Coagulopathy after traumatic brain injury: incidence, pathogenesis, and treatment options
Coagulopathy after traumatic brain injury: incidence, pathogenesis, and treatment options
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DOI：
10.1111/trf.12033
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发表时间：
2013-01-01
期刊：
影响因子：
2.9
通讯作者：
Maegele, Marc
中科院分区：
文献类型：
--
作者：
Maegele, Marc
创伤性脑损伤（TBI）后的凝血功能障碍是常见的，并且是与结果和预后相关的强有力的预测因素。创伤性脑损伤的凝血功能障碍的复杂病理生理机制是多因素的，仍然不明确。凝血异常的性质在严重TBI和伴有躯体损伤的非TBI之间是不同的。目前关于TBI后凝血障碍发展的假设包括低凝和高凝状态的组合，这两种状态由损伤的大小和程度促进，导致通过随后的缺血性和出血性损伤引起不同程度的继发性损伤。提出的潜在机制可能包括组织因子（TF）的释放、纤维蛋白溶解亢进、休克和灌注不足，从而触发蛋白C通路、弥散性血管内凝血和血小板功能障碍。创伤性脑损伤后的血液凝固障碍可能是可以治疗的，充分和及时的管理可以防止继发性损伤和不良结局。功能测定，如粘弹性测试可以支持早期检测，诊断和指导治疗。本文就脑外伤后凝血功能障碍的发生率、发病机制、诊断和治疗等方面进行综述。
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.