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Patients with traumatic brain injury(TBI)have various pathological conditions, such as direct cell destruction by external force, compression by hematoma, vascular injury, ischemia, complicated hypoxia, and hypotension. These pathological conditions occur simultaneously at the time of injury. In some cases, contaminated wounds may be treated, and infection patterns different from the scheduled neurosurgical cases should be managed. In cases of severe TBI, immunocompromised patients are considered to be at high risk of infection. Infection control during the initial stage of treatment affects patient prognosis. In addition, large craniotomy, including decompressive craniectomy, is required to manage intracranial pressure(ICP), which causes skin infection due to delayed wound healing. Furthermore, placement of drainage tubes and transducers for a long period of time might be necessary to manage ICP, and the patient is likely to develop surgical site infection(SSI). In this paper, we describe the characteristic surgical procedure and discuss ways to control SSI in TBI cases.

Neurological improvement occurs from the subacute to chronic phases in severe traumatic brain injury. We analyzed factors associated with improved neurological findings in the subacute phase, using data from the Japan Neurotrauma Data Bank (JNTDB). The subjects were 1345 patients registered in the JNTDB (Project 2015). Clinical improvement was evaluated by comparing the Glasgow Outcome Scale (GOS) at discharge and 6 months after injury. Of these patients, 157 with severe disability (SD) on the discharge GOS were examined to evaluate factors associated with neurological improvement in the subacute phase. Cases were defined as those with (group I) and without (group N) improvement: a change from SD at discharge to good recovery (GR) or moderate disability (MD) at 6 months after injury. Patient background, admission findings, treatment, and discharge destination were examined. In all patients, the favorable outcome (GR, MD) rate improved from 30.2% at discharge to 35.7% at 6 months after injury. Of SD cases at discharge, 44.6% had a favorable outcome at 6 months (group I). Patients in group I were significantly younger, and had a significantly lower D-dimer level in initial blood tests and a lower incidence of convulsions. In multivariate analysis, discharge to home was a significant factor associated with an improved outcome. Many SD cases at discharge ultimately showed neurological improvement, and the initial D-dimer level may be a predictor of such improvement. The environment after discharge from an acute care hospital may also contribute to an improved long-term prognosis.

Background: As the aging rate in the traumatic brain injury population increases, the number of patients taking antithrombotic drugs is also expected to increase among the population with traumatic brain injury; however, the utility or risk of reversal of such drugs is unclear. Therefore, we performed a retrospective cohort study of the effect of reversal of antithrombotic drugs on geriatric traumatic brain injury at our hospital., Methods: The study subjects included 83 patients(65 years or older)with intracranial traumatic lesions or skull fractures who were admitted to our hospital during 2013-2018. According to the hospital's protocol, we performed platelet transfusion in patients taking antiplatelet drugs, prothrombin complex concentrate(PCC)administration in patients taking warfarin and direct oral anticoagulants except dabigatran: factor IX complex before January 2018 and four-factor PCC after February 2018. We administered idarucizumab in the case of dabigatran. Fresh frozen plasma transfusion was additionally performed in operative cases., Results: Twenty-six patients took antithrombotic drugs. There was no significant difference in the ratio of talk and deteriorate, favorable outcome(Glasgow Outcome Scale: good recovery+moderate disability), and hospitalization period between the non-antithrombotic and antithrombotic administration groups involving reversal. The timing of antithrombotic drug resumption varied, but no major embolic event occurred during the follow-up period., Conclusion: This study suggests that reversal of antithrombotic drugs in geriatric traumatic brain injury may contribute to suppression of talk and deteriorate and lead to more favorable outcomes. As there are also contradictory reports about the utility of reversal, additional studies should be performed for confirmation.

Objective: Developed countries have rapidly aging populations and the use of antithrombotic drugs is increasing. We investigated the effects of antithrombotic drugs and reversal of these drugs in patients with geriatric traumatic brain injury (TBI)., Methods: Age, sex, mechanism of injury, Glasgow Coma Scale on admission, head computed tomography findings, antithrombotic therapy, acute exacerbation, and outcomes at discharge were examined in 711 patients with geriatric TBI, complicated with traumatic intracranial hemorrhage using data from the Japan Neurotrauma Data Bank Project 2015 (JNTDB P2015). These items were compared between patients who did and did not receive antithrombotic therapy. We also conducted a questionnaire survey of reversal of antithrombotic therapy at hospitals participating in the JNTDB P2015. Acute exacerbation was compared in hospitals that did and did not regularly use reversal of this therapy., Results: The major cause of injury was a fall. In head computed tomography, acute subdural hematoma was found in 65.7% of the subjects. Antithrombotic therapy was performed in 30.4% of subjects, and these subjects were significantly older than those who did not receive this therapy; many had a fall as the mechanism of injury, and the level of consciousness was significantly exacerbated with this therapy. In hospitals that performed regular reversal, late exacerbation of the level of consciousness was suppressed., Conclusions: Patients with geriatric TBI who are given antithrombotic drugs have a risk for late exacerbation, even if initially diagnosed with mild TBI. Therefore, there is a possibility that reversal of antithrombotic drugs is important to suppress the risk of deterioration of patients with TBI., (Copyright © 2019 Elsevier Inc. All rights reserved.)

d-dimer is a potential biomarker for the detection of traumatic brain injury (TBI). However, the mechanisms that trigger elevation of d-dimer in TBI remain unclear. The purpose of this study was to evaluate the reliability of d-dimer in blood as a biomarker for TBI and to determine the mechanisms involved in regulating its blood levels. Nine patients with moderate to severe isolated TBI (Glasgow Coma Scale [GCS] score 7-13) were admitted to our hospital from May 2013 to June 2014. Blood samples were collected from systemic arteries on arrival and at 1, 3, 5, and 7 days after injury. Blood levels of neuron specific enolase (NSE), d-dimer, and soluble tissue factor (sTF) were measured. NSE (33.4 ng/ml: normal <12.0 ng/ml) and d-dimer (56.1 μg/ml: normal <1.0 μg/ml) were elevated at admission and declined on day 1 after injury. At admission, there were significant correlations of d-dimer levels with NSE (R = 0.727, P = 0.026) and sTF (R = 0.803, P = 0.009) levels. The blood level of d-dimer accurately reflects the degree of brain tissue damage indicated by NSE levels. Our data suggest that release of sTF induced by brain tissue damage may activate the coagulation cascade, leading to elevation of d-dimer.