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INVITED COMMENTARIES
Year : 2006  |  Volume : 54  |  Issue : 4  |  Page : 347-348

Association between intravascular coagulopathy and outcome after traumatic brain injury


Departments of Anesthesiology and Critical Care and Pharmacology, University of Pennsylvania, Philadelphia, PA l9l04, USA

Correspondence Address:
William M Armstead
Departments of Anesthesiology and Critical Care and Pharmacology, University of Pennsylvania, Philadelphia, PA l9l04
USA
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Source of Support: None, Conflict of Interest: None


PMID: 17114832

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How to cite this article:
Armstead WM. Association between intravascular coagulopathy and outcome after traumatic brain injury. Neurol India 2006;54:347-8

How to cite this URL:
Armstead WM. Association between intravascular coagulopathy and outcome after traumatic brain injury. Neurol India [serial online] 2006 [cited 2019 Jul 23];54:347-8. Available from: http://www.neurologyindia.com/text.asp?2006/54/4/347/28096


It is now well accepted that much of the cerebral damage arising from traumatic brain injury (TBI) actually occurs secondarily at some temporally distant timepoint post insult.[1] While many factors such as hypoxia, hypotension and others may contribute to delayed cerebral vasosopasm and ischemia, more recent observations point toward the prominent role for disseminated intravascular coagulation.[2],[3] Because of the strong association between inravascular microthrombosis and neuronal necrosis in human TBI, intravascular coagulopathy should be considered as a potential cause of ischemia post insult.[4] Multiple studies have found changes in coagulation parameters in the systemic circulation within 24 h after TBI.[5] Changes in systemic blood coagulation probably reflect the cerebral intravascular coagulation process and their study permits the monitoring of central nervous system events post TBI. The present study focuses on the relationship between early changes (within the first 3 h) of systemic hemostatic and fibrinolytic markers after human TBI and indicators of outcome such as the Glascow Coma scale. This is a novel and non appreciated aspect of this research area. These data suggest that prothrombin time, partial thromboplastin time, fibrin degradation products and D-dimer levels may be useful prognostic indicators in head trauma patients. Such observations may have important implications in patient management.

 
  References Top

1.Bayir A, Kalkan E, Koηak S, Ahmet Ak, Cander C, Bodur S. Fibrinolytic markers and neurologic outcome in traumatic brain injury Neurol India 2006;54:363-5.  Back to cited text no. 1    
2.Stein C, Chen XH, Sinson G, Smith DH. Intravascular coagulation: A major secondary insult in non fatal traumatic brain injury. J Neurosurg 2002;97:1373-7.  Back to cited text no. 2    
3.Vavilala MS, Dunbar PJ, Rivara FP, Lam AM. Coagulopathy predicts poor outcome following head injury in children less than 16 years of age. J Neurosurg Anesthesiol 2001;13:13-8.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Stein SC, Graham Di, Chen XH, Smith DH. Association between intravacular microthrombosis and cerebral ischemia in traumatic brain injury. Neurosurg 2004;54:687-91.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Engstrom M. Romner B, Schalen W. Reinstrup B. Thrombocytopenia predicts progressive hemorrhage after head trauma. J Neurotrauma 2005;22:291-6.  Back to cited text no. 5    




 

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