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.