Atormac
Neurology India
menu-bar5 Open access journal indexed with Index Medicus
  Users online: 3307  
 Home | Login 
About Editorial board Articlesmenu-bullet NSI Publicationsmenu-bullet Search Instructions Online Submission Subscribe Videos Etcetera Contact
  Navigate Here 
 Search
 
  » Next article
  » Previous article 
  » Table of Contents
  
 Resource Links
  »  Similar in PUBMED
 »  Search Pubmed for
 »  Search in Google Scholar for
 »Related articles
  »  Article in PDF (121 KB)
  »  Citation Manager
  »  Access Statistics
  »  Reader Comments
  »  Email Alert *
  »  Add to My List *
* Registration required (free)  

 
  In this Article
 »  Abstract
 »  Materials and Me...
 »  Results
 »  Discussion
 »  References
 »  Article Figures
 »  Article Tables

 Article Access Statistics
    Viewed9017    
    Printed213    
    Emailed1    
    PDF Downloaded225    
    Comments [Add]    
    Cited by others 46    

Recommend this journal

 


 
ORIGINAL ARTICLE
Year : 2005  |  Volume : 53  |  Issue : 2  |  Page : 178-182

Change in tissue thromboplastin content of brain following trauma


1 Departments of Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh, India
2 Departments of Haematology, Postgraduate Institute of Medical Education and Research, Chandigarh, India
3 Departments of Forensic Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Date of Acceptance30-Mar-2005

Correspondence Address:
Ashis Pathak
Dept. of Neurosurgery, Postgraduate Institute of Medical, Education and Research, Chandigarh - 160 012
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.16404

Rights and Permissions

 » Abstract 

Background: Tissue thromboplastin (TTP) is an integral membrane protein contributing to coagulopathy after trauma of brain, which is a rich source of TTP. Aims: A study was undertaken to establish the TTP content of various areas of normal brain and estimate the changes in TTP activity of brain in response to varying degrees of trauma. Materials and Methods: Samples from different areas of brain of ten cadavers were used as controls and they were compared with contused brain tissue obtained after surgery in 25 head injury (HI) patients of varying severity. Results: In the study group, the TTP activity of the frontal, parietal, and temporal lobes after HI was significantly raised in contrast to that of the control group. The TTP activity was also significantly higher in the severe HI patients than those having moderate HI. The mode of injury and the time lapse after HI had no significant bearing on the TTP activity. Subjects above 40 years of age demonstrated a higher mean TTP activity after HI, though it was not statistically significant. Conclusion: The study provides quantitative data on TTP activity of normal brain and highlights the role of TTP in coagulopathy following HI through its increased activity after HI, more so in the severe HI group.


Keywords: Head injury, tissue thromboplastin, tissue factor


How to cite this article:
Pathak A, Dutta S, Marwaha N, Singh D, Varma N, Mathuriya S N. Change in tissue thromboplastin content of brain following trauma. Neurol India 2005;53:178-82

How to cite this URL:
Pathak A, Dutta S, Marwaha N, Singh D, Varma N, Mathuriya S N. Change in tissue thromboplastin content of brain following trauma. Neurol India [serial online] 2005 [cited 2019 Aug 23];53:178-82. Available from: http://www.neurologyindia.com/text.asp?2005/53/2/178/16404


Tissue thromboplastin (TTP), also called tissue factor (TF), plays a pivotal role in the coagulation cascade. It is considered as the physiological initiator of coagulation when it comes in contact with the blood at the site of an injury. Tissue thromboplastin catalyses the conversion of prothrombin to thrombin in the presence of Ca2+ in the initiation of blood coagulation.

Tissue thromboplastin activity is found in extracts of almost all tissues of the body, human brain being a rich source. The comparison of activities of TTP from 34 different areas of brain by Bjorkud et al . demonstrated a characteristic distribution pattern and a wide range of activities.[1] However, there is paucity in the literature on studies that give a quantitative measurement of TTP activity of other organs in their normal or pathological state.

Head injury (HI) is a common surgical emergency encountered in this fast-paced modern life. Coagulation disorders including disseminated intravascular coagulation (DIC) are well-known complications of HI recognized for decades.[2],[3],[4] Delayed brain changes following HI-like cerebral contusion or haematoma seem to appear as fresh progressive lesions in computerized tomography (CT) scans done at different intervals,[5] and sometimes patients of HI develop unexplained postoperative haematoma.

As several factors may be operating in the pathophysiology of post-HI-coagulation disorders including DIC, delayed cerebral contusion or postoperative cerebral haematoma, it stands to logic that this phenomenon might have something to do with the tissue thromboplastic content released as a result of trauma to the brain tissue, which is a known rich source of TTP. Though the TTP content of the brain has been estimated in normal individuals in one study till date,[1] the literature is lacking in data on alteration of the TTP content of various areas of the brain in response to trauma.

