Assessment of Platelet Function in Traumatic Brain Injury—A Retrospective Observational Study in the Neuro-Critical Care Setting

Abstract

Background: Despite seemingly functional coagulation, hemorrhagic lesion progression is a common and devastating condition following traumatic brain injury (TBI), stressing the need for new diagnostic techniques. Multiple electrode aggregometry (MEA) measures platelet function and could aid in coagulopathy assessment following TBI. The aims of this study were to evaluate MEA temporal dynamics, influence of concomitant therapy, and its capabilities to predict lesion progression and clinical outcome in a TBI cohort.Material and methods: Adult TBI patients in a neurointensive care unit that underwent MEA sampling were retrospectively included. MEA was sampled if the patient was treated with antiplatelet therapy, bled heavily during surgery, or had abnormal baseline coagulation values. We assessed platelet activation pathways involving the arachidonic acid receptor (ASPI), P2Y12 receptor, and thrombin receptor (TRAP). ASPI was the primary focus of analysis. If several samples were obtained, they were included. Retrospective data were extracted from hospital charts. Outcome variables were radiologic hemorrhagic progression and Glasgow Outcome Scale assessed prospectively at 12 months posttrauma. MEA levels were compared between patients on antiplatelet therapy. Linear mixed effect models and uni-/multivariable regression models were used to study longitudinal dynamics, hemorrhagic progression and outcome, respectively. results: In total, 178 patients were included (48% unfavorable outcome). ASPI levels increased from initially low values in a time-dependent fashion (p < 0.001). Patients on cyclooxygenase inhibitors demonstrated low ASPI levels (p < 0.001), while platelet transfusion increased them (p < 0.001). The first ASPI (p = 0.039) and TRAP (p = 0.009) were significant predictors of outcome, but not lesion progression, in univariate analyses. In multivariable analysis, MEA values were not independently correlated with outcome.

Influence of Blood–Brain Barrier Integrity on Brain Protein Biomarker Clearance in Severe Traumatic Brain Injury: A Longitudinal Prospective Study

“…40 Radiological brain injury progression upon subsequent examination was evaluated employing a similar strategy as in previous work. 8,41 Glasgow Outcome Scale 42 (GOS) was assessed as described previously. 27 In short, a neurorehabilitation board-certified physician (P.H.G.)…”

Does Complement-Mediated Hemostatic Disturbance Occur in Traumatic Brain Injury? A Literature Review and Observational Study Protocol

“…Presumably, trauma also initiates other processes that render platelets hypoactive despite the increased complement activity. The same pattern can also be seen in patients with TBI, where platelet function decreases in the first hours to days following injury [75]. Strengthening the hypothesis that complement activation leads to increased platelet activity, other studies have demonstrated that there is a correlation between MAC levels and plasma concentrations of prothrombin fragments 1 and 2, which are produced upon thrombin generation, in trauma patients with low C3a levels [27].…”

“…Our hypothesis is that increased complement activity will occur in patients with a prothrombotic phenotype following TBI, and those with decreased platelet aggregability will have a lower concentration of complement deposition on their platelet cell surfaces. Moreover, since there is often a recovery of platelet function after its initial decline [75], we believe that there will be a time-dependent variation in the amount of complement deposition on platelets that corresponds to the change in platelet function.…”

“…Evidence shows that TBI is followed by platelet dysfunction [75,76] and a decreased platelet count [77], both of which appear to increase the risk of bleeding [76,78,79].…”

Assessment and management of coagulopathy in neurocritical care

“…TEG with platelet mapping (TEG-PM, Haemoscope Corp., Niles, IL, USA) is a specific VHA that has been shown to correlate with platelet aggregometry and is able to detect platelet dysfunction due to APT and other coagulopa-thies. In neurocritically ill patients, such as those with subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH), or traumatic brain injury (TBI), platelet dysfunction may be seen even in the absence of APT use or failure of other organ systems and may confer worse outcomes [22][23][24].…”