Review of Temperature Management in Traumatic Brain Injuries.

Therapeutic hypothermia (TH) for severe traumatic brain injury has seen restricted application due to the outcomes of randomized controlled trials (RCTs) conducted since 2000. In contrast with earlier RCTs, recent trials have implemented active normothermia management in control groups, ensuring comparable intensities of non-temperature-related therapeutic interventions, such as neurointensive care. This change in approach may be a contributing factor to the inability to establish the efficacy of TH. Currently, an active temperature management method using temperature control devices is termed "targeted temperature management (TTM)". One of the goals of TTM for severe traumatic brain injury is the regulation of increased intracranial pressure, employing TTM as a methodology for intracranial pressure management. Additionally, fever in traumatic brain injury has been acknowledged as contributing to poor prognosis, underscoring the importance of proactively preventing fever. TTM is also employed for the preemptive prevention of fever in severe traumatic brain injury. As an integral component of current neurointensive care, it is crucial to precisely delineate the targets of TTM and to potentially apply them in the treatment of severe traumatic brain injury.

Endovascular Treatment for Posterior Communicating Artery Aneurysms with Oculomotor Nerve Palsy.

Objective: Coil embolization for the treatment of internal carotid artery-posterior communicating artery aneurysms (PComAAn) associated with oculomotor nerve palsy (ONP) remains controversial in terms of the therapeutic effect to improve ONP. Patients with PComAAn treated in our hospital were retrospectively analyzed to evaluate the effectiveness of coil embolization on ONP. Methods: Twenty-three patients who had coil embolization for PComAAn with ONP were included in the analysis. In the evaluation of postoperative outcome of ONP, complete resolution of all symptoms was considered as a total recovery. ONP with a few residual symptoms that are stable and not disabling was considered as a subtotal recovery and that with only a slight improvement as a partial recovery. Results: Preoperative ONP was complete palsy in 14 and partial palsy in nine cases. The mean maximum diameter of the aneurysms was 9.1 ± 3.5 mm (3-17 mm), and the mean time from the onset to treatment was 46.3 ± 98.4 days (0-300 days). The embolization state immediately after the procedure was complete occlusion in seven, neck remnant in eight, and body filling (BF) in eight cases. Total recovery was observed in nine, subtotal recovery in 11, and partial recovery in three cases. The mean time to any improvement in ONP was 6.0 ± 6.0 months (0.5-25 months). Comparing 20 cases with total plus subtotal recovery and three cases with partial recovery, five (25.0%) and three (100%) cases showed BF immediately after the procedure, respectively, which was statistically significant (P = 0.015). Conclusion: The analysis indicated that coil embolization for the treatment of PComAAn with ONP resulted in satisfactory recovery of ONP in 87% of the cases and the outcome of aneurysm embolization was related to improvement in ONP.

Case Series of Endovascular Therapy for Blood Blister-Like Aneurysm in Acute Phase.

Objective: Blood blister-like aneurysms (BBAs) of the internal carotid artery are highly challenging to treat due to their variable morphology and tendency for rupture and regrowth. Here, we report a single-institution experience of endovascular therapy (EVT) for BBA treatment. Methods: We retrospectively reviewed patients with ruptured BBA from 2006 to 2019. All patients in whom BBA was treated with EVT were included. Patients' aneurysmal characteristics, progression status, aneurysm occlusion on follow-up angiography, and modified Rankin Scale (mRS) score were recorded. Results: A total of 11 patients (5 women and 6 men) with the mean age of 46 ± 10 years were included in this study. As initial treatment, 9 patients were treated with stent-assisted coiling (SAC). Immediate angiographic results showed that 2 cases were body filling, 4 were neck remnant, and 3 were complete obliteration. Perioperative ischemic complications were not observed. On postoperative day 1, 2 patients suffered from rerupture, and their prognoses were poor. Retreatments were performed in 5 patients. Parent artery occlusion (PAO) was performed in 6 patients including 2 initial treatments and 4 retreatments. Symptomatic infarction developed in 2 patients. In 3 patients, bypass in combination with PAO was performed. Clinical data revealed discharge mRS scores of 0-2 and 3-6 in 4 and 7 patients, respectively. Conclusion: SAC is effective for the management of BBA. Careful follow-up and response are necessary after treatment with SAC.

