Outcome In Traumatic Brain Injury Patients Research Articles

Impact of fibrinogen level on the prognosis of patients with traumatic brain injury: a single-center analysis of 2570 patients

BackgroundFibrinogen may play an important role in the survival of trauma patients; however, its role in traumatic brain injury (TBI) and its correlation with disease prognosis remain poorly understood. The aims of this study were to determine the incidence of TBI-associated hypofibrinogenemia in patients with TBI and to evaluate the prognostic value of fibrinogen level with respect to mortality and clinical outcomes.MethodsA total of 2570 consecutive TBI patients were retrospectively studied. Prognostic evaluations were determined using the Glasgow Outcome Score (GOS) assessment 3 months after injury. The shape of the relationship between fibrinogen level and mortality or outcome was examined using cubic spline functions. Logistic regression analyses were conducted to identify the association between fibrinogen level and 3-month functional outcomes.ResultsFibrinogen concentrations < 2 g/L were observed in 992 (38.6%) patients at the time of admission. Multivariate analyses showed that for patients with fibrinogen levels < 2.0 g/L, those levels were an independent prognostic factor for 3-month mortality (odds ratio [OR], 0.91; 95% confidence interval [CI], 0.89–0.93; P < .001). By contrast, for patients with fibrinogen levels < 2.5 g/L, the levels were an independent prognostic factor for favorable outcomes at 3 months (OR, 1.654; 95% CI, 1.186–2.306; P = .003). Similar results were also seen for patients with fibrinogen levels > 3.0 g/L, with the levels being an independent prognostic factor for favorable outcomes at 3 months (OR, 0.771; 95% CI, 0.607–0.979; P = .033).ConclusionsFibrinogen is an independent prognostic factor for clinical outcomes in TBI patients. Maintaining the level of fibrinogen between 2.5 and 3 g/L may improve clinical outcomes in patients with TBI.

Lung Injury Is a Predictor of Cerebral Hypoxia and Mortality in Traumatic Brain Injury

Background: A major contributor to unfavorable outcome after traumatic brain injury (TBI) is secondary brain injury. Low brain tissue oxygen tension (PbtO2) has shown to be an independent predictor of unfavorable outcome. Although PbtO2 provides clinicians with an understanding of the ischemic and non-ischemic derangements of brain physiology, its value does not take into consideration systemic oxygenation that can influence patients' outcomes. This study analyses brain and systemic oxygenation and a number of related indices in TBI patients: PbtO2, partial arterial oxygenation pressure (PaO2), PbtO2/PaO2, ratio of PbtO2 to fraction of inspired oxygen (FiO2), and PaO2/FiO2. The primary aim of this study was to identify independent risk factors for cerebral hypoxia. Secondary goal was to determine whether any of these indices are predictors of mortality outcome in TBI patients.Materials and Methods: A single-centre retrospective cohort study of 70 TBI patients admitted to the Neurocritical Care Unit (NCCU) at Cambridge University Hospital in 2014–2018 and undergoing advanced neuromonitoring including invasive PbtO2 was conducted. Three hundred and three simultaneous measurements of PbtO2, PaO2, PbtO2/PaO2, PbtO2/FiO2, PaO2/FiO2 were collected and mortality at discharge from NCCU was considered as outcome. Generalized estimating equations were used to analyse the longitudinal data.Results: Our results showed PbtO2 of 28 mmHg as threshold to define cerebral hypoxia. PaO2/FiO2 found to be a strong and independent risk factor for cerebral hypoxia when adjusting for confounding factor of intracranial pressure (ICP) with adjusted odds ratio of 1.78, 95% confidence interval of (1.10–2.87) and p-value = 0.019. With respect to TBI outcome, compromised values of PbtO2, PbtO2/PaO2, PbtO2/FiO2, and PaO2/FiO2 were all independent predictors of mortality while considered individually and adjusting for confounding factors of ICP, age, gender, and cerebral perfusion pressure (CPP). However, when considering all the compromised values together, only PaO2/FiO2 became an independent predictor of mortality with adjusted odds ratio of 3.47 (1.20–10.04) and p-value = 0.022.Conclusions: Brain and Lung interaction in TBI patients is a complex interrelationship. PaO2/FiO2 seems to be a major determinant of cerebral hypoxia and mortality. These results confirm the importance of employing ventilator strategies to prevent cerebral hypoxia and improve the outcome in TBI patients.

Serum bilirubin level correlates with mortality in patients with traumatic brain injury.

