Background
Traumatic injuries are the leading cause of mortality in children and young adults, accounting for more than 45% of all deaths in patients 1–19 years of age in the USA.1–4 Furthermore, ongoing disability following non-fatal traumatic injury affects approximately 50% of pediatric patients.5–7 Due to hospital and long-term care expenses, the economic costs of pediatric trauma have been estimated at $14 billion in lifetime medical spending and $66 billion in present and future work loss.8–10 Despite its impact on outcomes, there is much to learn about the pathophysiological processes and clinical constellations that drive mortality and morbidity following pediatric injury.
In adults, trauma-induced coagulopathy (TIC) seems to play a critical role in outcomes following trauma. Historically, all TIC was thought to be related to patient management. Now termed iatrogenic coagulopathy, this type of coagulopathy has been attributed to (1) dilution of coagulation factors after crystalloid and red blood cell resuscitation, (2) blood loss and consumption due to ongoing bleeding and procedures, (3) hypothermia from exposure and infusion of unwarmed resuscitation fluids, and (4) resultant acidosis.11 Sixteen years ago, a distinct group of adult patients with trauma was described that present with coagulopathy prior to these exposures and interventions.12 This early coagulopathy, referred to as either early TIC or acute traumatic coagulopathy (ATC), is an endogenous biologic response that occurs nearly immediately after injury and is independent of iatrogenic causes of dysfunctional hemostasis.13 ATC is thought to be part of a pathway in which traumatic injury triggers a combination of mechanical tissue trauma, oxygen debt, and inflammation, which impairs coagulation and endothelial function.14 With an incidence of 25% in adults, ATC has been associated with increased transfusion requirements, a greater incidence of organ dysfunction, a longer intensive care unit and overall hospital stay, and a fourfold increase in mortality in the adult population.11–13 15 16
There are a handful of retrospective studies describing ATC in the pediatric population.17–21 While all have identified the presence of pediatric ATC, the incidence varies widely between studies (8.4%–57%).17–21 In addition, all of these prior studies have found an association between pediatric ATC and mortality (OR 2.2 to 4.2). However, none have quantified the impact of ATC on multiple organ dysfunction syndrome (MODS). In pediatric populations, MODS is associated with an increased risk of mortality as well as short-term morbidity and serves as a validated proxy for poor outcomes when mortality rates may be too low to quantify the full effect of a clinical condition.22 Because MODS has not been evaluated in pediatric ATC, the true impact of pediatric ATC may be significantly under-represented by prior studies focused on mortality. Given the significance of trauma in the pediatric population and this important limitation in prior pediatric ATC studies, the objective of this work is to describe the incidence and outcomes in pediatric ATC with specific focus on the relationship between pediatric ATC and MODS.