Department of Neurological Surgery, University of California, San Francisco, California 94110, USA.
Neurosurgery. 2012 Jun;70(6):1334-45. doi: 10.1227/NEU.0b013e31824d179b.
Traumatic brain injury has long been associated with abnormal coagulation parameters, but the exact mechanisms underlying this phenomenon are poorly understood. Coagulopathy after traumatic brain injury includes hypercoagulable and hypocoagulable states that can lead to secondary injury by either the induction of microthrombosis or the progression of hemorrhagic brain lesions. Multiple hypotheses have been proposed to explain this phenomenon, including the release of tissue factor, disseminated intravascular coagulation, hyperfibrinolysis, hypoperfusion with protein C activation, and platelet dysfunction. The diagnosis and management of these complex patients are difficult given the lack of understanding of the underlying mechanisms. The goal of this review is to summarize the current knowledge regarding the mechanisms of coagulopathy after blunt traumatic brain injury. The current and emerging diagnostic tools, radiological findings, treatment options, and prognosis are discussed.
创伤性脑损伤长期以来一直与异常凝血参数有关，但这种现象的确切机制尚不清楚。创伤性脑损伤后的凝血功能障碍包括高凝状态和低凝状态，这两种状态都可能通过诱导微血栓形成或进展性出血性脑损伤而导致继发性损伤。已经提出了多种假说来解释这一现象，包括组织因子释放、弥散性血管内凝血、纤维蛋白溶解亢进、蛋白 C 激活伴低灌注以及血小板功能障碍。由于对潜在机制缺乏了解，这些复杂患者的诊断和管理存在困难。本综述的目的是总结目前关于钝性创伤性脑损伤后凝血功能障碍机制的知识。讨论了目前和新兴的诊断工具、影像学发现、治疗选择和预后。
