Switching gears a little bit, our next speaker will be Andrew Gaiot, speaking on the effect of platelet dysfunction on outcomes in traumatic brain injury. Good afternoon. Thank you for the opportunity of speaking to you today. I'm a second year medical student at the University of Missouri. Coagulopathy is a common complication in traumatic brain injury, and it's been associated with poor outcomes, including delayed hematoma expansion, poor functional outcomes, and increased mortality. TBI has also been associated with as an independent risk factor for platelet dysfunction. And many patients present with TBI have prior use of platelet-inhibiting medications due to prior strokes, coronary artery disease, and venous thromboembolism. So many patients that present with TBI will have a high risk of platelet dysfunction. Thromboelastography has been widely adopted in many trauma centers as a point-of-care assay to evaluate coagulopathy. It's a viscoelastic study, so basically it's measuring the strength of a forming thrombus over time. And by evaluating various parameters shown on the curve on the right, you're able to evaluate coagulation factor function, platelet function, and thrombolysis. And TAG with platelet mapping has also been used in some operative applications, including cardiac surgery, to guide transfusion of blood products. So the goals of our project were to evaluate the incidence and severity of TAG abnormalities in TBI patients and identify which factors contributed to the platelet dysfunction and also to evaluate whether transfusing platelets would improve the TAG assay results and also influence patient outcomes. So we enrolled adult patients with non-penetrating TBI. In order to be included in the study, patients were required to have an identifiable lesion on the CT scan, which could be any kind of intracranial hemorrhage, hematoma, or skull fracture. We performed a TAG with platelet mapping assay on the patients at admission and then repeated again at 24 hours. The patients that were found to have ADP inhibition greater than 60% were transfused one unit of platelets, and then the TAG assay was repeated again one hour later. Additionally, there was a small number of patients included in our study which were admitted for severe multisystem trauma that were transfused multiple units of platelets along with other blood products. So the outcomes that we were interested in our study included in-hospital mortality, the Glasgow outcome score at discharge, as well as the progression of CT lesion at 24 hours. So did the hematoma expand, remain stable, or decrease in size? And we also evaluated the estimated blood loss during surgery and the surgeon's perception of the difficulty obtaining hemostasis. So during our study period, 179 patients were admitted, which met the inclusion criteria. 155 of those patients had the TAG assay performed on admission. Twenty-nine patients underwent a neurosurgical procedure, and 36 received a platelet transfusion. We found that 40% of the patients in our study had an ADP inhibition greater than 60%, which is a threshold that other studies and clinical applications have considered as clinically significant platelet dysfunction. We started by evaluating the ADP inhibition compared to the Glasgow Coma Scale. So defining severe TBI as GCS 3 to 8, moderate TBI GCS 9 to 12, and mild TBI GCS 13 to 15. We found that the mild TBI group had a statistically significant lower ADP inhibition compared to the moderate and severe TBI group. And this suggests that there may be a dose-dependent relationship between the severity of TBI and the degree of platelet dysfunction. Next, we looked at the effect of transfusing platelets on the TAG assay results. So patients that did not receive a transfusion showed a mean increase of about 12% in ADP inhibition at the follow-up TAG assay. Patients that were transfused platelets showed a mean decrease of about 12%. However, the difference here was not statistically significant. I would like to point out that we did have a relatively small sample size, especially in the patients that did not receive a platelet transfusion and then had the follow-up assay performed at 24 hours. But potentially, there's a clinically significant effect here within the confidence interval. Additional results that did show statistical significance, patients with polytrauma showed higher ADP inhibition compared to isolated TBI. And patients taking P2Y12 inhibiting medication showed higher ADP inhibition. And also, patients who received platelet transfusions had higher mortality. I'd like to point out the significant confounding factor that the patients with the most severe injuries are more likely to receive platelet transfusions, likely explaining the higher mortality in that group. But we did not see any associations with alcohol consumption, the type of lesion on the CT scan, or lesion expansion at 24 hours. We also did not see an association between the ADP inhibition and the difficulty with obtaining hemostasis during surgery. So in conclusion, we've shown that the mild TBI is associated with less ADP inhibition compared to moderate and severe TBI. Transfusing platelets did not have a significant effect on the tag assay results and did not appear to improve outcomes. So we feel that the decision to transfuse platelets in TBI patients should not be made solely based on the tag assay results. Some potential areas for further study include, we'd like to look at a larger sample of patients undergoing neurosurgery. We had a small sample size there. And clearly, those are the patients at the most risk of complications due to difficulty obtaining hemostasis in the intra- and perioperative period. We'd also like to look at the effect of transfusing more than one unit of platelets in a patient with a normal platelet count. One unit of platelets may not be enough to have a significant effect on the tag assay results or possibly a clinically significant effect on outcomes. And then a better understanding of the mechanism of platelet dysfunction may help determine what the most appropriate treatment for these patients are. I'd like to acknowledge my faculty mentor, Dr. Lutovsky at the University of Missouri for his guidance on this project. And thank you for allowing me to speak today. Thank you.

platelet dysfunction

traumatic brain injury

coagulopathy

thromboelastography

transfusing platelets