Temporal and spatial changes in reactive astrogliosis examined by 18F-THK5351 positron emission tomography in a patient with severe traumatic brain injury.

BACKGROUND: The positron emission tomography (PET) radioligand 18F-THK5351 is now used to evaluate monoamine oxidase B expression in the reactive astrogliosis seen in various central nervous diseases. Traumatic brain injury (TBI) is known to induce reactive astrogliosis in the lesion site. This is a first report to examine the spatial and temporal changes in reactive astrogliosis as evaluated by 18F-THK5351 after a severe TBI. CASE PRESENTATION: A 27-year-old man suffering from a severe TBI with multiple brain contusions was examined using 18F-THK5351 PET/CT in the subacute and chronic phases after the injury. The first PET scan, performed 46 days after the TBI, showed intense uptake of 18F-THK5351 in and around the brain contusions. The second PET scan, performed 271 days after the TBI, showed reduced uptake of 18F-THK5351 at the original sites of the brain contusions and increased uptakes in the white matter surrounding the contusions and the corpus callosum. The patient exhibited sustained improvement of neuropsychological impairment between the two PET examinations and remarkable recovery from the severe TBI. CONCLUSIONS: There were evident temporal and spatial changes in 18F-THK5351 uptake in the traumatized brain between the two PET examinations. These changes may have been related to the remarkable neurological recovery in this patient. The degree and distribution of reactive astrogliosis detected by 18F-THK5351 PET may be useful in assessing pathophysiology and predicting prognosis in TBI patients.

Hydrocephalus Following Experimental Subarachnoid Hemorrhage in Rats with Different Aerobic Capacity.

Low aerobic capacity is considered to be a risk factor for stroke, while the mechanisms underlying the phenomenon are still unclear. The current study looked into the impacts of different aerobic capacities on early brain injury in a subarachnoid hemorrhage (SAH) model using rats bred for high and low aerobic capacity (high-capacity runners, HCR; low-capacity runners, LCR). SAH was modeled with endovascular perforation in HCR and LCR rats. Twenty-four hours after SAH, the rats underwent behavioral testing and MRI, and were then euthanized. The brains were used to investigate ventricular wall damage, blood-brain barrier breakdown, oxidative stress, and hemoglobin scavenging. The LCR rats had worse SAH grades (p < 0.01), ventricular dilatation (p < 0.01), ventricular wall damage (p < 0.01), and behavioral scores (p < 0.01). The periventricular expression of HO-1 and CD163 was significantly increased in LCR rats (p < 0.01 each). CD163-positive cells were co-localized with HO-1-positive cells. The LCR rats had greater early brain injuries than HCR rats. The LCR rats had more serious SAH and extensive ventricular wall damage that evolved more frequently into hydrocephalus. This may reflect changes in iron handling and neuroinflammation.

Association between physical restraint requirement and unfavorable neurologic outcomes in subarachnoid hemorrhage.

BACKGROUND: Physical restraint has been commonly indicated to patients with brain dysfunction in neurocritical care. The effect of physical restraints on outcomes of critically ill adults remains controversial as no randomized controlled trials have compared its safety and efficacy, and the association between physical restraint requirement and neurological outcome in patients with subarachnoid hemorrhage (SAH) has not been fully examined. The aim of this study was to examine the association between physical restraint requirement and neurological outcomes in patients with SAH. METHODS: A single-center, retrospective study was conducted on patients with acute phase SAH treated for > 72 h in the intensive care unit from 2014 to 2020. Patients were divided into three groups based on the amount of time required for physical restraint during the first 24-72 h after admission: no, intermittent, and continuous use of physical restraint. Unfavorable neurologic outcome, assessed using the modified Rankin scale upon hospital discharge, has been considered as primary end point. RESULTS: Overall, 101 patients were included in the study, with 52 patients (51.5%) having unfavorable neurological outcomes. Among them, 46 patients (45.5%) did not use physical restraint, and 55 (54.5%) patients used physical restraint during the first 24-72 h after admission: 26 (25.7%) intermittent and 29 (28.7%) continuous. Multivariable logistic regression analysis showed that continuous use of physical restraint during the first 24-72 h after admission was significantly associated with unfavorable neurological outcomes in patients with SAH (odds ratio, 3.54; 95% confidence interval, 1.05-13.06; p = 0.042) compared with no physical restraint. CONCLUSIONS: Continuous use of physical restraint during the first 24-72 h after admission was more significantly associated with unfavorable neurological outcomes than no physical restraint among patients with SAH during the acute phase.

