Hyperfibrinolysis in severe isolated traumatic brain injury may occur without tissue hypoperfusion: a retrospective observational multicentre study.
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.
['Hayakawa|Mineji|M|', 'Maekawa|Kunihiko|K|', 'Kushimoto|Shigeki|S|', 'Kato|Hiroshi|H|', 'Sasaki|Junichi|J|', 'Ogura|Hiroshi|H|', 'Matsuoka|Tetsuya|T|', 'Uejima|Toshifumi|T|', 'Morimura|Naoto|N|', 'Ishikura|Hiroyasu|H|', 'Hagiwara|Akiyoshi|A|', 'Takeda|Munekazu|M|', 'Kaneko|Naoyuki|N|', 'Saitoh|Daizoh|D|', 'Kudo|Daisuke|D|', 'Kanemura|Takashi|T|', 'Shibusawa|Takayuki|T|', 'Furugori|Shintaro|S|', 'Nakamura|Yoshihiko|Y|', 'Shiraishi|Atsushi|A|', 'Murata|Kiyoshi|K|', 'Mayama|Gou|G|', 'Yaguchi|Arino|A|', 'Kim|Shiei|S|', 'Takasu|Osamu|O|', 'Nishiyama|Kazutaka|K|']
D000328:Adult D000368:Aged D001780:Blood Coagulation Tests D000070642:Brain Injuries, Traumatic D005260:Female D006801:Humans D015601:Injury Severity Score D007564:Japan D008297:Male D008875:Middle Aged D012189:Retrospective Studies D014193:Trauma Centers
Hyperfibrinolysis Traumatic brain injury Hypoperfusion Coagulopathy Disseminated intravascular coagulation