Traumatic brain injury (TBI) has long been associated with coagulopathy; however, the time course of coagulation/fibrinolytic parameters in the acute phase of TBI remains unclear. The purpose of the study was to analyze the time course of coagulation/fibrinolytic parameters in the acute phase of TBI and to elucidate parameter relationships to prognosis. We retrospectively evaluated 234 patients with severe isolated TBI with initial blood samples obtained no more than 1 h after injury. Platelet count, prothrombin time, activated partial thromboplastin time (aPTT), plasma levels of fibrinogen, and D-dimer were measured on arrival in the emergency department and 3, 6, and 12 h after injury. Multivariate logistic regression analysis was performed to identify risk factors for poor prognosis at each time point. From hospital admission to 12 h after injury, an elevated D-dimer level was a significant negative prognostic indicator (admission: p < 0.0001; 3 h after injury: p = 0.0005; 6 h after injury: p = 0.005; 12 h after injury: p = 0.0009). An upward trend of aPTT on admission and 3 h after injury was also a significant negative prognostic indicator (admission: p = 0.0011; 3 h after injury: p = 0.013). On multivariate logistic regression analysis, which included all initial variables, independent risk factors for poor prognosis included older age (p = 0.0005), low Glasgow Coma Scale score (p < 0.0001), high Abbreviated Injury Score (p = 0.015), aPTT >30.2 sec (p = 0.019), and elevated D-dimer level (p = 0.0005). We concluded that D-dimer is the best coagulation/fibrinolytic parameter to monitor for prediction of outcome.
Our findings suggest that global end-diastolic volume index impacts both delayed cerebral ischemia and pulmonary edema after subarachnoid hemorrhage. Maintaining global end-diastolic volume index slightly above normal levels has promise as a fluid management goal during the treatment of subarachnoid hemorrhage.
Physician-directed prophylactic triple-H administration was not associated with improved clinical outcomes or quantitative hemodynamic indicators for intravascular volume. Further, GEDI-directed intervention studies are warranted to better define management algorithms for SAH patients with the aim of preventing DCI.
Background:Coagulopathy and old age have been associated with poor outcomes in traumatic brain injury (TBI) patients; however, the relationships of coagulopathy and age with the acute phase of TBI remain unclear. We hypothesized that coagulation/fibrinolytic abnormalities are more severe in older patients in the acute phase of TBI and may explain, in part, their poor outcome.Methods:We analyzed the relationship between coagulation/fibrinolytic parameters and age in the acute phase of TBI by retrospectively evaluating 274 patients with initial blood samples obtained no more than 1 hour after injury. Measurement of platelet count, prothrombin time, activated partial thromboplastin time, plasma levels of fibrinogen, and D-dimer was done in the emergency department on arrival as well as 3, 6, and 12 hours following injury. Values were compared between patients aged 16–55 years (group 1) and those aged older than 55 years (group 2) with an Abbreviated Injury Score (AIS)-head of 3–5 to identify any relationship between these parameters and age.Results:When groups 1 and 2 were matched for AIS-head, plasma levels of D-dimer in group 2 were significantly higher than those in group 1 from hospital admission to 12 hours after injury. The Glasgow Outcome Scale scores at 3 months post-injury of group 2 with AIS 4 and 5 were significantly lower than those of group 1 (both P < 0.0001).Conclusions:Fibrinolytic abnormalities are more severe in older acute-phase TBI patients, which may be a factor associated with their poor prognosis.
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