Coagulopathy and Traumatic Brain Injury: Overview of New Diagnostic and Therapeutic Strategies
Coagulopathy is a common sequela of traumatic brain injury. Consumptive coagulopathy and secondary hyperfibrinolysis are associated with hypercoagulability. In addition, fibrinolytic pathways are hyperactivated as a result of vascular endothelial cell damage in the injured brain. Coagulation and fib...
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| Format: | Article |
| Language: | English |
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The Japan Neurosurgical Society
2022-06-01
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| Series: | Neurologia Medico-Chirurgica |
| Subjects: | |
| Online Access: | https://www.jstage.jst.go.jp/article/nmc/62/6/62_2022-0018/_pdf/-char/en |
| _version_ | 1818114811467137024 |
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| author | Ryuta NAKAE Yasuo MURAI Akio MORITA Shoji YOKOBORI |
| author_facet | Ryuta NAKAE Yasuo MURAI Akio MORITA Shoji YOKOBORI |
| author_sort | Ryuta NAKAE |
| collection | DOAJ |
| description | Coagulopathy is a common sequela of traumatic brain injury. Consumptive coagulopathy and secondary hyperfibrinolysis are associated with hypercoagulability. In addition, fibrinolytic pathways are hyperactivated as a result of vascular endothelial cell damage in the injured brain. Coagulation and fibrinolytic parameters change dynamically to reflect these pathologies. Fibrinogen is consumed and degraded after injury, with fibrinogen concentrations at their lowest 3-6 h after injury. Hypercoagulability causes increased fibrinolytic activity, and plasma levels of D-dimer increase immediately after traumatic brain injury, reaching a maximum at 3 h. Owing to disseminated intravascular coagulation in the presence of fibrinolysis, the bleeding tendency is highest within the first 3 h after injury, and often a condition called “talk and deteriorate” occurs. In neurointensive care, it is necessary to measure coagulation and fibrinolytic parameters such as fibrinogen and D-dimer routinely to predict and prevent the development of coagulopathy and its negative outcomes. Currently, the only evidence-based treatment for traumatic brain injury with coagulopathy is tranexamic acid in the subset of patients with mild-to-moderate traumatic brain injury. Coagulation and fibrinolytic parameters should be closely monitored, and treatment should be considered on a patient-by-patient basis. |
| first_indexed | 2024-12-11T03:56:39Z |
| format | Article |
| id | doaj.art-1d69703d8f1240949e5d367f386690e2 |
| institution | Directory Open Access Journal |
| issn | 1349-8029 |
| language | English |
| last_indexed | 2024-12-11T03:56:39Z |
| publishDate | 2022-06-01 |
| publisher | The Japan Neurosurgical Society |
| record_format | Article |
| series | Neurologia Medico-Chirurgica |
| spelling | doaj.art-1d69703d8f1240949e5d367f386690e22022-12-22T01:21:46ZengThe Japan Neurosurgical SocietyNeurologia Medico-Chirurgica1349-80292022-06-0162626126910.2176/jns-nmc.2022-00182022-0018Coagulopathy and Traumatic Brain Injury: Overview of New Diagnostic and Therapeutic StrategiesRyuta NAKAE0Yasuo MURAI1Akio MORITA2Shoji YOKOBORI3Department of Emergency and Critical Care Medicine, Nippon Medical School HospitalDepartment of Neurological Surgery, Nippon Medical School HospitalDepartment of Neurological Surgery, Nippon Medical School HospitalDepartment of Emergency and Critical Care Medicine, Nippon Medical School HospitalCoagulopathy is a common sequela of traumatic brain injury. Consumptive coagulopathy and secondary hyperfibrinolysis are associated with hypercoagulability. In addition, fibrinolytic pathways are hyperactivated as a result of vascular endothelial cell damage in the injured brain. Coagulation and fibrinolytic parameters change dynamically to reflect these pathologies. Fibrinogen is consumed and degraded after injury, with fibrinogen concentrations at their lowest 3-6 h after injury. Hypercoagulability causes increased fibrinolytic activity, and plasma levels of D-dimer increase immediately after traumatic brain injury, reaching a maximum at 3 h. Owing to disseminated intravascular coagulation in the presence of fibrinolysis, the bleeding tendency is highest within the first 3 h after injury, and often a condition called “talk and deteriorate” occurs. In neurointensive care, it is necessary to measure coagulation and fibrinolytic parameters such as fibrinogen and D-dimer routinely to predict and prevent the development of coagulopathy and its negative outcomes. Currently, the only evidence-based treatment for traumatic brain injury with coagulopathy is tranexamic acid in the subset of patients with mild-to-moderate traumatic brain injury. Coagulation and fibrinolytic parameters should be closely monitored, and treatment should be considered on a patient-by-patient basis.https://www.jstage.jst.go.jp/article/nmc/62/6/62_2022-0018/_pdf/-char/entraumatic brain injuryblood coagulation disordersfibrinolysisfibrinogenfibrin fibrinogen degradation products |
| spellingShingle | Ryuta NAKAE Yasuo MURAI Akio MORITA Shoji YOKOBORI Coagulopathy and Traumatic Brain Injury: Overview of New Diagnostic and Therapeutic Strategies Neurologia Medico-Chirurgica traumatic brain injury blood coagulation disorders fibrinolysis fibrinogen fibrin fibrinogen degradation products |
| title | Coagulopathy and Traumatic Brain Injury: Overview of New Diagnostic and Therapeutic Strategies |
| title_full | Coagulopathy and Traumatic Brain Injury: Overview of New Diagnostic and Therapeutic Strategies |
| title_fullStr | Coagulopathy and Traumatic Brain Injury: Overview of New Diagnostic and Therapeutic Strategies |
| title_full_unstemmed | Coagulopathy and Traumatic Brain Injury: Overview of New Diagnostic and Therapeutic Strategies |
| title_short | Coagulopathy and Traumatic Brain Injury: Overview of New Diagnostic and Therapeutic Strategies |
| title_sort | coagulopathy and traumatic brain injury overview of new diagnostic and therapeutic strategies |
| topic | traumatic brain injury blood coagulation disorders fibrinolysis fibrinogen fibrin fibrinogen degradation products |
| url | https://www.jstage.jst.go.jp/article/nmc/62/6/62_2022-0018/_pdf/-char/en |
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