Traumatic Brain Injury by Weight-Drop Method Causes Transient Amyloid-ß Deposition and Acute Cognitive Deficits in Mice.

There has been growing awareness of the correlation between an episode of traumatic brain injury (TBI) and the development of Alzheimer's disease (AD) later in life. It has been reported that TBI accelerated amyloid-ß (Aß) pathology and cognitive decline in the several lines of AD model mice. However, the short-term and long-term effects of TBI by the weight-drop method on amyloid-ß pathology and cognitive performance are unclear in wild-type (WT) mice. Hence, we examined AD-related histopathological changes and cognitive impairment after TBI in wild-type C57BL6J mice. Five- to seven-month-old WT mice were subjected to either TBI by the weight-drop method or a sham treatment. Seven days after TBI, the WT mice exhibited significantly lower spatial learning than the sham-treated WT mice. However, 28 days after TBI, the cognitive impairment in the TBI-treated WT mice recovered. Correspondingly, while significant amyloid-ß (Aß) plaques and amyloid precursor protein (APP) accumulation were observed in the TBI-treated mouse hippocampus 7 days after TBI, the Aß deposition was no longer apparent 28 days after TBI. Thus, TBI induced transient amyloid-ß deposition and acute cognitive impairments in the WT mice. The present study suggests that the TBI could be a risk factor for acute cognitive impairment even when genetic and hereditary predispositions are not involved. The system might be useful for evaluating and developing a pharmacological treatment for the acute cognitive deficits.

Association of Brain CD163 Expression and Brain Injury/Hydrocephalus Development in a Rat Model of Subarachnoid Hemorrhage.

Hemoglobin contributes to brain cell damage and death following subarachnoid hemorrhage (SAH). While CD163, a hemoglobin scavenger receptor, can mediate the clearance of extracellular hemoglobin it has not been well-studied in SAH. In the current study, a filament perforation SAH model was performed in male rats. T2-weighted and T2*-weighted scans were carried out using a 7.0-Tesla MR scanner 24 h after perforation. T2 lesions and hydrocephalus were determined on T2-weighted images. A grading system based on MRI was used to assess SAH severity. The effects of SAH on CD163 were determined by immunohistochemistry staining and Western blots. SAH led to a marked increase in CD163 levels in cortex, white matter and periventricular regions from days 1 to 7. CD163 stained cells were co-localized with neurons, microglia/macrophages, oligodendrocytes and cleaved caspase-3-positive cells, but not astrocytes. Furthermore, CD163 protein levels were increased in rats with higher SAH grades, the presence of T2 lesions on MRI, or hydrocephalus. In conclusion, CD163 expression is markedly upregulated after SAH. It is associated with more severe hemorrhage, as well as MRI T2 lesion and hydrocephalus development.

Feasibility and Safety of Intravascular Temperature Management for Severe Heat Stroke: A Prospective Multicenter Pilot Study.

OBJECTIVES: Heat stroke is a life-threatening condition with high mortality and morbidity. Although several cooling methods have been reported, the feasibility and safety of treating heat stroke using intravascular temperature management are unclear. This study evaluated the efficacies of conventional treatment with or without intravascular temperature management for severe heat stroke. DESIGN: Prospective multicenter study. SETTING: Critical care and emergency medical centers at 10 tertiary hospitals. PATIENTS: Patients with severe heat stroke hospitalized during two summers. INTERVENTIONS: Conventional cooling with or without intravascular temperature management. MEASUREMENTS AND MAIN RESULTS: Cooling efficacy, Sequential Organ Failure Assessment score, occurrence rate of serious adverse events, and prognosis based on the modified Rankin Scale and Cerebral Performance Category. Patient outcomes were compared between five centers that were prospectively assigned to perform conventional cooling (control group: eight patients) and five centers that were assigned to perform conventional cooling plus intravascular temperature management (intravascular temperature management group: 13 patients), based on equipment availability. Despite their higher initial temperatures, all patients in the intravascular temperature management group reached the target temperature of 37°C within 24 hours, although only 50% of the patients in the control group reached 37°C (p < 0.01). The intravascular temperature management group also had a significant decrease in the Sequential Organ Failure Assessment score during the first 24 hours after admission (4.0 vs 1.5; p = 0.04). Furthermore, the intravascular temperature management group experienced fewer serious adverse events during their hospitalization, compared with the control group. The percentages of favorable outcomes at discharge and 30 days after admission were not statistically significant. CONCLUSIONS: 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.

