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Neurology India
Medknow Publications on behalf of the Neurological Society of India
ISSN: 0028-3886 EISSN: 1998-4022
Vol. 54, Num. 4, 2006, pp. 347-347

Neurology India, Vol. 54, No. 4, October-December, 2006, pp. 347

Invited Commentaries

The coagulation system: A vulnerable system and a potential therapeutic aimpoint in treatment of traumatic brain injury

Department of Anaesthesia and Intensive Care, Lund University Hospital, Lund
Correspondence Address:Department of Anaesthesia and Intensive Care, Lund University Hospital, Lund

Code Number: ni06119

The authors of the paper "Fibrinolytic markers and neurologic outcome in traumatic brain injury" in this issue of Neurology India have studied an aspect of traumatic brain injury (TBI) that is gaining an increasing amount of interest.[1] They have found that activation and impairment of the coagulation system occur very early after TBI. It is previously known that impairment occurs, but it has never been systematically studied this early before. They have also found that admission Glasgow Coma scale levels and mortality correlate to such an early impairment.

These results support several other findings in the literature of correlations between activation and impairment of the coagulation and impaired outcome. One interesting aspect of this that may offer a therapeutic option is that impairment of the coagulation has been linked to growth of posttraumatic intracerebral contusions after admission[2],[3] Growth of intracerebral contusions has in turn been linked to an impaired outcome.[4] Combining these observations it lies close to hand to hypothesize that inhibiting the growth of contusions could potentially lead to improved outcome. One way to inhibit such growth could potentially, as suggested by the authors of the article and by others, be to use prohemostatic agents in the treatment of TBI patients.

At the same time it is important to be aware that inside contusions the microcirculation is impaired and that microthrombi are formed. Causing an overwhelming procoagulant situation may be associated with a risk of creating an increased amount of microthrombi, thereby jeopardizing the microcirculation. Deleterious effects of an impaired microcirculation have, however, not been shown to be associated with an impaired outcome, while growth of contusions has been associated with impaired outcome.

In the light of these informations it may seem appropriate to initiate studies of prohemostatic or antifibrinolytic agents in the treatment of TBI. The choice of agent may be difficult, but some guidance may potentially be found in recent studies of prohemostatic and antifibrinolytic agents in treatment of other kinds of intracranial hemorrhage. One study has found that administration of tranexamic acid to patients suffering from subarachnoid hemorrhage until the aneurysm has been secured decreases the rate of rebleeding.[5] Another recent study has found that administration of recombinant factor VIIa (rFVIIa) to patients with spontaneous intracerebral hemorrhage decreases the growth of the hemorrhage and improves outcome.[6] These studies may provide some guidance also in the search for better treatment for TBI patients. An early phase II study of rFVIIa administered to TBI patients with signs of hemorrhagic contusions on an early CT scan, most likely the first study of this kind, has recently recruited its last patient and we are awaiting the report from this study with great interest.


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 SC, Young GS, Talucci RC, Greenbaum BH, Ross SE. Delayed brain injury after head trauma: Significance of coagulopathy. Neurosurgery 1992;30:160-5.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.Engstrom M, Romner B, Schalen W, Reinstrup P. Thrombocytopenia predicts progressive hemorrhage after head trauma. J Neurotrauma 2005;22:291-6.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Stein SC, Spettell C, Young G, Ross SE. Delayed and progressive brain injury in closed-head trauma: Radiological demonstration. Neurosurgery 1993;32:25-31.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Hillman J, Fridriksson S, Nilsson O, Yu Z, Saveland H, Jakobsson KE. Immediate administration of tranexamic acid and reduced incidence of early rebleeding after aneurysmal subarachnoid hemorrhage: A prospective randomized study. J Neurosurg 2002;97:771-8.  Back to cited text no. 5  [PUBMED]  
6.Mayer SA, Brun NC, Begtrup K, Broderick J, Davis S, Diringer MN, et al . Recombinant activated factor VII for acute intracerebral hemorrhage. N Engl J Med 2005;352:777-85.  Back to cited text no. 6    

Copyright 2006 - Neurology India

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