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.

Coagulopathy is a common sequela of traumatic brain injury. Consumptive coagulopathy and secondary hyperfibrinolysis are associated with hypercoagulability. In addition, fibrinolytic pathways are hyperactivated as a result of vascular endothelial cell damage in the injured brain. Coagulation and fibrinolytic parameters change dynamically to reflect these pathologies. Fibrinogen is consumed and degraded after injury, with fibrinogen concentrations at their lowest 3-6 h after injury. Hypercoagulability causes increased fibrinolytic activity, and plasma levels of D-dimer increase immediately after traumatic brain injury, reaching a maximum at 3 h. Owing to disseminated intravascular coagulation in the presence of fibrinolysis, the bleeding tendency is highest within the first 3 h after injury, and often a condition called "talk and deteriorate" occurs. In neurointensive care, it is necessary to measure coagulation and fibrinolytic parameters such as fibrinogen and D-dimer routinely to predict and prevent the development of coagulopathy and its negative outcomes. Currently, the only evidence-based treatment for traumatic brain injury with coagulopathy is tranexamic acid in the subset of patients with mild-to-moderate traumatic brain injury. Coagulation and fibrinolytic parameters should be closely monitored, and treatment should be considered on a patient-by-patient basis.

Transcranial Doppler (TCD) is widely accepted to monitor cerebral vasospasm after subarachnoid hemorrhage (SAH); however, its predictive value remains controversial. To investigate the predictive reliability of an increase in the mean blood flow velocity (mBFV) ratio of the ipsilateral to contralateral middle cerebral arteries (I/C mBFV) compared with the conventional absolute flow velocity. We retrospectively investigated the clinical and radiologic data of consecutive patients with SAH admitted from July 2003 to August 2009 who underwent TCD ultrasonography. The highest mBFV value in bilateral middle cerebral arteries was recorded, while delayed cerebral ischemia (DCI) was defined as neurological deficits or computed tomographic evidence of cerebral infarction caused by vasospasm. The ipsilateral side was defined as the side with higher mBFV value when evaluating the I/C mBFV. We thus elucidated the reliability of this rate in comparison with the conventional method for predicting DCI with receiver operating characteristic (ROC) analysis. One hundred and forty-two patients were retrospectively analyzed with specific data from 1262 TCD studies. The ROC curve showed that the overall predictive value for DCI had an area under the curve of 0.86 (95% confidence interval: 0.76-0.96) when the I/C mBFV was used vs 0.80 (0.71-0.88) when the absolute flow velocity was used. The threshold value that best discriminated between patients with and without DCI was I/C mBFV of 1.5. In patients with SAH, the I/C mBFV demonstrated a more significant correlation to vasospasm than the absolute mean flow velocity.

Traumatic brain injury (TBI) is associated with coagulation/fibrinolysis disorders. We retrospectively evaluated 61 TBI cases transported to hospital within 1 h post-injury. Levels of thrombin-antithrombin III complex (TAT), D-dimer, and plasminogen activator inhibitor-1 (PAI-1) were measured on arrival and 3 h, 6 h, 12 h, 1 day, 3 days and 7 days after injury. Multivariate logistic regression analysis was performed to identify prognostic factors for coagulation and fibrinolysis. Plasma TAT levels peaked at admission and decreased until 1 day after injury. Plasma D-dimer levels increased, peaking up to 3 h after injury, and decreasing up to 3 days after injury. Plasma PAI-1 levels increased up to 3 h after injury, the upward trend continuing until 6 h after injury, followed by a decrease until 3 days after injury. TAT, D-dimer, and PAI-1 were elevated in the acute phase of TBI in cases with poor outcome. Multivariate logistic regression analysis showed that D-dimer elevation from admission to 3 h after injury and PAI-1 elevation from 6 h to 1 day after injury were significant negative prognostic indicators. Post-TBI hypercoagulation, fibrinolysis, and fibrinolysis shutdown were activated consecutively. Hyperfibrinolysis immediately after injury and subsequent fibrinolysis shutdown were associated with poor outcome.

OBJECTIVE: The authors sought to demonstrate that hemorrhagic transformation of ischemic lesions is the main cause of delayed intracerebral hemorrhage (ICH) after Pipeline embolization device (PED) treatment and to estimate the rate of hemorrhagic transformation of new postprocedure ischemic lesions.METHODS: Patients who underwent PED placement (PED group) from November 2015 to March 2017 or stent-mediated embolization (EN group) from December 2010 to October 2015 were retrospectively analyzed. Pre- and postprocedural MR images and 6-month follow-up MR images for each patient were scored for the presence of postprocedural bland ischemic and hemorrhagic lesions using diffusion-weighted MRI (DWI) and T2*-weighted MRI (T2*WI), respectively.RESULTS: The PED group comprised 28 patients with 30 intracranial aneurysms, and the EN group comprised 24 patients with 27 intracranial aneurysms. The mean number of ischemic lesions on DWI 1 day postprocedure was higher in the PED group than in the EN group (5.2 vs 2.7, p = 0.0010). The mean number of microbleeds detected on T2*WI 6 months postprocedure was higher in the PED group than in the EN group (0.6 vs 0.15, p = 0.028). A total of 36.7% of PED-treated patients exhibited new microbleeds on T2*WI at 6 months postprocedure, with at least 77.8% of these lesions representing hemorrhagic transformations of the new ischemic lesions observed on day 1 postprocedure. The rate of adjunctive coil embolization (27.3% vs 0.0%, p = 0.016) and the mean number of ischemic lesions observed 1 day postprocedure (6.6 vs 4.3, p = 0.020) were predictors of subsequent microbleeds in the PED group.CONCLUSIONS: New microbleeds detected using T2*WI at 6 months postprocedure were more common after PED treatment than after stent-mediated embolization. Approximately three-quarters of these lesions were hemorrhagic transformations of new ischemic lesions observed on day 1 postprocedure. Prevention of intraprocedural or postprocedural infarcts is necessary to reduce the risk of hemorrhagic complications following PED placement.