Association between dexmedetomidine use and neurological outcomes in aneurysmal subarachnoid hemorrhage patients: A retrospective observational study.

PURPOSE: Recent studies in animal subarachnoid hemorrhage (SAH) models have reported that dexmedetomidine (DEX) use demonstrates significantly better neurological outcomes. This study aimed to evaluate whether DEX use is associated with favorable neurological outcomes (FO) in SAH patients. MATERIALS AND METHODS: We retrospectively reviewed all SAH patients between 2009 and 2017. We calculated the total dosage of DEX administered for the first 24h after admission. All patients were classified into no use, low dosage, and standard dosage group. Multivariate analysis was performed to clarify the association between DEX use and FO (modified Ranking Scale score of 0-2 at hospital discharge). RESULTS: There were 161 patients with 55.3% of FO. On univariate analysis, there were significant differences with regard to age, Hunt and Kosnik (H&K) grade, and DEX use. Multivariate analysis showed that age, H&K grade, and low dosage DEX (rather than no use) (odds ratio (OR) 3.17; 95% confidence interval (CI), 1.24-8.53; p=0.02) were significantly associated with FO. However, standard dosage DEX was not a significant factor (OR, 0.75; 95% CI, 0.25-2.16; p=0.59). CONCLUSIONS: Low dosage DEX during the first 24h after admission was associated with FO in SAH patients.

Blood Glucose Variability: A Strong Independent Predictor of Neurological Outcomes in Aneurysmal Subarachnoid Hemorrhage.

PURPOSE: In patients with aneurysmal subarachnoid hemorrhage (SAH), increased glucose variability (GV) is associated with increased mortality and cerebral infarction; however, there are no reports demonstrating an association between GV and neurological outcome. This study investigated whether GV had an independent effect on neurological outcomes in patients with SAH in the intensive care unit. MATERIALS AND METHODS: Consecutive adult patients hospitalized with SAH between January 1, 2009, and May 31, 2015 (N = 122) were retrospectively reviewed. Univariate/multivariate analyses were performed to identify independent predictors of poor neurological outcome. Patients were divided according to the mean glucose level (80-139 vs 140-200 mg/dL) and further subdivided using quartiles (Q) of the standard deviation (SD, representing variability) of the glucose level (Q1, Q2 + 3, and Q4). RESULTS: Unfavorable neurological outcomes occurred in 44.2% of the patients. On multiple regression analysis, age, Hunt and Kosnik grade, SD of glucose (odds ratio [OR], 1.09; 95% confidence interval [CI], 1.02-1.17; P < .01), and minimum blood glucose level (OR, 0.95; 95% CI, 0.91-0.99; P < .01) were significantly associated with unfavorable neurological outcomes. Both groups (mean glucose levels: 80-139 and 140-200 mg/dL groups) had increasing unfavorable neurological outcomes with increasing SD of glucose (Q1, 15.0%; Q2 + 3, 40.0%; Q4, 52.4% and Q1, 44.4%; Q2 + 3, 50%; Q4, 88.9% in the 80-139 and 140-200 mg/dL groups, respectively). Patients with minimum glucose of <90 mg/dL comprised >50% of unfavorable neurological outcome. CONCLUSION: Increased GV was an independent predictor of unfavorable neurological outcomes in patients with SAH.

Clinical characteristics of non-convulsive status epilepticus diagnosed by simplified continuous electroencephalogram monitoring at an emergency intensive care unit.

