Fibrinogen metabolic responses to trauma

Abstract Coagulation complications are significant contributors to morbidity and mortality in trauma patients. Although the lethal triad of hypothermia, acidosis and coagulopathy has been recognized for over a decade, the underlying mechanisms related to the development of coagulopathy remain unclear. Recent data suggest that decreased fibrinogen levels contribute to the development of coagulation disorders. Thus, regulation of fibrinogen availability, not fully understood at present, may play an important role in survival of trauma patients. This review summarizes the recent findings of the studies that have explored mechanisms related to changes in fibrinogen availability following trauma-related events. Trauma alters fibrinogen metabolism in a variety of ways: hemorrhage – accelerated fibrinogen breakdown; hypothermia – inhibited fibrinogen synthesis; and, acidosis – accelerated fibrinogen breakdown. However, hemorrhage, hypothermia andcidosis all result in a consistent outcome of fibrinogen availability deficit, supporting the notion of fibrinogen supplementation in trauma patients with coagulation defects. Future prospective clinical trials are needed to confirm the beneficial effects of fibrinogen supplementation in trauma patients with bleeding complications.