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Review
. 2018 May 3;131(18):2001-2006.
doi: 10.1182/blood-2017-11-784108. Epub 2018 Mar 5.

Coagulopathy induced by traumatic brain injury: systemic manifestation of a localized injury

Affiliations
Review

Coagulopathy induced by traumatic brain injury: systemic manifestation of a localized injury

Jianning Zhang et al. Blood. .

Abstract

Traumatic brain injury (TBI)-induced coagulopathy is a common and well-recognized risk for poor clinical outcomes, but its pathogenesis remains poorly understood, and treatment options are limited and ineffective. We discuss the recent progress and knowledge gaps in understanding this lethal complication of TBI. We focus on (1) the disruption of the brain-blood barrier to disseminate brain injury systemically by releasing brain-derived molecules into the circulation and (2) TBI-induced hypercoagulable and hyperfibrinolytic states that result in persistent and delayed intracranial hemorrhage and systemic bleeding.

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Conflict of interest statement

Conflict-of-interest disclosure: The authors declare no competing financial interests.

Figures

Figure 1.
Figure 1.
CT images of 2 TBI patients. The first patient suffered from subdural hematoma after a step fall (A) and developed diffused cerebral bleeding immediately after decompressive craniectomy (B). The second patient suffered from progressive subdural hematoma after a car accident (C-D) and developed delayed subdural and intracerebral hematomas after decompressive cranioctomy (E-F).
Figure 2.
Figure 2.
Schematic pathways for consumptive coagulopathy induced by TBI. (A) Hemostasis is triggered by platelet adhesion and aggregation at the site of vascular injury and stabilized by crosslinked fibrin polymers to form a hemostatic plug. (B) The tissue factor and anionic phospholipid-rich microvesicles (BDMVs and exMTs) from injured brain cells are released into the circulation to provide microplatforms for tenase assembly. Thrombin thus produced (1) cleaves fibrinogen to generate fibrin, (2) activates platelets, and (3) activates endothelial cells to generate platelet and endothelial cell MVs. The blood cell–derived MVs further amplify the coagulation initiated by BDMVs and exMTs. Endothelial cells activated by MVs, thrombin, and fibrin also induce the acute release of tPA, which initiates early fibrinolysis. All of these processes occur in the fluid phase of the blood, without the local vascular injury and blood-derived factors found in trauma patients with hemorrhagic shock. EC, endothelial cells; FVa, activated factor V; FVII, coagulation factor VII; FXa, activated factor X; PS, phosphatidylserine; TF, tissue factor.

References

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