfunction.
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    Whole Blood, Fixed Ratio, or Goal-Directed Blood Component Therapy for the Initial Resuscitation of Severely Hemorrhaging Trauma Patients: A Narrative Review
    (MDPI, 2021-01-17) Walsh, Mark; Moore, Ernest E.; Moore, Hunter B.; Thomas, Scott; Kwaan, Hau C.; Speybroeck, Jacob; Marsee, Mathew; Bunch, Connor M.; Stillson, John; Thomas, Anthony V.; Grisoli, Annie; Aversa, John; Fulkerson, Daniel; Vande Lune, Stefani; Sjeklocha, Lucas; Tran, Quincy K.; Medicine, School of Medicine
    This narrative review explores the pathophysiology, geographic variation, and historical developments underlying the selection of fixed ratio versus whole blood resuscitation for hemorrhaging trauma patients. We also detail a physiologically driven and goal-directed alternative to fixed ratio and whole blood, whereby viscoelastic testing guides the administration of blood components and factor concentrates to the severely bleeding trauma patient. The major studies of each resuscitation method are highlighted, and upcoming comparative trials are detailed.