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.

Thrombomodulin (TM), which is located in the surface of the endothelium in the arteries, veins, and capillaries of major organs such as the brain, lungs, liver, kidneys, skeletal muscles, and gastrointestinal tract, is one of several indicators of endothelial injury. Von Willebrand factor (vWf), which is synthesized by endothelial cells, is also an endothelial specific glycoprotein. The serum level of vWf increases in response to various stimuli without endothelial injury. An elevated serum level of vWf may suggest endothelial activation in severe head injury. We hypothesize that the degree of cerebral endothelial activation or injury depends on the type of head injury and that measuring the TM and vWf is useful for predicting delayed traumatic intracerebral hematoma (DTICH), produced by weakness of the vessel wall, occuring either as a direct or indirect effect of head injury. The values of vWf in focal brain injury (ranging from 332.5 +/- 52.8% to 361.7 +/- 86.2%) were significantly higher than those in diffuse axonal injury from 2 h to 7 days after the injury occurred (ranging from 201.6 +/- 59.5% to 242.5 +/- 51.7%). The serum level of TM in focal brain injury (ranging from 3.84 +/- 1.54 to 4.12 +/- 1.46 U/mL) was higher than that in diffuse axonal injury (ranging from 2.96 +/- 0.63 to 3.67 +/- 1.70 U/mL), but these differences were not statistically significant. In patients with DTICH, TM was significantly higher than in patients without DTICH (p < 0.01). The results of our study demonstrate that the degree of endothelial activation in focal brain injury was significantly higher than in diffuse brain injury. In addition, the serum level of TM in patients with DTICH was significantly higher than in patients without DTICH. These findings suggest that cerebral tissue injury is often accompanied by cerebral endothelial activation, and that these two phenomena should be distinguished from each other. The levels of serum TM and vWf appear to be good indicators of the cerebral endothelial injury and of endothelial activation in severe head injury.

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The combination of intravascular temperature management and conventional cooling was safe and feasible for treating severe heat stroke. The results indicate that better temperature management may help prevent organ failure. A large randomized controlled trial is needed to validate our findings.

Our study suggests the usefulness of measurement of cortical cellular pH by intracranial tonometer for evaluating the severity of focal anaerobic cerebral metabolism and predicting patient prognosis.