BACKGROUND
Complex cranial vault reconstruction (CCVR) is a surgery primarily performed in infants and young children for repair of craniosynostosis.1 CCVR is an intricate and high-risk procedure involving extensive scalp dissection and multiple osteotomies, resulting in hemorrhage and need for transfusion.2–4Although coagulopathy related to CCVR has been attributed to dilutional anemia, there is emerging evidence for alternative mechanisms for disrupted hemostasis in highly invasive surgical procedures.5–9 This type of “trauma-induced coagulopathy” (TIC) has been distinguished from simple hemodilution and hypothermia.6,10–13 Additional contributing factors for coagulopathy in acute injury states include activation of protein C, endothelial injury, platelet dysfunction, complement activation, and altered fibrinolysis.6,10,12,13
CCVR is considered to be a type of controlled trauma.14 As such, exploring the mechanisms of TIC in this population is key to improving outcomes. Control of hyperfibrinolysis through use of antifibrinolytics has been shown to improve bleeding outcomes.15–17 Other mechanisms of TIC are being explored, but are not fully elucidated.18–21 One limitation to such analysis is the inadequacy of standard clinical coagulation testing to provide a picture of global hemostasis.19,21,22 Conventional pro-coagulant based assays prothrombin time (PT) and partial thromboplastin time (PTT) provide limited information about procoagulant protein function, but fail to capture other factors affecting hemostasis, including fibrinolysis, inflammation, and changes in platelet function.8,19,23 However, the PT and PTT assays are relatively inexpensive, widely available, and provide rapid feedback. Currently, most clinical teams must rely on these assays to assess hemostatic function in CCVR patients and to decide on clinical interventions.