Coagulopathy prediction in traumatic brain injury

Traumatic brain injury (TBI) represents a significant public health concern. Besides the initial primary injury, a defining point of TBI is causing secondary, delayed damage through inflammatory biochemical processes. Among the complications arising from this inflammatory response, coagulopathy emerges as a critical concern. With an overall prevalence of 32.7 %, TBI-induced coagulopathy significantly contributes to increased mortality rates and unfavorable patient outcomes, through its clinical manifestations, such as progressive hemorrhagic injury (PHI). This chapter investigates biomarkers capable of accurately detecting coagulopathy and PHI in TBI, evaluating their potential utility based on statistical evidence from various studies and exploring their possible association in the biochemical processes guiding or following TBI-induced coagulopathy. Notably, glucose emerges as a standout candidate, exhibiting a sensitivity of 91.5 % and specificity of 87.5 % for predicting coagulopathy. Furthermore, interleukin-33, with a sensitivity of 93.3 % and specificity of 66.7 %, and galectin-3, with a sensitivity of 67.7 % and specificity of 85.5 %, are promising for PHI. Despite these encouraging findings, significant efforts remain necessary to translate biomarker diagnostic utility into clinical practice effectively. Further research and validation studies are imperative to elucidate the intricate biochemical processes underlying TBI-induced coagulopathy and to refine the clinical application of biomarkers for improved patient management and outcomes in real-world settings.