A renewed understanding of Trauma Induced Coagulopathy (TIC) has implicated platelets as a crucial mediator and potential therapeutic target in hemostasis. While the importance of abnormal coagulation tests is well described in trauma, there is a paucity of data regarding the role of platelets in coagulopathy. New coagulation models, namely the cell-based-model of hemostasis, have refocused attention toward the platelet and endothelium as key regulators of clot formation. Although platelet dysfunction has been associated with worse outcomes in trauma, the mechanisms which platelet dysfunction contributes to coagulopathy are poorly understood. The goal of this review article is to outline recent advances in understanding hemostasis and the ensuing cellular dysfunction that contributes to the exsanguination of a critically injured patient.