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Hyperfibrinolysis in severe isolated traumatic brain injury may occur without tissue hypoperfusion : a retrospective observational multicentre study

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/67457

Title: Hyperfibrinolysis in severe isolated traumatic brain injury may occur without tissue hypoperfusion : a retrospective observational multicentre study
Authors: Hayakawa, Mineji Browse this author →KAKEN DB
Maekawa, Kunihiko Browse this author
Kushimoto, Shigeki Browse this author →KAKEN DB
Kato, Hiroshi Browse this author
Sasaki, Junichi Browse this author
Ogura, Hiroshi Browse this author →KAKEN DB
Matsuoka, Tetsuya Browse this author
Uejima, Toshifumi Browse this author
Morimura, Naoto Browse this author
Ishikura, Hiroyasu Browse this author
Hagiwara, Akiyoshi Browse this author
Takeda, Munekazu Browse this author
Kaneko, Naoyuki Browse this author
Saitoh, Daizoh Browse this author →KAKEN DB
Kudo, Daisuke Browse this author →KAKEN DB
Kanemura, Takashi Browse this author
Shibusawa, Takayuki Browse this author
Furugori, Shintaro Browse this author
Nakamura, Yoshihiko Browse this author
Shiraishi, Atsushi Browse this author
Murata, Kiyoshi Browse this author
Mayama, Gou Browse this author
Yaguchi, Arino Browse this author
Kim, Shiei Browse this author
Takasu, Osamu Browse this author
Nishiyama, Kazutaka Browse this author
Keywords: Coagulopathy
Disseminated intravascular coagulation
Hypoperfusion
Hyperfibrinolysis
Traumatic brain injury
Issue Date: 23-Aug-2017
Publisher: BioMed Central
Journal Title: Critical care
Volume: 21
Start Page: 222
Publisher DOI: 10.1186/s13054-017-1811-1
Abstract: Background: Hyperfibrinolysis is a critical complication in severe trauma. Hyperfibrinolysis is traditionally diagnosed via elevated D-dimer or fibrin/fibrinogen degradation product levels, and recently, using thromboelastometry. Although hyperfibrinolysis is observed in patients with severe isolated traumatic brain injury (TBI) on arrival at the emergency department (ED), it is unclear which factors induce hyperfibrinolysis. The present study aimed to investigate the factors associated with hyperfibrinolysis in patients with isolated severe TBI. Methods: We conducted a multicentre retrospective review of data for adult trauma patients with an injury severity score >= 16, and selected patients with isolated TBI (TBI group) and extra-cranial trauma (non-TBI group). The TBI group included patients with an abbreviated injury score (AIS) for the head >= 4 and an extra-cranial AIS < 2. The non-TBI group included patients with an extra-cranial AIS >= 3 and head AIS < 2. Hyperfibrinolysis was defined as a D-dimer level >= 38 mg/L on arrival at the ED. We evaluated the relationships between hyperfibrinolysis and injury severity/tissue injury/tissue perfusion in TBI patients by comparing them with non-TBI patients. Results: We enrolled 111 patients in the TBI group and 126 in the non-TBI group. In both groups, patients with hyperfibrinolysis had more severe injuries and received transfusion more frequently than patients without hyperfibrinolysis. Tissue injury, evaluated on the basis of lactate dehydrogenase and creatine kinase levels, was associated with hyperfibrinolysis in both groups. Among patients with TBI, the mortality rate was higher in those with hyperfibrinolysis than in those without hyperfibrinolysis. Tissue hypoperfusion, evaluated on the basis of lactate level, was associated with hyperfibrinolysis in only the non-TBI group. Although the increase in lactate level was correlated with the deterioration of coagulofibrinolytic variables (prolonged prothrombin time and activated partial thromboplastin time, decreased fibrinogen levels, and increased D-dimer levels) in the non-TBI group, no such correlation was observed in the TBI group. Conclusions: Hyperfibrinolysis is associated with tissue injury and trauma severity in TBI and non-TBI patients. However, tissue hypoperfusion is associated with hyperfibrinolysis in non-TBI patients, but not in TBI patients. Tissue hypoperfusion may not be a prerequisite for the occurrence of hyperfibrinolysis in patients with isolated TBI.
Rights: http://creativecommons.org/licenses/by/4.0/
Type: article
URI: http://hdl.handle.net/2115/67457
Appears in Collections:北海道大学病院 (Hokkaido University Hospital) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 早川 峰司

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