2008 Volume 31 Issue 1 Pages 32-36
Object. Brain injury is known to result in disordered haemostasis. The significant prolongation of coagulapathy was taken to support activation of the extrinsic pathway of the coagulation cascade by tissue thromboplastin, as a result of brain parenchymal injury. We experienced to difficult of treatment of brain parenchymal hemorrhage in decompression craniotomy, and poor outcome.
Methods. The objective of this study was to determine the clinical significance of coagulation and fibrinogenolysis in 178 patients with head injury.
Results. The result of univariate analyses for survival and non-survival was determining association between clinical factor (age, GCS, ISS), hemocoagulative factor and mortality. When simultaneously adjusting for all these factor in multivariate analysis, initial GCS and plasma D-dimer values was independent predicting factor of mortality. Mortality was most strongly related to initial GCS and plasma D-dimer values by ROC curve. In Computed Tomography of brain findings, we found plasma D-dimer value measured within 1 hr after head injury were higher in patients with a focal brain injury group than a diffuse brain injury. The peak of plasma D-dimer values peak was between 3 h to 4 h within head injury from changes of plasma D-dimer values after sever head injury by 19 patients data of 1, 3, 6, 12 hr.
Conclusions. Fibrinogenolysis of increased plasma D-dimer value associated a prediction of mortality and a degree of brain parenchymal damage influenced for the systemic haemostasis in early phase within 1 hr after head injury and increasing within 3 hr to 4 hr after head injury, there is an initial hypercoagulable stage followed by 6 hr after head injury. Therefore, it is important for us to recognize haemostatic disorders at treatment of head injury in acute phase.
