Department of Trauma and Orthopedic Surgery, Institute for Research in Operative Medicine (IFOM), University of Witten/Herdecke, Cologne-Merheim Medical Center, Cologne, Germany.
Transfusion. 2013 Jan;53 Suppl 1:28S-37S. doi: 10.1111/trf.12033.
Coagulopathy after traumatic brain injury (TBI) is frequent and represents a powerful predictor related to outcome and prognosis. The complex pathophysiological mechanisms of the coagulopathy of TBI are multifactorial and remain still undefined. The nature of the coagulation abnormalities differs between severe TBI and non-TBI with somatic injuries. The current hypothesis for the development of coagulopathy after TBI includes combinations of both hypo- and hypercoagulable states promoted by the magnitude and the extent of the injury resulting in a variable degree of secondary injury via subsequent ischemic and hemorrhagic lesioning. The proposed underlying mechanisms may comprise the release of tissue factor (TF), hyperfibrinolysis, shock, and hypoperfusion thus triggering the protein C pathway, disseminated intravascular coagulation, and platelet dysfunction. Hemocoagulative disorders after TBI may be amenable to treatment, and adequate and timely management may protect from secondary injury and poor outcomes. Functional assays such as viscoelastic tests may be supportive in early detection, diagnosis, and guidance of treatment. This review summarizes the current understanding with regard to frequency, pathogenesis, diagnosis, and treatment of the coagulopathy after TBI.
创伤性脑损伤（TBI）后的凝血功能障碍很常见，是与结局和预后相关的强有力预测因素。TBI 凝血功能障碍的复杂病理生理机制是多因素的，目前仍未完全明确。严重 TBI 和伴有躯体损伤的非 TBI 之间的凝血异常性质不同。目前认为 TBI 后凝血功能障碍的发生包括由损伤的程度和范围引起的低凝和高凝状态的组合，导致通过随后的缺血和出血性损伤产生不同程度的继发性损伤。潜在的发病机制可能包括组织因子（TF）释放、纤维蛋白溶解亢进、休克和低灌注，从而触发蛋白 C 途径、弥散性血管内凝血和血小板功能障碍。TBI 后的血液凝固障碍可能可以进行治疗，充分和及时的治疗可能有助于防止继发性损伤和不良结局。诸如粘弹性测试等功能检测可能有助于早期检测、诊断和治疗指导。本文总结了 TBI 后凝血功能障碍的频率、发病机制、诊断和治疗的最新认识。