The present study was aimed to: (1) establish the TTP content of various areas of normal brain, (2) estimate the changes in TTP content of various areas of brain in response to trauma, (3) establish any correlation of TTP levels in the brain vis-à-vis severity of HI.


 » Materials and Methods Top


The present study was conducted over a 2-year time frame with the approval of the Institute Research Committee, who looked into the ethical considerations of the study before giving the approval.

Control group

The control group comprised ten cadavers of patients who died of conditions not affecting normal coagulation. The brain tissues were harvested within 6 h of death during medicolegal postmortem examination in the Department of forensic medicine. Tissue samples from different areas of brain were collected with the valid consent of legal heirs of the deceased. Brain tissue samples were collected from the following areas: (a) gray and white matter of all lobes, (b) thalamus, (c) optic nerve and tract, (d) pons, (e) medulla oblongata, (f) cerebellum, and (g) mid brain.

Study group (head-injury patients)

Twenty-five patients with HI admitted under the neurosurgical services of the Institute were included in the study. All the cases underwent surgery after admission once they were found to have a normal screening coagulation profile.

There were 22 male and 3 female patients of which 19 (76%) patients sustained HI in roadside accidents, and 6 (24%) patients had a history of fall from height. Age ranged between 14 and 70 years (mean 42.96 ± 18.84), with 15 patients below 50 years of age, 5 in the fifth decade, and the remaining 5 above 60 years of age.

Location of contusion of the brains was classified according to the predominant lobe involved. Patients were divided into three groups according to the severity of injury using the Glasgow Coma Scale (GCS): Minor HI (Group A: GCS 13-15), moderate HI (Group B: GCS 9-12), and severe HI (Group C: CGS 3-8). Accordingly, 2 (8%) patients fell in Group A, 11 (44%) in Group B, and 12 (48%) in Group C at the time of admission. All patients underwent detailed neurological examination. The level of consciousness varied from patient to patient. Twelve patients were put on assisted ventilation before or after admission.

CT scan findings

A CT scan revealed cerebral contusion involving one or more than one lobe in all the patients. Four patients had associated skull fracture, two had associated SDH, one had SAH and intraventricular hemorrhage and the remaining one had associated EDH. Eleven (44%) patients had predominantly frontal lobe contusion followed by temporal lobe contusion in six (24%) and parietal lobe contusion in eight (32%). No patient had contusion of the occipital lobe.

Nineteen (76%) patients were operated on within 8-24 h of admission. The rest were operated on late due to delay in admission or late deterioration. All patients underwent craniotomy and evacuation of contused brain tissue, which was collected for estimation of TTP activity after washing with saline to remove blood clots.

Collection and processing of brain tissue

Contused brain tissue samples from patients and normal brain tissue samples from the control group were collected in sterile saline immediately after resection in the operation theatre or autopsy room as per the case. The specimens were delivered to the laboratory within 15 min of collection. If that was not feasible, the collected specimen was preserved in autoclaved normal saline in a refrigerator at 4°C. Each tissue was washed several times with normal saline to remove blood and other tissue fluids, minced, and then homogenized in a tissue homogenizer using a tight pestle. The homogenate was centrifuged at 8000 g for 30 min and nonhomogenized tissue debris was discarded. The protein content of the supernatant was estimated by Lowry's method[6] and the sample was stored at -20°C until further analysis.

The tissue homogenate (TH) was thawed immediately before use and diluted in normal saline to a final protein concentration of 1 mg/ml-1 before use in coagulation studies.[7]

Assay of brain TTP activity

Plasma recalcification time was noted after addition of 0.1 ml of TH to 0.1 ml of normal pooled plasma. This was compared with a standard TTP calibration curve. Standard graph was plotted using commercially available recombinant human thromboplastin. The clotting time obtained with 1 mg/ml protein concentration of recombinant human thromboplastin was taken to represent 100% TTP activity. Contused brain TTP was thus expressed as percentage activity of recombinant human TTP.

The TTP activity of different areas of normal brain was tabulated and the mean TTP value of individual areas of normal brain was established. The TTP activity of contused or traumatized brain tissue collected from patients of HI was estimated and compared with the corresponding mean value of control subjects. The results were analyzed subsequently after tabulation using unpaired t -test.

As ours is a tertiary referral center, all the patients were discharged for convalescence and further management to the local hospital. However, due to various logistic problems a satisfactory data on the follow up of these patients could not be obtained.


