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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.

Burr hole surgery in the emergency room can be lifesaving for patients with acute subdural hematoma (ASDH). In the first part of this study, a strategy of combined burr hole surgery, a period of intracranial pressure (ICP) monitoring, and then craniotomy was examined for safe and effective treatment of ASDH. Since 2012, 16 patients with severe ASDH with indications for burr hole surgery were admitted to Kenwakai Otemachi Hospital. From 2012 to 2016, craniotomy was performed immediately after burr hole surgery (emergency [EM] group, n = 10). From 2017, an ICP sensor was placed before burr hole surgery. After a period for correction of traumatic coagulopathy, craniotomy was performed when ICP increased (elective [EL] group, n = 6). Patient background, bleeding tendency, intraoperative blood transfusion, and outcomes were compared between the groups. In the second part of the study, ICP was measured before and after burr hole surgery in seven patients (including two of the six in the EL group) to assess the effect of this surgery. Activated partial thromboplastin time (APTT) and prothrombin time-international normalized ratio (PT-INR) were significantly prolonged after craniotomy in the EM group, but not in the EL group, and the EM group tended to require a higher intraoperative transfusion volume. The rate of good outcomes was significantly higher in the EL group, and ICP was significantly decreased after burr hole surgery. These results suggest the value of burr hole surgery followed by ICP monitoring in patients with severe ASDH. Craniotomy can be performed safely using this method, and this may contribute to improved outcomes.

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.

Introduction: Elevated intracranial pressure(ICP)can cause secondary brain injury after severe traumatic brain injury(TBI), and ICP is the key factor that determines the outcome. Therefore, prediction of elevation of ICP during the course of the injury would allow for more effective care of patients with severe TBI. In this study, we investigated predictive factors for elevation of ICP in patients with severe acute subdural hematoma(ASDH)., Methods: Twenty patients with severe isolated ASDH were admitted to our hospital between January 2009 and April 2016. The patients were divided into two groups with a maximum ICP of ≥20mmHg(elevated ICP group)and <20mmHg(normal ICP group). Age, mechanism of injury, Glasgow Coma Scale score on admission, initial head computed tomography findings, vital signs, serological and blood gas examinations, initial ICP, and clinical outcome were evaluated., Results: The elevated ICP group had significantly higher initial ICP(5.0±3.1 vs. 30±22.4mmHg, p<0.01), arterial oxygen pressure(151.2±68.3 vs. 314.2±197.1mmHg, p<0.05), and activated partial thromboplastin time(APTT;28.17±3.1 vs. 35.96±8.0, p<0.05)at admission, and significantly lower fibrinogen level(273.3±65.1 vs. 188.1±82.4mg/dL, p<0.05)and favorable outcome rate(p<0.01)., Conclusions: Our results show that high initial ICP, APTT, and arterial oxygen and low fibrinogen levels are associated with ICP elevation in patients with severe ASDH. These factors might be useful for the indication of therapeutic methods such as decompressive craniectomy.

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.

Objective: Traditionally, angiographic vasospasm (aVS) has been thought to cause delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH). However, successful treatment of aVS alone does not result in improved neurological outcome. Therefore, there may be other potential causes of poor neurological outcome, including spreading depolarization (SD). A recent study showed beneficial effects of cilostazol on DCI and neurological outcome. The present prospective clinical trial and experimental study focused on effects of cilostazol on SDs., Methods: Fifty aSAH patients were treated with clip ligation and randomly assigned to a cilostazol (n = 23) or control group (n = 27). Effects of cilostazol on DCI, aVS, and SDs, measured with subdural electrodes, were examined. The effect of cilostazol on SD-induced perfusion deficits (spreading ischemia) was assessed in an aSAH-mimicking model., Results: There was a trend for less DCI in the cilostazol group, but it did not reach our threshold for statistical significance (13.0% vs 40.0%, odds ratio = 0.266, 95% confidence interval [CI] = 0.059-1.192, p = 0.084). However, the total SD-induced depression duration per recording day (22.2 vs 30.2 minutes, β = -251.905, 95% CI = -488.458 to -15.356, p = 0.043) and the occurrence of isoelectric SDs (0 vs 4 patients, β = -0.916, 95% CI = -1.746 to -0.085, p = 0.037) were significantly lower in the cilostazol group. In rats, cilostazol significantly shortened SD-induced spreading ischemia compared to vehicle (Student t test, difference = 30.2, 95% CI = 5.3-55.1, p = 0.020)., Interpretation: Repair of the neurovascular response to SDs by cilostazol, as demonstrated in the aSAH-mimicking model, may be a promising therapy to control DCI. Ann Neurol 2018;84:873-885., (© 2018 American Neurological Association.)

Thrombosed giant aneurysm of the V1 segment of the vertebral artery is rare, and there is controversy regarding the optimal method of treatment in this portion. Here, we report a thrombosed giant aneurysm of the V1 segment of the vertebral artery with a good clinical course with endovascular proximal artery occlusion of the vertebral artery. A 59-year-old woman presented with a large mass in the left side of the neck. Echographic examination revealed a mass measuring 42 × 38 × 48 mm in the left neck. Angiography showed a thrombosed giant aneurysm of the V1 segment of the left vertebral artery. Endovascular proximal artery occlusion of the vertebral artery was performed, and the aneurysm lessened gradually. Although a number of procedures have been developed to treat extracranial vertebral artery aneurysms, endovascular proximal artery occlusion is a good option to treat aneurysms in this portion.

Kupffer cells (KCs) are involved in the progression of liver diseases such as hepatitis and liver cancer. Several members of the fatty acid binding proteins (FABPs) are expressed by tissue macrophages, and FABP7 is localized only in KCs. To clarify the role of FABP7 in the regulation of KC function, we evaluated pathological changes of Fabp7 knockout mice during carbon tetrachloride-induced liver injury. During liver injury in Fabp7 knockout mice, serum liver enzymes were increased, cytokine expression (tumor necrosis factor-α, monocyte chemoattractant protein-1, and transforming growth factor-β) was decreased in the liver, and the number of KCs in the liver necrotic area was significantly decreased. Interestingly, in the FABP7-deficient KCs, phagocytosis of apoptotic cells was impaired, and expression of the scavenger receptor CD36 was markedly decreased. In chronic liver injury, Fabp7 knockout mice showed less fibrogenic response to carbon tetrachloride compared with wild-type mice. Taken together, FABP7 is involved in the liver injury process through its regulation of KC phagocytic activity and cytokine production. Such modulation of KC function by FABP7 may provide a novel therapeutic approach to the treatment of liver diseases., (Copyright © 2014 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)