As a catabolic product of hemoglobin, bilirubin has been confirmed playing an important role in the development of various central nervous system disease. The aim of this study is to explore the correlation between serum bilirubin level and mortality in patients with traumatic brain injury (TBI).Patients admitted with traumatic brain injury (TBI) in our hospital between January 2015 and January 2018 were enrolled in this study. Clinical and laboratory data of 361 patients were retrospectively collected to explore the independent risk factors of mortality.The comparison of baseline characteristics showed that non-survivors had lower Glasgow Coma Scale (GCS) (P < .001) and higher level of serum total bilirubin (TBIL) (P < .001) and direct bilirubin (DBIL) (P < .001). We found that only GCS (P < .001), glucose (P < .001), lactate dehydrogenase (LDH) (P = .042) and DBIL (P = .005) were significant risk factors in multivariate logistic regression analysis. GCS and DBIL had comparable AUC value (0.778 vs 0.750, P > .05) on predicting mortality in TBI patients. The AUC value of the combination of GCS and DBIL is higher than the single value of these two factors (P < .05). Moreover, predictive model 1 consisted of GCS, glucose, LDH and DBIL had the highest AUC value of 0.894.DBIL is a significant risk factor of mortality in TBI patients. Assessing the level of DBIL is beneficial for physicians to evaluate severity and predict outcome for TBI patients.

Hubungan Kadar Natrium Serum dengan Outcome Klinis pada Pasien Cedera Kepala Berat di RSUD Abdul Wahab Sjahranie Samarinda

Recently, Traumatic Brain Injury (TBI) has high mortality in the world. In severe TBI, secondary brain injury can occur. ElectrSolyte disorders are the most common in secondary brain insult especially sodium disorders. It remains unclear whether hyponatremia or hypernatremia can cause worse clinical outcome in TBI patients. This study aimed to determine association between serum sodium level with clinical outcome in severe TBI patients at RSUD Abdul Wahab Sjahranie Samarinda. A cross sectional analytical study by taking samples to the patients with diagnosed severe TBI (GCS ≤ 8) which were hospitalized at RSUD Abdul Wahab Sjahranie Samarinda in the period of January-December 2018 that complied inclusion and exclusion criteria. Research variables are sodium serum level and clinical outcome that was assessed by structured interviews for Glasgow Outcome Scale (GOS). The relationship between variables was done using the Fisher's Exact test. A total of 41 severe TBI patients were administered. The characteristics of the sample were the most patients in 20s-40s (46.3%), patients were dominated by male (82.9%) and the most common CT scan characteristic were epidural hematoma (29.3%). The most of patients showed normonatremia in 25 patients (61%), 9 patients (22%) had hypernatremia and 7 patients (17.1%) had hyponatremia. The most clinical outcome on severe TBI patients were worse outcome with 70.7% while good outcome with 29.3%. Statistical result showed there’s no association between serum sodium level (hyponatremia and hypernatremia) with clinical outcome in severe TBI patients with p values, 1.000 and 0.225, respectively. There’s no association between serum sodium level with clinical outcome in severe TBI patients.

CRP Albumin ratio is positively associated with poor outcome in patients with traumatic brain injury

ObjectivesThe C-reactive protein/albumin ratio (CAR), a novel inflammation-based index, has been proved useful in predicting outcome of various diseases. We designed this study to explore the prognostic value of CAR in patients with traumatic brain injury (TBI). Patients and methodsWe retrospectively included 151 patients diagnosed with TBI and collected related clinical and laboratory data. Univariate and multivariate logistic regression were conducted to find independent risk factors of mortality. Then, we incorporated CAR into prognostic model and drew receiver operating characteristic (ROC) curve of models. Finally, we compared the predictive value of different models by evaluating the area under the receiver operating characteristic curves (AUC). ResultsIn this study, a total of 54 patients had poor survival outcome with mortality rate of 35.8 %. Results of multivariate analysis showed that GCS score in admission (OR 0.700, 95 %Cl 0.570−0.860, p=0.001), acute kidney injury (AKI) (OR 3.952, 95Cl 1.631−9.577, p=0.002) and CAR (OR 1.202, 95Cl 1.039−1.390, p=0.013) were independently associated with in-hospital mortality. The AUC value of predictive model composed of the above three factors was higher than GCS or CAR alone. ConclusionCAR is an independent risk factor of mortality in patients with TBI. Incorporating CAR into predictive model could increase the value in predicting outcome of TBI patients.

Apoptosis in cerebrospinal fluid as outcome predictors in severe traumatic brain injury: An observational study.