 » Results Top


Control group

The TTP activity of different areas of the brain was estimated in ten cadavers as control, which is depicted in [Table - 1]. The TTP activity from different areas of the brains of ten cadavers was studied as per inclusion criteria for control group and TTP activity was estimated as per description in the methodology. The overall mean TTP activity of control group was 75.084% ± 29.6 (range 25-146%). The control samples were divided into two groups - lobar and nonlobar samples. The lobar samples consisted of brain tissue from frontal, temporal, parietal, and occipital lobes. The nonlobar group consisted of optic nerve, medulla oblongata, pons, mid brain, thalamus, and cerebellum. In the lobar control group, mean TTP activity was 83.85% ± 31.29 (range 27-146%) while in nonlobar group, it was 70.63 ± 27.76 (range 25%-136%). In the nonlobar group, the highest mean TTP activity was seen in pons (136%) and lowest activity in mid brain (25%). Comparing the lobar control samples and nonlobar control samples, the unpaired ' t ' test was found to be statistically significant ( t = 2.216; P =0.029).

TTP activity of study group

The TTP activity from brain tissue of 25 HI patients was estimated. The mean value of TTP activity of the study group was 164.76% ± 72.78 (range 82-350%). The frontal lobe was the most common site (44%) for lobar contusion. This was followed by temporal (32%) and parietal lobes (24%), respectively. No patient had occipital lobe contusion. In 8 (32%) patients, the TTP activity was above 200%, while in 14 (56%) patients, TTP activity ranged between 100 and 200%. The remaining three (12%) patients had TTP activity below 100% but greater than 50%. The mean TTP activity as per different lobes affected in the study group is depicted in [Table - 2], with parietal lobe showing the highest activity.

Comparison of the TTP activity of corresponding lobes of both control and study groups show that the overall TTP activity in the study group is significantly raised in comparison to the control group ( t = 5.3; P £ 0.001).

Twelve of twenty-five cases that belonged to the severe HI group had TTP activity that ranged between 110 and 350% (mean value of 204.1 ± 78.83). Eleven patients with moderate HI had TTP activity ranging between 94 and 240% (mean 136% ± 43.56). Two patients suffered mild HI [Figure - 1]. The comparison between moderate and severe HI groups established a statistically significant difference in TTP activity ( t = 2.53; P = 0.019). The mean TTP activity of the severe HI group was higher than the mild HI group but it failed to reach a statistical significance.

Tissue thromboplastin activity of different lobes of normal brain was compared with corresponding lobes with contused brain tissue. The mean TTP activity of contused brain from three lobes (frontal, temporal, and parietal) was higher than that of normal brain. This difference was statistically significant for all the lobes (frontal lobe t = 3.02, P = 0.007; parietal lobe t = 3.73, P = 0.002, temporal lobe t = 2.26, P = 0.038).

Tissue thromboplastin activity versus mode of injury was correlated between two groups where HI was sustained by (i) fall from height (six patients) and (ii) roadside accident (19 patients). The mean TTP activity of the former group was 156.67 ± 79.63 (range 82-300%) and the latter was 167.32 ± 72.61 (range 92-350%). The difference was not statistically significant ( t = 0.3; P = 0.76).

Tissue thromboplastin activity was correlated with the interval between the time of injury and surgery. The patients were divided between two groups where surgery was performed (1) within 8-24 h and (2) those operated after 24 h. The mean TTP activity of patients operated after 24 h was 162.17 ± 54.12 and of those operated within 8-24 h 165.58 ± 79.03; the correlation was not statistically significant ( t = 0.098; P = 0.92).

On correlation of the TTP activity of contused brain tissue with the age of patients, it was found that patients above 40 years of age showed a higher mean TTP activity (mean 182 ± 63.4; range 110-300%) than those below 40 years of age (mean 142.82 ± 80.87; range 82-350%). The correlation, however, failed to reach a statistical significance ( t = 1.36; P = 0.18).


 » Discussion Top


Since the description of the cascade system of coagulation for the first time in 1964, it has long been recognized that with an injured subendothelium the surface of adherent platelets plays an essential role in initiating and supporting coagulation reactions. Early observation on blood clotting established the potent ability of certain tissue extracts, notably from brain and lung, to initiate fibrin formation. These tissue extracts (thromboplastins) were found to contain two ingredients responsible for this activity - a phospholipid component and a protein component. This led to the discovery of tissue factor (TF), an integral membrane protein expressed by cells in most extra-vascular tissues. Tissue factor is not present in the plasma but is supplied by exogenous tissue. It is known that TF is not always extrinsic to the circulatory system but is expressed on the surface of vascular endothelial cells and leucocytes under certain pathological conditions, whereby it is thought to contribute to associated coagulopathy.[8]

Comparison of the TTP activity of different areas of normal brain demonstrated a wide range of variations.[1] It was also noted that the distinct distribution pattern was unrelated to tissue vascularization and white and gray matter had similar activities. The highest activity was observed in olfactory bulb and tract. Regions associated with the limbic system, second cranial nerve and primary visual structures and lower part of the brain stem also have a very high-procoagulant activity. High TTP activity seemed to occur in phylogenetically older parts of the brain.

