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Critical Care
Published in: Critical Care 1/2017

Open Access 01-12-2017 | Research

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

Authors: Mineji Hayakawa, Kunihiko Maekawa, Shigeki Kushimoto, Hiroshi Kato, Junichi Sasaki, Hiroshi Ogura, Tetsuya Matsuoka, Toshifumi Uejima, Naoto Morimura, Hiroyasu Ishikura, Akiyoshi Hagiwara, Munekazu Takeda, Naoyuki Kaneko, Daizoh Saitoh, Daisuke Kudo, Takashi Kanemura, Takayuki Shibusawa, Shintaro Furugori, Yoshihiko Nakamura, Atsushi Shiraishi, Kiyoshi Murata, Gou Mayama, Arino Yaguchi, Shiei Kim, Osamu Takasu, Kazutaka Nishiyama

Published in: Critical Care | Issue 1/2017

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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.
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Metadata
Title
Hyperfibrinolysis in severe isolated traumatic brain injury may occur without tissue hypoperfusion: a retrospective observational multicentre study
Authors
Mineji Hayakawa
Kunihiko Maekawa
Shigeki Kushimoto
Hiroshi Kato
Junichi Sasaki
Hiroshi Ogura
Tetsuya Matsuoka
Toshifumi Uejima
Naoto Morimura
Hiroyasu Ishikura
Akiyoshi Hagiwara
Munekazu Takeda
Naoyuki Kaneko
Daizoh Saitoh
Daisuke Kudo
Takashi Kanemura
Takayuki Shibusawa
Shintaro Furugori
Yoshihiko Nakamura
Atsushi Shiraishi
Kiyoshi Murata
Gou Mayama
Arino Yaguchi
Shiei Kim
Osamu Takasu
Kazutaka Nishiyama
Publication date
01-12-2017
Publisher
BioMed Central
Published in
Critical Care / Issue 1/2017
Electronic ISSN: 1364-8535
DOI
https://doi.org/10.1186/s13054-017-1811-1

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