The purpose of this review is to summarize the current understanding of the role of aberrant platelet biology in trauma-induced coagulopathy (TIC), discuss the evidence for platelet transfusions in the management of hemorrhaging trauma patients, and review emerging platelet-based hemostatic adjuncts. Advances in the study of post-injury platelet biology have led to the discovery of pathways associated with altered platelet activation and aggregation observed in the context of TIC. Impaired platelet aggregation after injury has recently been associated with histone driven modifications in platelet structureand function, alterations in calcium signaling, and alterations in von Willebrand factor (vWF) platelet interactions. Furthermore, studies have identified several soluble factors in plasma which may play a role in inhibiting platelets after injury. Lastly, loss of the normal regulatory and bidirectional relationships of platelets with the endothelium and with fibrinolytic pathways may additionally play key roles in TIC. Importantly, the use of platelet transfusions as a treatment for hemorrhage control is not “one size fits all”—the benefit in several circumstances may be outweighed by risks, and there is a lack of demonstrated effectiveness for certain populations. Therefore, current efforts are underway to develop platelet based and platelet mimetic hemostatic agents, and to improve the effectiveness of platelet transfusions while mitigating the risks. Our understanding of how injury leads to altered platelet behavior contributing to TIC has grown substantially but remains incomplete. Decoding the complex biologic interface of platelets with the endothelium, fibrinolysis, and inflammatory pathways will lead to a more complete understanding of platelets and of TIC. Platelet transfusions remain the mainstay of treatment as part of balanced and goal-directed resuscitation, but through advancing knowledge of the underlying biology, safer, targeted, and more effective therapies may emerge.