The first case with definite evidence of DIC associated with a massive HI was reported by Keimowitz and Annis in 1973.[9] Vander Sande et al[10] described the relationship of CT and coagulation abnormalities to clinical features in 55 patients with blunt HI. They concluded that (a) FDP concentration reflected the amount of brain tissue damage rather than its location, (b) in the absence of other causes of DIC, coagulation studies may be more sensitive than CT scanning in demonstrating brain contusion. It was interpreted that the finding of high FDP with a combination of hemorrhagic lesion in the brain and mass effect was a confirmation of hypothesized infusion of TTP into the circulation consequent to head trauma.

Scherer et al[11] tried to determine the degree of regional and systemic coagulation activation soon after isolated severe HI. They studied 24 trauma victims, of which 20 patients had isolated severe HI (GCS £ 8) and four patients with isolated bone fractures. It was concluded that within 6 h after severe isolated HI, systemic procoagulant overflow from the traumatized cerebral microvasculature proceeds to thrombin level and is then inhibited by antithrombin III. Regional and systemic hypercoagulability and increased D-dimer concentrations appear to be common among HI patients. Increased procoagulant and consecutive fibrinolytic turnover may, therefore, spark DIC in this patient group.

Various earlier studies established coagulation abnormalities in HI[2],[3],[4] leading to DIC also.[9],[12],[13],[14] All these studies highlighted the role of TTP in the genesis of coagulation abnormalities in HI. The present study is a step ahead to establish the above postulate and prove the role of TTP in the causation of coagulation disorders after HI. There is a statistically significant correlation of TTP activity between moderate and severe HI. Hirashima et al . tried to determine whether TF might be a marker of brain injury caused by SAH and cerebral vasospasm.[15] Using a sensitive enzyme immunoassay, the authors measured the TF in CSF of patients with SAH. As the concentration of TF in CSF was increased fivefold in comparison to plasma after the onset of SAH, it was believed that TF was released from the brain with its concentration paralleling the degree of tissue injury. Hence, the release of TF after brain injury may initiate coagulation disorders. Drawing a parallel example in HI, which is very frequently associated with SAH, evidence from present study establishes the role of TTP activity as a marker of HI. The high level of TTP activity correlated with the severity of HI. The mechanism of release of TTP after HI is yet to be established. Postulated mechanisms suggest that there may be increased synthesis or there is an enhanced release of TTP following trauma or surface expression of TTP activity already present in the contused brain tissue. However, further research needs to be done in this direction.

Robert et al . described the development of a mutant of human TF as a specific antagonist of the extrinsic pathway of blood coagulation and tested this mutant in a rabbit model of arterial thrombosis.[16]

Creasey et al . (1993) showed the role of tissue factor pathway inhibitor (TFPI) in reducing mortality from  Escherichia More Details coli and septic shock.[17] This fact leads to the assumption of the role of an analogue of TFPI in the management of moderate to severe HI patients, who are at a greater risk of coagulation disorder or DIC.

The present study not only attempts to establish a quantitative data on basal TTP activity in different areas of normal brain tissue but also establishes the role of TTP in the promotion of coagulation disorders in HI patients, with its potential to act as a prognostic indicator. On the whole, the study highlighted the role of TTP activity in severe HI, as there is significant difference in TTP activity of this group from the moderate HI patients.

The patients of HI were taken up for surgery after they had a normal screening coagulation profile but postoperative screening coagulation tests were not included in the data as these were bound to have secondary alterations by the insult of surgery on the brain and blood transfusion, which was required in some cases. However, there remains a scope for future study using more sensitive and specific activation markers of coagulation to establish any correlation between coagulation changes and TTP activity of the brain tissue.

The present study is the first of its kind in which the TTP activity of brain parenchyma after HI has been quantified, as earlier studies have used only the hematological changes subsequent to head trauma as a parameter to prognosticate HI.[18],[19],[20] This might have some implications in the management of HI in future. However, further studies are required on a larger number of patients to endorse the above findings. Patients with moderate to severe HI with evidence of coagulation disturbances may at a later date benefit from adjunctive therapy with mutant TF or with TFPI.



