Fletcher-Sandersjöö Alexander, Sebghati Jennifer, Thelin Eric Peter
Department of Clinical Neuroscience, Karolinska InstitutetBioclinicum J5:20, 171 64, Solna, Stockholm, Sweden.
Department of Neurosurgery, Karolinska University Hospital, Stockholm, Sweden.
Acta Neurochir (Wien). 2025 May 19;167(1):146. doi: 10.1007/s00701-025-06549-w.
Coagulopathy following traumatic brain injury (TBI) is increasingly being recognized as a determinant of hematoma expansion and outcome. Unlike systemic trauma, where coagulopathy is often driven by hemorrhagic shock, TBI appears to induce a unique brain-derived hemostatic response. In this review, we discuss the mechanisms underlying TBI-induced coagulopathy, its diagnostic challenges, and association with hematoma expansion. We further evaluate evidence from randomized trials targeting coagulopathy in TBI, including interventions such as tranexamic acid, plasma, recombinant Factor VIIa, and fibrinogen. While several studies show proof of concept, clinical benefit remains inconsistent, likely due to issues of timing, heterogeneity, and underpowered study design. Moving forward, ultra-early and individualized approaches guided by real-time hemostatic monitoring may offer the most promising path. A better understanding of the temporal and mechanistic dynamics of coagulopathy will be essential for improving treatment strategies and patient outcomes.
创伤性脑损伤（TBI）后的凝血病越来越被认为是血肿扩大和预后的一个决定因素。与系统性创伤不同，系统性创伤中的凝血病通常由失血性休克驱动，而TBI似乎会引发一种独特的脑源性止血反应。在这篇综述中，我们讨论了TBI诱导凝血病的潜在机制、其诊断挑战以及与血肿扩大的关联。我们进一步评估了针对TBI凝血病的随机试验证据，包括诸如氨甲环酸、血浆、重组凝血因子VIIa和纤维蛋白原等干预措施。虽然多项研究显示了概念验证，但临床益处仍然不一致，这可能是由于时机、异质性和研究设计力度不足等问题。展望未来，由实时止血监测指导的超早期和个体化方法可能提供最有前景的途径。更好地理解凝血病的时间和机制动态对于改善治疗策略和患者预后至关重要。