Aim: The present study aimed to elucidate the clinical characteristics of non-convulsive status epilepticus (NCSE) in patients with altered mental status (AMS). Methods: This single-center retrospective study comprised 149 patients who were hospitalized between March 1, 2015 and September 30, 2015 at the emergency intensive care unit (ICU) of the Kagawa University Hospital (Kagawa, Japan). The primary outcome was NCSE incidence. The secondary outcome was the comparison of duration of ICU stay, hospital stay, and a favorable neurological outcome, as assessed using the modified Rankin Scale score, at discharge from our hospital between patients with and without NCSE. Favorable neurological outcome and poor neurological outcome were defined as modified Rankin Scale scores of 0-2 and 3-6, respectively. Results: Simplified continuous electroencephalogram was used to monitor 36 patients (median age, 68 years; 69.4% males) with acute AMS; among them, NCSE was observed in 11 (30.1%) patients. Rates of favorable neurological outcome, duration of ICU stay, and hospital stay were not significantly different between the NCSE and non-NCSE groups (P = 0.45, P = 0.30, and P = 0.26, respectively). Conclusion: Approximately 30% of the patients with AMS admitted to emergency ICUs developed NCSE. The outcomes of AMS patients with and without NCSE did not differ significantly when appropriate medical attention and antiepileptic drugs were initiated. Simplified continuous electroencephalogram monitoring may be recommended in patients with AMS in emergency ICU to obtain early detection of NCSE followed by appropriate intervention.

Serial blood lactate measurements and its prognostic significance in intensive care unit management of aneurysmal subarachnoid hemorrhage patients.

PURPOSE: This study assesses the behavior of serial blood lactate measurements during intensive care unit (ICU) stay to identify prognostic factors of unfavorable neurological outcomes (UO) in patients with aneurysmal subarachnoid hemorrhage (SAH). METHODS: We retrospectively reviewed all patients who were consecutively hospitalized with SAH between 2009 and 2016. Arterial blood lactate levels were routinely obtained on admission and every 6h in the ICU. Univariate/multivariate analyses were performed to identify independent predictors of UO (modified Rankin scale of 3-6 upon hospital discharge). RESULTS: There were 145 patients with 46% of UO. Initially, increased lactate levels reached maximum levels during the first 24h and then decreased to within the normal range. Then, the levels slightly increased again to within the normal range for the next 24h, especially in UO. On multiple regression analysis, lactate levels measured at 24h, and 48h after admission were strong predictors of UO. Lactate level measured at 48h after admission demonstrated the greatest accuracy and the highest specificity (area under the curve, 0.716; sensitivity, 40%; specificity, 92.1%). CONCLUSIONS: The lactate level at 48h after admission was the most accurate predictor of UO with a high specificity in SAH patients.

Target Serum Sodium Levels During Intensive Care Unit Management of Aneurysmal Subarachnoid Hemorrhage.

INTRODUCTION: Dysnatremia commonly occur in the intensive care unit (ICU) management of patients with aneurysmal subarachnoid hemorrhage (SAH). However, detailed management strategies have not been provided even by current guidelines. The purposes of this study were to examine the association of abnormal serum sodium levels with unfavorable neurologic outcomes and to identify the target range of serum sodium in patients with SAH. METHODS: We retrospectively reviewed all patients who were consecutively hospitalized with a confirmed diagnosis of SAH between January 2009 and December 2015. Univariate/multivariate analyses were performed to identify the independent predictors of an unfavorable neurologic outcome (modified Rankin scale of 3-6 upon hospital discharge). RESULTS: There were 131 patients included in this study. Unfavorable neurologic outcomes occurred in 45% of patients. On multiple regression analysis, age, Hunt and Kosnik grade, and serum sodium levels in the ICU at the maximum [odds ratio (OR), 1.18; 95% CI, 1.05-1.35; P < 0.01] and minimum (OR, 0.88; 95% CI, 0.77-0.99; P = 0.048) values were significantly associated with unfavorable neurologic outcomes. The receiver operating characteristic curve analysis showed that the cut-off serum sodium levels were 145 mmol/L for maximum value and 132 mmol/L for minimum value. Patients with hyponatremia and hypernatremia during the first 2 weeks in the ICU accounted for 88.2% of patients with an unfavorable neurologic outcome; whereas, those with normal sodium levels accounted for only 15.6%. CONCLUSIONS: In patients with SAH, both hyponatremia and hypernatremia during ICU management were significantly associated with unfavorable neurologic outcomes.

Data on amyloid precursor protein accumulation, spontaneous physical activity, and motor learning after traumatic brain injury in the triple-transgenic mouse model of Alzheimer׳s disease.