 
 » References Top

1.Bjorkud E, Storm-Mathisen J, Storm E, Prydz H. Localisation of tissue thromboplastin in human brain. Thromb Diath Hemorrha 1979;37:91-7.  Back to cited text no. 1    
2.Tikk A, Noormaa U. The significance of cerebral and systemic disseminated intravascular coagulation in early prognosis of brain injury. Acta Neurochir (Wien) 1978;28:96-7.  Back to cited text no. 2    
3.Clark JA, Finelle RE, Netsky MG. Disseminated intravascular coagulation following cranial trauma. J Neurosurg 1980;52:266-9.  Back to cited text no. 3    
4.Selladurai BM, Vickneswaran M, Duraisamy S, Atan M. Coagulopathy in acute head injury - a study of its role as a prognostic indicator. Br J Neurosurg 1997;11:398-404.  Back to cited text no. 4  [PUBMED]  
5.Stein SC, Young GS, Talucci RC, Green Baum BH, Ross Se. Delayed brain injury after head trauma: significance of coagulopathy. Neurosurg 1992;30:160-5.  Back to cited text no. 5    
6.Sidney PC, Colowich Nathan OK. Methods in Enzymology. New York: Academic Press Inc. Publishers; 1957. p. III 448.  Back to cited text no. 6    
7.Sarode R, Marwaha N, Gupta NM. Procoagulant activity of human tumors: Existence of Xa and thrombin like activities. Br J Cancer 1990;61:29-31.  Back to cited text no. 7  [PUBMED]  
8.Davic EW, Ratnoff OD. Waterfall sequence for Intrinsic blood clotting. Science 1964;145:1310.  Back to cited text no. 8    
9.Keimowitz RM, Annis BL. Disseminated intravascular coagulation associated with massive brain injury. J Neurosurg 1973;39:178-80.  Back to cited text no. 9  [PUBMED]  
10.Vander Sande JJ, Velkamp JJ, Bockhout Mussert RJ, Vielvaje GJ. Haemostasis and computerised tomography in head injury, their relationship to clinical features. J Neurosurg 1981;55:718-24.  Back to cited text no. 10    
11.Scherer RU, Spangubug P. Procoagulant activity in patients with isolated severe head trauma. Crit Care Med 1998;26:149-56.   Back to cited text no. 11    
12.Preston EE, Malia RG, Shown MJ, Timperley WR, Blackburn EK. Disseminated intravascular coagulation as a consequence of cerebral damage. J Neurol Neurosurg Psy 1974;37:241-8.  Back to cited text no. 12    
13.Vecht CJ, Sinilsilinga CT, MinderhondJM. Disseminated intravascular coagulation and head injury. J Neurol Neurosurgery Psy 1975;38:567-71.  Back to cited text no. 13    
14.Drayer BP, Poser CM. Disseminated intravascular coagulation and head trauma: Two cases studies. JAMA 1975;131:174-5.  Back to cited text no. 14    
15.Hirashima Y, Nakamura S, Suzuki M, Kurimoto M, Endo S, Ogawa A, et al . Cerebrospinal fluid tissue factor and thrombin-anti-thrombin III complex as indicators of tissue injury after subarachanoid haemorrhage. Stroke 1997;28:1660-70.  Back to cited text no. 15    
16.Robert FK, Cranio JR, Mark PO, Nishit M, Pal S, David L, et al . A soluble tissue factor mutant is a selective anticoagulant and antithrombic agent. Blood 1997;89:3219-27.  Back to cited text no. 16    
17.Creasey AA, Chang ACK, Feign L, Wiin TC, Taylor FB Jr. Hinshaw LB. Tissue factor pathway inhibitor reduces mortality from Escherichia coli septic shock J Clin Invest 1993;91:2850-60.  Back to cited text no. 17    
18.Ghosh S. Frequency and prognostic significance of disseminated intravascular coagulation and other coagulation disorders following acute cranio-cervical trauma. Unpublished dissertation work in collaboration with Departments of Neurosurgery and Haematology, PGIMER, Chandigarh, 1989.  Back to cited text no. 18    
19.Sharma MS. Emergency biochemical triage: Slide latex agglutination for fibrin degradation products (D-dimer) in acute craniocerebral trauma. Unpublished dissertation work in collaboration with Departments of Neurosurgery and Haematology, PGIMER, Chandigarh, 1989.  Back to cited text no. 19    
20.Kuo JR, Chou TJ, Chio CC. Coagulopathy as a parameter to predict the outcome in head injury patients - analysis of 61 cases. J Clin Neurosci 2004;11:710-4.  Back to cited text no. 20  [PUBMED]  [FULLTEXT]


Figures

[Figure - 1]

Tables

[Table - 1], [Table - 2]

