• Casey H Halpern, Patrick M Reilly, Alan R Turtz, and Sherman C Stein.
• Department of Neurosurgery, Hospital of the University of Pennsylvania, 3400 Spruce Street, Third Floor, Silverstein Pavilion, Philadelphia, PA 19104, USA. casey.halpern@uphs.upenn.edu
• J. Neurotrauma. 2008 Aug 1;25(8):997-1001.

AbstractTraumatic coagulopathy has several possible mechanisms. In traumatic brain injury (TBI), the principal process involves the release of tissue factor (TF). There is no agreement how common this mechanism is following general trauma. Furthermore, when TF-induced coagulopathy occurs, it is unknown whether the source of TF (TBI or extracranial trauma) influences the course of coagulopathy. We undertook this investigation to address both questions. The temporal course of prothrombin times (PTs) were recorded in a group (n = 441) with isolated TBI (head Abbreviated Injury Scale [AIS] >or= 3, non-head AIS < 3) and a group (n = 101) with extracranial trauma (non-TBI; non-head AIS >or= 3; head AIS < 3). Data were arranged according to preset time intervals after injury. The PT values in both groups were elevated and not significantly different for the first 12 h after trauma. Values then fell to normal in TBI patients, but remained elevated in non-TBI injury. Traumatic coagulopathy can be explained at least in part by TF release into the general circulation with activation of the coagulation cascade in both TBI and non-TBI. We hypothesize that the different time courses of coagulopathy represented by PT values in these populations were due to reconstitution of the blood-brain barrier, although further investigation is warranted. Peripheral hematologic studies may not reflect persistent coagulopathy in cerebral circulation.

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