Coagulopathy after severe pediatric trauma

Abstract

Trauma remains the leading cause of morbidity and mortality in the United States among children aged 1 to 21 years. The most common cause of lethality in pediatric trauma is traumatic brain injury. Early coagulopathy has been commonly observed after severe trauma and is usually associated with severe hemorrhage and/or traumatic brain injury. In contrast to adult patients, massive bleeding is less common after pediatric trauma. The classical drivers of trauma-induced coagulopathy include hypothermia, acidosis, hemodilution, and consumption of coagulation factors secondary to local activation of the coagulation system after severe traumatic injury. Furthermore, there is also recent evidence for a distinct mechanism of trauma-induced coagulopathy that involves the activation of the anticoagulant protein C pathway. Whether this new mechanism of posttraumatic coagulopathy plays a role in children is still unknown. The goal of this review is to summarize the current knowledge on the incidence and potential mechanisms of coagulopathy after pediatric trauma and the role of rapid diagnostic tests for early identification of coagulopathy. Finally, we discuss different options for treating coagulopathy after severe pediatric trauma.

Figure 1. Current hypothesis for the development of coagulation abnormalities after blunt traumatic brain injury

A combination of hypocoagulable and hypercoagulable states triggered by the extent of brain injury will lead to secondary injury by way of ischemic and hemorrhagic lesions. Figure modified from [123].

Figure 2. Typical tracings of viscoelastic coagulation devices

A, upper side: Thrombelastograph (TEG®) tracing: r = reaction time; K = kinetics; α = slope between r and k; MA = maximum amplitude; CL = clot lysis. B, lower side: Rotation Thrombelastography (RoTEM®) tracing: CT = clotting time; CFT = clot formation time; α = slope of tangent at 2 mm amplitude; MCF = maximal clot firmness; LY = Lysis. Figure modified from [105].

Figure 3. Potential mechanisms involved in the trauma-induced coagulopathy in children

There is much adult literature detailing mechanisms and drivers of acute traumatic coagulopathy (ATC) and iatrogenic coagulopathy (IC). The classical physiologic drivers include hypothermia, acidosis, dilution secondary to intravenous administration of crystalloids and consumption of coagulation factors and might be similar between children and adults, although there is a limited description of these mechanisms in pediatric trauma. There is recent evidence for a distinct mechanism for early ATC in patients who have not been exposed to the traditional coagulopathy triggers and that may involve the activation of the anticoagulant protein C pathway, the Weibel-Palade body degradation and glycocalyx shedding. Whether these new mechanisms of ATC play a role in children is still unknown. TM: Thrombomodulin, TPA: tissue plasminogen activator, PAI-1: plasminogen activator inhibitor −1. Figure modified from [76] and [124].

Figure 4. Treatment of acute traumatic coagulopathy in children

This cartoon represents the coagulation cascade and the effect of potential therapeutic approaches for treating acute traumatic coagulopathy in children. PCC: prothrombin complex concentrate. Figure modified from [125].