This article has been cited by
1 Overpressure blast injury-induced oxidative stress and neuroinflammation response in rat frontal cortex and cerebellum
Hale Z. Toklu,Zhihui Yang,Sehkar Oktay,Yasemin Sakarya,Nataliya Kirichenko,Michael K. Matheny,Judy Muller-Delp,Kevin Strang,Philip J. Scarpace,Kevin K.W. Wang,Nihal Tümer
Behavioural Brain Research. 2018; 340: 14
[Pubmed] | [DOI]
2 Coagulopathy and haemorrhagic progression in traumatic brain injury: advances in mechanisms, diagnosis, and management
Marc Maegele,Herbert Schöchl,Tomas Menovsky,Hugues Maréchal,Niklas Marklund,Andras Buki,Simon Stanworth
The Lancet Neurology. 2017; 16(8): 630
[Pubmed] | [DOI]
3 Mortality in severely injured children: experiences of a German level 1 trauma center (2002 – 2011)
Carsten Schoeneberg,Marc Schilling,Judith Keitel,Manuel Burggraf,Bjoern Hussmann,Sven Lendemans
BMC Pediatrics. 2014; 14(1)
[Pubmed] | [DOI]
4 Mortality in severely injured elderly patients: a retrospective analysis of a German level 1 trauma center (2002–2011)
Carsten Schoeneberg,Thomas Probst,Marc Schilling,Alexander Wegner,Bjoern Hussmann,Sven Lendemans
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. 2014; 22(1)
[Pubmed] | [DOI]
5 Early Platelet Dysfunction in a Rodent Model of Blunt Traumatic Brain Injury Reflects the Acute Traumatic Coagulopathy Found in Humans
Deborah L. Donahue,Julia Beck,Braxton Fritz,Patrick Davis,Mayra J. Sandoval-Cooper,Scott G. Thomas,Robert A. Yount,Mark Walsh,Victoria A. Ploplis,Francis J. Castellino
Journal of Neurotrauma. 2014; 31(4): 404
[Pubmed] | [DOI]
6 Relationship Between Systemic Thrombogenic or Thrombolytic Indices and Acute Increase of Spontaneous Intracerebral Hemorrhage
Tack Geun Cho,Jong Chul Lee,Seung Won Park,Chan Chung,Taek Kyun Nam,Sung Nam Hwang
Journal of Cerebrovascular and Endovascular Neurosurgery. 2014; 16(3): 159
[Pubmed] | [DOI]
7 Coagulopathy after traumatic brain injury: incidence, pathogenesis, and treatment options
Marc Maegele
Transfusion. 2013; 53: 28S
[Pubmed] | [DOI]
8 Epidemiology, risk stratification and outcome of severe pediatric trauma [Epidemiologie, risikostratifizierung und behandlungsergebnisse nach schwerem kindlichen trauma]
Kipfmueller, F. and Wyen, H. and Borgman, M.A. and Spinella, P.C. and Wirth, S. and Maegele, M.
Klinische Padiatrie. 2013; 225(1): 34-40
[Pubmed]
9 Coagulopathy after pediatric traumatic brain injury: Association or causality?
Bruins, B.B. and Kilbaugh, T.J. and Friess, S.H.
Pediatric Critical Care Medicine. 2012; 13(4): 491-492
[Pubmed]
10 The 4G/4G genotype of the PAI-1 (Serpine-1) 4G/5G polymorphism is associated with decreased lung allograft utilization
Sapru, A. and Zaroff, J.G. and Pawlikowska, L. and Liu, K.D. and Khush, K.K. and Baxter-Lowe, L.A. and Hayden, V. and Menza, R.L. and Convery, M. and Lo, V. and Poon, A. and Kim, H. and Young, W.L. and Kukreja, J. and Matthay, M.A.
American Journal of Transplantation. 2012; 12(7): 1848-1854
[Pubmed]
11 Glasgow Coma Scale as a predictor for hemocoagulative disorders after blunt pediatric traumatic brain injury*
Peiniger, S. and Nienaber, U. and Lefering, R. and Braun, M. and Wafaisade, A. and Borgman, M.A. and Spinella, P.C. and Maegele, M.
Pediatric Critical Care Medicine. 2012; 13(4): 455-460
[Pubmed]
12 Coagulopathy after traumatic brain injury
Laroche, M. and Kutcher, M.E. and Huang, M.C. and Cohen, M.J. and Manley, G.T.
Neurosurgery. 2012; 70(6): 1334-1345
[Pubmed]
13 CRASH-2 (Clinical Randomisation of an Antifibrinolytic in Significant Haemorrhage) Intracranial Bleeding Study: The effect of tranexamic acid in traumatic brain injury - a nested, randomised, placebo-controlled trial
Perel, P. and Al-Shahi Salman, R. and Kawahara, T. and Morris, Z. and Prieto-Merino, D. and Roberts, I. and Sandercock, P. and Shakur, H. and Wardlaw, J.
Health Technology Assessment. 2012; 16(13): I-53
[Pubmed]
14 Serum D-dimer as a predictor of mortality in patients with acute spontaneous intracerebral hemorrhage