This data article contains supporting information regarding the research article entitled "Traumatic brain injury accelerates amyloid-ß deposition and impairs spatial learning in the triple-transgenic mouse model of Alzheimer׳s disease" (H. Shishido, Y. Kishimoto, N. Kawai, Y. Toyota, M. Ueno, T. Kubota, Y. Kirino, T. Tamiya, 2016) [1]. Triple-transgenic (3×Tg)-Alzheimer׳s disease (AD) model mice exhibited significantly poorer spatial learning than sham-treated 3×Tg-AD mice 28 days after traumatic brain injury (TBI). Correspondingly, amyloid-ß (Aß) deposition within the hippocampus was significantly greater in 3×Tg-AD mice 28 days after TBI. However, data regarding the short-term and long-term influences of TBI on amyloid precursor protein (APP) accumulation in AD model mice remain limited. Furthermore, there is little data showing whether physical activity and motor learning are affected by TBI in AD model mice. Here, we provide immunocytochemistry data confirming that TBI induces significant increases in APP accumulation in 3×Tg-AD mice at both 7 days and 28 days after TBI. Furthermore, 3×Tg-AD model mice exhibit a reduced ability to acquire conditioned responses (CRs) during delay eyeblink conditioning compared to sham-treated 3×Tg-AD model mice 28 days after TBI. However, physical activity and motor performance are not significantly changed in TBI-treated 3×Tg-AD model mice.

Traumatic brain injury accelerates amyloid-ß deposition and impairs spatial learning in the triple-transgenic mouse model of Alzheimer's disease.

Several pathological and epidemiological studies have demonstrated a possible relationship between traumatic brain injury (TBI) and Alzheimer's disease (AD). However, the exact contribution of TBI to AD onset and progression is unclear. Hence, we examined AD-related histopathological changes and cognitive impairment after TBI in triple transgenic (3×Tg)-AD model mice. Five- to seven-month-old 3×Tg-AD model mice were subjected to either TBI by the weight-drop method or a sham treatment. In the 3×Tg-AD mice subjected to TBI, the spatial learning was not significantly different 7 days after TBI compared to that of the sham-treated 3×Tg-AD mice. However, 28 days after TBI, the 3×Tg-AD mice exhibited significantly lower spatial learning than the sham-treated 3×Tg-AD mice. Correspondingly, while a few amyloid-ß (Aß) plaques were observed in both sham-treated and TBI-treated 3×Tg-AD mouse hippocampus 7 days after TBI, the Aß deposition was significantly greater in 3×Tg-AD mice 28 days after TBI. Thus, we demonstrated that TBI induced a significant increase in hippocampal Aß deposition 28 days after TBI compared to that of the control animals, which was associated with worse spatial learning ability in 3×Tg-AD mice. The present study suggests that TBI could be a risk factor for accelerated AD progression, particularly when genetic and hereditary predispositions are involved.

Association Between Comorbidities, Nutritional Status, and Anticlotting Drugs and Neurologic Outcomes in Geriatric Patients with Traumatic Brain Injury.

BACKGROUND: Several studies using trauma data banks and registers showed that age, Glasgow Coma Scale (GCS), Injury Severity Score, and intraventricular hemorrhage were independent factors for neurologic outcomes in geriatric patients with traumatic brain injury (TBI). However, these analyses did not comprehensively evaluate factors particularly associated with geriatric patients. We aimed to identify factors particularly associated with geriatric patients that affect neurologic outcomes in TBI. METHODS: Patients aged ≥65 years who were hospitalized consecutively in Kagawa University Hospital with severe TBI between 1 January 2008 and 31 October 2015 were retrospectively reviewed. We evaluated background factors particularly associated with geriatric patients, including comorbidities (Charlson Comorbidity Index [CCI]), nutritional status (serum albumin level), and presence/absence of antiplatelet and anticoagulant drugs, in addition to baseline characteristics. Multivariate analyses were performed to identify independent predictors of unfavorable neurologic outcomes (UO), as defined as a Glasgow Outcome Scale score of 1-3 at discharge from hospital. The association between CCI and UO was evaluated in a subgroup analysis. RESULTS: UO occurred in 65.0% of 140 patients. Multivariate analyses showed that the CCI (odds ratio, 1.91; 95% confidence interval, 1.21-3.29; P = 0.011), age, and GCS were independent predictors of UO. In subgroup analyses of patients with an initial GCS score of 13-15, the rate of UO significantly increased with CCI score (CCI 0, 35.5%; CCI 1 or 2, 39.4%; CCI >2, 83.3%; P < 0.01). CONCLUSIONS: CCI was an independent predictor of UO in geriatric patients with severe TBI.

