摘要
Traumatic brain injury （TBI）： Despite improved supportive and rehabilitative care of TBI patients, TBI remains a leading cause of death and disability worldwide. To date, no effective pharmacological treatments are available for TBI. The mechanisms underlying brain damage and repair following TBI are complex and not completely understood. Coagulopathy after TBI is frequent and an independent prognostic factor for unfavorable outcome and prognosis （Stein and Smith, 2004）. It may be amenable to treatment, and effective management of coagulopathy may protect from secondary injury and poor outcomes. Although the main challenge for TBI management is to address the risk of hypocoagulopathy with prolonged bleeding and progression of hemorrhagic lesions, the risk of hypercoagulopathy with an increased microthrombosis formation warrants investigation to reduce neurological deficits after TBI.
Traumatic brain injury （TBI）： Despite improved supportive and rehabilitative care of TBI patients, TBI remains a leading cause of death and disability worldwide. To date, no effective pharmacological treatments are available for TBI. The mechanisms underlying brain damage and repair following TBI are complex and not completely understood. Coagulopathy after TBI is frequent and an independent prognostic factor for unfavorable outcome and prognosis （Stein and Smith, 2004）. It may be amenable to treatment, and effective management of coagulopathy may protect from secondary injury and poor outcomes. Although the main challenge for TBI management is to address the risk of hypocoagulopathy with prolonged bleeding and progression of hemorrhagic lesions, the risk of hypercoagulopathy with an increased microthrombosis formation warrants investigation to reduce neurological deficits after TBI.