Chun-Cheng Chiu, Yi-Nong Li, Leng-Jye Lin, Cheng-Ting Hsiao, Kuang-Yu Hsiao, I.-Chuan Chen
Journal of Clinical Neuroscience. 2012;
[VIEW] | [DOI]
15 The 4G/4G Genotype of the PAI-1 (Serpine-1) 4G/5G Polymorphism Is Associated with Decreased Lung Allograft Utilization : 4G/4G Genotype and Decreased Lung Allograft Utilization
American Journal of Transplantation. 2012; : no
[VIEW] | [DOI]
16 Coagulopathy After Traumatic Brain Injury
Mathieu Laroche,Matthew E. Kutcher,Michael C. Huang,Mitchell Jay Cohen,Geoffrey T. Manley
Neurosurgery. 2012; 70(6): 1334
[Pubmed] | [DOI]
17 Coagulopathy after pediatric traumatic brain injury
Benjamin B. Bruins,Todd J. Kilbaugh,Stuart H. Friess
Pediatric Critical Care Medicine. 2012; 13(4): 491
[Pubmed] | [DOI]
18 Glasgow Coma Scale as a predictor for hemocoagulative disorders after blunt pediatric traumatic brain injury*
Sigune Peiniger,Ulrike Nienaber,Rolf Lefering,Maximilian Braun,Arasch Wafaisade,Matthew A. Borgman,Philip C. Spinella,Marc Maegele
Pediatric Critical Care Medicine. 2012; 13(4): 455
[Pubmed] | [DOI]
19 The character of haemostatic disorders and level of protein S-100 in acute ischaemic stroke can affect survival in the first week of follow-up
Maria Jastrzebska,Kornel Chelstowski,Aldona Siennicka,Halina Grzelec,Anna Bajer-Czajkowska,Marta Rybicka,Jeremy Clark,Przemyslaw Nowacki
Blood Coagulation & Fibrinolysis. 2011; 22(5): 388
[Pubmed] | [DOI]
20 Balanced massive transfusion ratios in multiple injury patients with traumatic brain injury
Sigune Peiniger, Ulrike Nienaber, Rolf Lefering, Maximilian Braun, Arasch Wafaisade, Sebastian Wutzler, Matthew Borgmann, Philip C Spinella, Marc Maegele
Critical Care. 2011; 15(1): R68
[VIEW] | [DOI]
21 Rol del factor VII recombinante activado en pacientes neuroquirúrgicos y neurocríticos
P. Rama-Maceiras,I. Ingelmo-Ingelmo,N. Fàbregas-Julià,J. Hernández-Palazón
Neurocirugía. 2011; 22(3): 209
[Pubmed] | [DOI]
22 The natural history of trauma-related coagulopathy: Implications for treatment
Engels, P.T. and Rezende-Neto, J.B. and Al Mahroos, M. and Scarpelini, S. and Rizoli, S.B. and Tien, H.C.
Journal of Trauma - Injury, Infection and Critical Care. 2011; 71(5 SUPPL.1): S448-S455
[Pubmed]
23 The character of haemostatic disorders and level of protein S-100 in acute ischaemic stroke can affect survival in the first week of follow-up: A pilot study
Jastrzȩbska, M. and Chełstowski, K. and Siennicka, A. and Grzelec, H. and Bajer-Czajkowska, A. and Rybicka, M. and Clark, J. and Nowacki, P.
Blood Coagulation and Fibrinolysis. 2011; 22(5): 388-395
[Pubmed]
24 The role of recombinant activated factor VII in neuro-surgical and neurocritical patients [Rol del factor VII recombinante activado en pacientes neuroquirúrgicos y neu-rocríticos]
Rama-Maceiras, P. and Ingelmo-Ingelmo, I. and Fàbregas-Julià, N. and Hernández-Palazón, Y.J.
Neurocirugia. 2011; 22(3): 209-223
[Pubmed]
25 The Natural History of Trauma-Related Coagulopathy: Implications for Treatment :
Paul T. Engels, Joao B. Rezende-Neto, Mohammed Al Mahroos, Sandro Scarpelini, Sandro B. Rizoli, Homer C. Tien
The Journal of Trauma Injury Infection and Critical Care. 2011; 71: S448
[VIEW] | [DOI]
26 Disseminated intravascular coagulation associated with ventriculoperitoneal shunt surgery: Case report
Frazier, J.L., Bova, G.S., Jockovic, K., Hunt, E.A., Lee, B., Ahn, E.S.
Journal of Neurosurgery: Pediatrics. 2010; 5(3): 1-2
[Pubmed]
27 Acute Coagulopathy in Isolated Blunt Traumatic Brain Injury
Arasch Wafaisade, Rolf Lefering, Thorsten Tjardes, Sebastian Wutzler, Christian Simanski, Thomas Paffrath, Philipp Fischer, Bertil Bouillon, Marc Maegele
Neurocritical Care. 2010; 12(2): 211
[VIEW] | [DOI]
28 Disseminated intravascular coagulation associated with ventriculoperitoneal shunt surgery : Case report
James L. Frazier, G. Steven Bova, Kathryn Jockovic, Elizabeth A. Hunt, Benjamin Lee, Edward S. Ahn
