Purpose of review: Homeostasis represents a delicate balance between hemostatic and fibrinolytic processes. This balance permits arrest of hemorrhage after mild injury but prevents thrombosis from occurring under normal circumstances. Trauma disturbs the equilibrium between hemostatic and fibrinolytic processes, frequently producing either a hypocoagulable state or a hypercoagulable state depending on the severity of injury, degree of hemorrhage, and the nature of the resuscitation. The purpose of this review is to describe the epidemiology and pathophysiology of coagulopathy after trauma and to discuss novel methods of treating it.
Recent findings: Published reports during the past year focus on the pathophysiology of coagulopathy after trauma and novel methods of treatment. Individual effects of hypothermia and acidosis on clotting factors and platelet function have been described. The effects of varying resuscitation fluids on coagulopathy have also been described as well as the course of coagulopathy over time. Recombinant factor VIIa has emerged as a popular therapy for traumatic coagulopathy although a prospective randomized trial has yet to be published. The efficacy of several new dressings for the local control of hemorrhage has been reported.
Summary: Changes in coagulation following trauma are characterized by a complex series of events that may result in either a hypocoagulable or a hypercoagulable state. Routinely analyzed coagulation parameters do not adequately describe this state and they are deficient for guiding its therapy. Several promising new agents are available for treating hemorrhage in coagulopathic trauma patients that should result in improved survival.