Pathophysiology, Mortality, Treatment of Acute Phase of Haemostatic Disorders of Traumatic Brain Injury
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- Takayama Yasuhiro
- Department of Critical Care Medicine, Nihon Medical School of Medicine
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- Yokota Hiroyuki
- Department of Critical Care Medicine, Nihon Medical School of Medicine
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- Sato Hidetaka
- Department of Critical Care Medicine, Nihon Medical School of Medicine
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- Naoe Yasutaka
- Department of Critical Care Medicine, Nihon Medical School of Medicine
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- Araki Takashi
- Department of Critical Care Medicine, Nihon Medical School of Medicine
Bibliographic Information
- Other Title
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- 頭部外傷に伴う凝固・線溶系障害からみた病態, 予後, 治療について
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Description
Disordered haemostasis is a known complication following traumatic brain injury. In the event of brain parenchymal injury, coagulapathy is significantly prolonged to support activation of the extrinsic pathway of the coagulation cascade by tissue thromboplastin. We experienced such a difficult to treat brain parenchymal hemorrhage in decompression craniotomy that resulted in a poor outcome. <br> In this study, we focus on hemorrhage due to the fibrinogenolysis effect of second brain injury and patient outcome. We also show the importance of monitoring haemostatic markers when treating traumatic brain injury and provide practical guidelines. <br> The objective of this study was to determine the clinical significance of coagulation and fibrinogenolysis in 247 patients with traumatic brain injury and compare the shift of haemostatic markers. <br> Univariate analyses for survival and non-survival was performed by determining the association between clinical factor (age, GCS, ISS), hemocoagulative factor and mortality. When simultaneously adjusting for all these factors in multivariate analysis, patient age, initial GCS and plasma D-dimer values were found to be independent predicting factors of mortality. Mortality was most strongly related to an age greater than 57 years, an initial GCS of 7 points and a less than 50 μg/ml of plasma D-dimer value level. As for haemostatic marker shifting dynamic change in the short-term after traumatic brain injury, we found that coagulation and fibrinogenolysis initially increase within the first 3 hours, the secondary inhibitor of fibrinogenolysis increases within 6 hours, and that fibrinogen increases over 6 hours after brain injury. The most important factor in haemostatic shift was the peak of plasma D-dimer values within 3 hours after brain injury. <br> Fibrinogenolysis with an increased plasma D-dimer value was associated with a prediction of mortality and the degree that the brain parenchymal damage influenced systemic haemostasis in the early phase within 1 hour after brain injury and increases within 3 hours after brain injury. There is also an initial hypercoagulable stage that follows 6 hours after brain injury. Therefore, it is important for us to recognize haemostatic disorders when treating brain injury in the acute phase and practical use should be made of haemostatic shift values after brain injury.
Journal
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- Japanese Journal of Neurosurgery
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Japanese Journal of Neurosurgery 22 (11), 837-841, 2013
The Japanese Congress of Neurological Surgeons
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Details 詳細情報について
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- CRID
- 1390282679382630784
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- NII Article ID
- 10031196800
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- NII Book ID
- AN10380506
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- ISSN
- 21873100
- 0917950X
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- Text Lang
- ja
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- Data Source
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- JaLC
- Crossref
- CiNii Articles
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- Abstract License Flag
- Disallowed