Background
Although global pediatric mortality rates related to trauma have improved over the past 30 years, hemorrhage remains a leading cause of potentially preventable death in this population.1–3 Traumatic brain injury is the leading cause of death overall in pediatric trauma patients and progression of traumatic head bleeds can contribute significantly to long-term disability.1 3 4 Identifying and treating trauma-induced coagulopathy in this population will be paramount as we strive to continue improving trauma outcomes in these patients.
While many factors contribute to trauma-induced coagulopathy, hypofibrinogenemia has been identified as predictor of poor outcomes in adult trauma patients.5–7 Fibrinogen plays a key role in the coagulation cascade as its activated substrate fibrin is used in combination with platelets to form the final product of hemostasis, clot.8 The source of hypofibrinogenemia in the trauma patient is likely multifactorial. Increased consumption in the setting of hemorrhage and clot formation likely plays a role. Other factors that likely contribute to hypofibrinogenemia include dilution secondary to fluid administration, decreased synthesis in the setting of hypothermia, and decreased utilization secondary to increased levels of protein C and thrombomodulin often found in trauma coagulopathy.6 9–13
Fibrinogen levels can be calculated using several different methods including: the Clauss fibrinogen assay, levels derived from a prothrombin time standard curve, and viscoelastic studies.14 Traditional measurements may take up to 80 min to provide results, while viscoelastic tests such as thrombelastography (TEG) can provide results in <15 min. Several studies have demonstrated that K-time, α-angle, and maximum amplitude (MA) are reliable in diagnosing hypofibrinogenemia.15 16 An α-angle <60 has been previously demonstrated to correlate strongly to traditional Clauss fibrinogen assay.16 These modalities offer an opportunity to rapidly identify and intervene on hypofibrinogenemia in the trauma patient.
To date, the role that hypofibrinogenemia plays in the pediatric patient population has not been a source of significant investigation. Leeper et al identified abnormalities in fibrinolysis to be an independent risk factor for mortality in pediatric trauma patients, with fibrinolysis shutdown being a particularly poor indicator.17 Given the prevalence of hypofibrinogenemia in trauma patients and its association with mortality, the role of fibrinogen replacement has been a topic of increased attention. It has been suggested that early correction of hypofibrinogenemia may lead to improved outcomes and the early administration of fresh frozen plasma or fibrinogen in patients with hypofibrinogenemia is recommended by the Task Force for Advanced Bleeding Care in Trauma.18–20 Whether this applies to the pediatric population is unknown. If pediatric patients with hypofibrinogenemia are predominantly dying because of hemorrhage, rapid correction of coagulopathy would be of the utmost importance. To better answer this question, a full understanding of the prevalence and outcomes of pediatric patients with hypofibrinogenemia is needed. The aim of this study was to evaluate the role that fibrinogen plays in the pediatric trauma patient receiving massive transfusion. It is hoped that a better understanding of this aspect of trauma coagulopathy will help inform what role cryoprecipitate and other concentrated fibrinogen products play in the initial resuscitation of traumatically injured pediatric patients.