Invasive group B streptococcal infection in a patient with post splenectomy for hypersplenism secondary to liver cirrhosis and portal hypertension.

BACKGROUND: Splenectomy in patients with liver cirrhosis (LC) is expected to become more common owing to its efficacy on portal hemodynamics. In this report we describe an alarming case of group B streptococcus (GBS) infection after splenectomy in a patient with LC. METHODS: A 72-year-old woman with a history of LC was admitted to our emergency department because of respiratory failure. The patient had received left lateral segmentectomy of the liver and splenectomy three months before admission. Pulmonary examination revealed significant wheezing during inspiration and expiration, but no crackles and stridor. Chest radiography and CT showed no infiltrates. A presumptive diagnosis of bronchial asthma caused by upper respiratory infection was made. Four days after admission, GBS infection was confirmed by blood culture and penicillin G was administered. Antibiotics were given intravenously for a total of 12 days. RESULTS: The patient was discharged on the 12th day after admission. CONCLUSIONS: Although efficacy of splenectomy in patients with LC has been reported, immune status should be evaluated for a longer period. Patients who have undergone splenectomy are highly susceptible to bacteria; moreover, LC itself is an independent risk factor for mortality in patients with sepsis. Since prophylaxis against GBS has not been established, immediate action should be taken. Emergency physicians should be aware of invasive GBS infection in the context of the critical risk factors related to splenectomy and LC, particularly the expected increase of splenectomy performed in LC patients.

Successful treatment of non-convulsive status epilepticus diagnosed using bedside monitoring by a combination of amplitude-integrated and two-channel simplified electroencephalography.

Case: A 66-year-old man developed disturbed consciousness and right hemiparesis with transient convulsions in the right arm. Bedside monitoring using a combination of amplitude-integrated electroencephalography and two-channel simplified electroencephalography revealed intermittent episodes of 1-3 Hz δ waves lasting for approximately 5 min, consistent with non-convulsive status epilepticus. Fosphenytoin (22.5 mg/kg/day) and levetiracetam (1,000 mg) prevented right arm convulsions but did not restore consciousness. The two-channel simplified electroencephalography also showed an intermittent periodic δ wave pattern in the Fp1-C3 channel. Conventional electroencephalography revealed a polymorphic δ activity that was abolished by 2.5 mg diazepam, thus confirming the diagnosis of non-convulsive status epilepticus. Outcome: The patient recovered completely with the antiepileptic drug combination. Conclusion: Immediate initiation of bedside monitoring using amplitude-integrated electroencephalography and two-channel simplified electroencephalography allows early detection of non-convulsive status epilepticus in patients with disturbed consciousness, which considerably improves the prognosis.

Role of lipocalin 2 in intraventricular haemoglobin-induced brain injury.

OBJECTIVE: Our recent studies have shown that blood components, including haemoglobin and iron, contribute to hydrocephalus development and brain injury after intraventricular haemorrhage (IVH). The current study investigated the role of lipocalin 2 (LCN2), a protein involved in iron handling, in the ventricular dilation and neuroinflammation caused by brain injury in a mouse model of IVH. DESIGN: Female wild-type (WT) C57BL/6 mice and LCN2-deficient (LCN2-/-) mice had an intraventricular injection of haemoglobin, and control mice received an equivalent amount of saline. MRI was performed presurgery and postsurgery to measure ventricular volume and the brains were used for either immunohistochemistry or western blot. RESULTS: Ventricular dilation was observed in WT mice at 24 h after haemoglobin (25 mg/mL, 20 µL) injection (12.5±2.4 vs 8.6±1.5 mm3 in the control, p<0.01). Western blotting showed that LCN2 was significantly upregulated in the periventricular area (p<0.01). LCN2 was mainly expressed in astrocytes, whereas the LCN2 receptor was detected in astrocytes, microglia/macrophages and neurons. Haemoglobin-induced ventricle dilation and glia activation were less in LCN2-/- mice (p<0.01). Injection of high-dose haemoglobin (50 mg/mL) resulted in lower mortality in LCN2-/- mice (27% vs 86% in WT; p<0.05). CONCLUSIONS: Intraventricular haemoglobin caused LCN2 upregulation and ventricular dilation. Haemoglobin resulted in lower mortality and less ventricular dilation in LCN2-/- mice. These results suggest that LCN2 has a role in haemoglobin-induced brain injury and may be a therapeutic target for IVH.