Journal of Neurosurgery Pediatrics. 2010; 5(3): 306
[VIEW] | [DOI]
29 Hemostatic and hemorrhagic problems in neurosurgical patients
Ruediger Gerlach, Manuela Krause, Volker Seifert, Klaus Goerlinger
Acta Neurochirurgica. 2009; 151(8): 873
[VIEW] | [DOI]
30 Coagulopathy in Severe Traumatic Brain Injury: A Prospective Study
Peep Talving, Rodd Benfield, Pantelis Hadjizacharia, Kenji Inaba, Linda S. Chan, Demetrios Demetriades
The Journal of Trauma Injury Infection and Critical Care. 2009; 66(1): 55
[VIEW] | [DOI]
31 Low-dose recombinant factor VIIa for trauma patients with coagulopathy
Deborah M. Stein,Richard P. Dutton,John R. Hess,Thomas M. Scalea
Injury. 2008; 39(9): 1054
[Pubmed] | [DOI]
32 RECOMBINANT FACTOR VIIA IN TRAUMATIC INTRACEREBRAL HEMORRHAGE
Raj K. Narayan,Andrew I.R. Maas,Lawrence F. Marshall,Franco Servadei,Brett E. Skolnick,Michael N. Tillinger
Neurosurgery. 2008; 62(4): 776
[Pubmed] | [DOI]
33 Disseminated Intravascular Coagulation After Craniotomy
Jeffrey J. Pasternak, Dana N. Hertzfeldt, Sharm R. Stanger, Kirsten R. Walter, Travis D. Werts, Mary E. S. Marienau, William L. Lanier
Journal of Neurosurgical Anesthesiology. 2008; 20(1): 15
[VIEW] | [DOI]
34 Neuroanesthesiology Review—2007
Jeffrey J. Pasternak, William L. Lanier
Journal of Neurosurgical Anesthesiology. 2008; 20(2): 78
[VIEW] | [DOI]
35 Coagulation disorder in cranioencephalic trauma [Trastornos de coagulación en trauma craneoencefalico]
De Mejía, M.C.N. and Caicedo, M.V. and Torres, J.A. and Tovar, J.A.
Revista Colombiana de Anestesiologia. 2008; 36(3): 199-206
[Pubmed]
36 Recombinant factor viia in traumatic intracerebral hemorrhage: Results of a dose-escalation clinical trial
Narayan, R.K. and Maas, A.I.R. and Marshall, L.F. and Servadei, F. and Skolnick, B.E. and Tillinger, M.N.
Neurosurgery. 2008; 62(4): 776-786
[Pubmed]
37 Coagulation disorders after traumatic brain injury
B. S. Harhangi, E. J. O. Kompanje, F. W. G. Leebeek, A. I. R. Maas
Acta Neurochirurgica. 2008; 150(2): 165
[VIEW] | [DOI]
38 Aggressive Organ Donor Management Protocol
Joseph DuBose,Ali Salim
Journal of Intensive Care Medicine. 2008; 23(6): 367
[Pubmed] | [DOI]
39 Trastornos de coagulación en trauma craneoencefálico
M.C. Niño de Mejía,M.V. Caicedo,J.A. Torres,J.A. Tovar
Revista Colombiana de Anestesiología. 2008; 36(3): 199
[Pubmed] | [DOI]
40 Low-dose recombinant factor VIIa for trauma patients with coagulopathy
Stein, D.M., Dutton, R.P., Hess, J.R., Scalea, T.M.
Injury. 2008; 39(9): 1-2
[Pubmed]
41 Aggressive organ donor management protocol
DuBose, J., Salim, A.
Journal of Intensive Care Medicine. 2008; 23(6): 1-2
[Pubmed]
42 Coagulation disorder in cranioencephalic trauma | [Trastornos de coagulación en trauma craneoencefalico]
De Mejía, M.C.N., Caicedo, M.V., Torres, J.A., Tovar, J.A.
Revista Colombiana de Anestesiologia. 2008; 36(3): 1-2
[Pubmed]
43 Neuroanesthesiology review - 2007
Pasternak, J.J., Lanier, W.L.
Journal of Neurosurgical Anesthesiology. 2008; 20(2): 1-2
[Pubmed]
44 Correlation of a high D-dimer level with poor outcome in traumatic intracranial hemorrhage
J.-R. Kuo, K.-C. Lin, C.-L. Lu, H.-J. Lin, C.-C. Wang, C. H. Chang
European Journal of Neurology. 2007; 14(10): 1073
[VIEW] | [DOI]
45 Safety of rFVIIa in hemodynamically unstable polytrauma patients with traumatic brain injury: Post hoc analysis of 30 patients from a prospective, randomized, placebo-controlled, double-blind clinical trial
Kluger, Y., Riou, B., Rossaint, R., Rizoli, S.B., Boffard, K.D., Choong, P.T., Warren, B., Tillinger, M.
Critical Care. 2007; 11: Art- R85
[Pubmed]
46 Fibrinolytic markers and neurologic outcome in traumatic brain injury
Bayir, A., Kalkan, E., Kocak, S., Ak, A., Cander, B., Bodur, S.
Neurology India. 2006; 54(4): 363-365
[Pubmed]



 

Top
Print this article  Email this article
Previous article Next article
Online since 20th March '04
Published by Wolters Kluwer - Medknow