Coagulation is a complex cascade whose intact functioning is essential in helping control hemorrhage after injury. While traditionally ascribed to the combined effects of acidosis, hypothermia, factor consumption and factor dilution, coagulopathy is also directly related to injury as well as hypofibrinogenemia and hyperfibrinolysis. Low fibrinogen concentration is readily determined with standard laboratory profiling, but direct analysis of hyperfibrinolysis relies on either thromboelastography or rotational thromboelastometry. Both conditions offer opportunities for therapeutic intervention, and inhibition or abrogation of hyperfibrinolysis in particular may significantly improve survival in patients with injury and massive hemorrhage. Herein, we explore the underpinnings of trauma associated coagulopathy, the basic science behind the role of fibrinogen in acute traumatic coagulopathy, and the rationale behind and the data derived from management of hypofibrinogenemia as well as hyperfibrinolysis.