Traumatic Coagulopathy: The Effect of Brain Injury

Abstract

Traumatic 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.

Venous thromboembolism in the setting of pediatric traumatic brain injury

“…Long-bone fractures, direct endothelial disruption, release of tissue factors associated with neurotrauma, hypercoagulability from inflammation, and venous stasis from prolonged bed rest may be contributing factors in the increased risk of VTE in this TBI population. 7,9,10,16,17 Finally, nonaccidental trauma was found to be an independent risk factor for VTE in our study population. Patients with nonaccidental trauma in our sample were younger, with a median of 0 years of age (interquartile range [IQR] 0-1 years).…”

“…These findings are in keeping with other reports in the literature that have identified VTE risk factors. 5,6,9,17,20,22,26,27 In particular, Vu et al 27 performed a cross-sectional study using the 1997, 2000, and 2003 KID to determine the risk factors for VTE in the hospitalized pediatric population. They found older age, thoracoabdominal and orthopedic surgery, obesity, malignancy, inflammatory bowel disease, and longer hospitalization to be independent risk factors for VTE.…”

Hypocoagulability in Traumatic Brain Injury as Measured by Traditional Means and Thrombelastography

“…A variety of mechanisms have been hypothesized including alterations in the release of tissue factor, platelet dysfunction, consumptive coagulopathy, and the activation of protein C pathways secondary to hypoperfusion [12,[23][24][25][26][27][28][29][30][31].…”

Coagulation disorder in moderate to severe traumatic brain injuries

“…Pondaag 3 defi ned coagulopathy as a fi brinogen level below 130 mg/dl and FDP values greater than 40 gm/ml. Halpern 6 defi ned coagulopathy in his study as PT above normal range of 10.3-13.4 seconds. Lozance, 4 Selladurai 8 and Olson 9 defi ned coagulopathy as a DIC score below 6.…”

“…1 Many studies have suggested possible adverse effects of disseminated intravascular coagulation and other coagulopathies on outcome of the patients. [2][3][4][5][6][7] Post-traumatic coagulopathy, in particular, appears to be linked to secondary cerebral injury. 5,8 Although the extent of this process is yet to be elucidated fully, coagulation abnormalities are evident soon after trauma.…”