Coagulation and fibrinolysis after head injury

Introduction

It is believed that abnormal coagulation and fibrinolysis is a frequent complication in patients with head injury, and this abnormality is initiated by the released of thromboplastin (tissue factor) from damaged brain. But some authors [1,2] reported that the activation of coagulation and fibrinolysis after head injury is not the specific phenomenon comparing with the population of trauma victim. Recently, we have been able to measure some molecular markers of coagulation and fibrinolysis system in clinical setting. We compared coagulation and fibrinolysis activity of trauma and head injury patients using the molecular markers.

Materials and methods

Blood samples were collected in 1, 3 and 5 days after onset from 31 trauma patients (TR) (patients with head-Abbreviated Injury Score (AIS) = 3 were excluded), 12 head injury (HI) patients (patients with other system AIS = 3 were excluded) and 27 cerebrovascular disease patients (CVD) (patients with intracranial hemorrhage or subarachnoid hemorrhage), and thrombin-antithrombin III complex (TAT), a 2 plasmin inhibitor plasmin complex (PIC), D-dimer, plasminogen activator inhibitor (PAI-1), tissue plasminogen activator (tPA)-PAI-I complex (tPAI-C), thrombomodulin (TM) and protein C activity (PCA) were measured.

Results

PCA and PAI- I on 1 day had good correlation with injury severity score (ISS). TAT, D-dimer and PAI-1 of TR were significantly (P < 0.05) higher than those of CVD, and PCA of TR were significantly lower than those of CVD, but there were no difference between TR and HI.

Conclusions

HI and TR had significantly activation of coagulation and fibrinolysis compared with CVD, but there were no evidence that HI had significantly activation of coagulation and fibrinolysis compared with TR.

Table 1 Table (abstract P022)