Traumatic brain injury (TBI), due to its high mortality and morbidity, is an important research topic. Apoptosis plays a pathogenic role in a series of neurological disorders, from neurodegenerative diseases to acute neurological lesions.In this study, we analyzed the association between apoptosis and the Glasgow Outcome Scale (GOS), to examine the potential of apoptosis as a biomarker for a TBI outcome. Patients with severe TBI were recruited at the Department of Neurosurgery, Wujin Hospital Affiliated with Jiangsu University, between January 2018 and December 2019. As a control group, healthy subjects were recruited. The concentrations of caspase-3, cytochrome c, sFas, and caspase-9 in the cerebrospinal fluid (CSF) were analyzed by enzyme-linked immunosorbent assay (ELISA). The association between the GOS and the clinical variables age, sex, initial Glasgow Coma Scale (GCS) score, intracranial pressure (ICP), cerebral perfusion pressure (CPP), initial computed tomography (CT) findings, and apoptotic factors was determined using logistic regression. The area under the receiver operator characteristic (ROC) curve (AUC), and thus the sensitivity and specificity of each risk factor, were obtained.The levels of caspase-3, cytochrome c, sFas, and caspase-9 in the TBI group were significantly higher than those in the control group (P < .05). The logistic regression results showed that ICP and caspase-3 were significant predictors of outcome at 6 months post-TBI (P < .05). The AUC was 0.925 and 0.888 for ICP and caspase-3, respectively. However, the AUC for their combined prediction was 0.978, with a specificity and sensitivity of 96.0% and 95.2%, respectively, showing that the combined prediction was more reliable than that of the 2 separate factors.We demonstrated that caspase-3, cytochrome C, sFas, and caspase-9 were significantly increased in the CSF of patients following severe TBI. Furthermore, we found that ICP and caspase-3 were more reliable for outcome prediction in combination, rather than separately.

EPO treatment does not alter acute serum profiles of GFAP and S100B after TBI: A brief report on the Australian EPO-TBI clinical trial

PurposeTo determine the diagnostic and prognostic value of glial fibrillary acidic protein (GFAP) and S100B after traumatic brain injury (TBI) in an Erythropoietin (EPO) clinical trial and examine whether EPO therapy reduces biomarker concentrations. Materials and MethodsForty-four patients with moderate-to-severe TBI were enrolled to a sub-study of the EPO-TBI trial. Patients were randomized to either Epoetin alfa 40,000 IU or 1 ml sodium chloride 0.9 as subcutaneous injection within 24 h of TBI. ResultsGFAP and S100B were measured in serum by ELISA from D0 (within 24 h of injury, prior to EPO/vehicle administration) to D5. Biomarker concentrations were compared between injury severities, diffuse vs. focal TBI, 6-month outcome scores (GOS-E) and EPO or placebo treatments. At D0 GFAP was significantly higher than S100B (951 pg/mL vs. 476 pg/mL, p = 0.018). ROC analysis of S100B at 1D post-injury distinguished favorable vs. unfavorable outcomes (area under the curve = 0.73; p = 0.01). EPO did not reduce concentration of either biomarker. ConclusionsElevated serum concentrations of GFAP and S100B after TBI reflect a robust, acute glial response to injury. Consistent with lack of improved outcome in TBI patients treated with EPO and prior findings on neuronal and axonal markers, glial biomarker concentrations and acute profiles were not affected by EPO.

Increased Brain Tissue Oxygen Monitoring Threshold to Improve Hospital Course in Traumatic Brain Injury Patients

IntroductionThis article is a retrospective analysis of the neurosurgical census at our institution to determine an optimal threshold for brain tissue oxygenation (PbtO2). The use of brain tissue oxygen monitoring has been in place for approximately three decades but data suggesting optimal thresholds to improve outcomes have been lacking. Though there are multiple modalities to monitor cerebral oxygenation, the monitoring of brain tissue oxygen tension has been deemed the gold standard. Still, it is not clear exactly how reductions in PbtO2 should be treated or what appropriate thresholds to treat might be. The aim of our study was to determine if our threshold of 28 mmHg for a good functional outcome could be correlated to the Glasgow Coma Scale (GCS) and Glasgow Outcome Scale (GOS).MethodsA retrospective analysis of the Arrowhead Regional Medical Center (ARMC) Neurosurgery Census was performed. Patients from 2017-2019 who had placement of Licox® cerebral oxygen monitoring sensors (Integra® Lifesciences, Plainsboro Township, New Jersey) were included in the analysis. Fifteen patients were consecutively identified, all of which presented with traumatic brain injury (TBI). Data on age, gender, days in the intensive care unit (ICU), days before discharge or end of medical care, admission GCS, hospital length of stay, GOS, maximum and minimum PbtO2 values for five days following insertion, minimum and maximum intracranial pressures (ICPs), and brain temperature were included for analysis. Patient data were separated into two groups; those with consistently higher PbtO2 scores (≥ 28 mmHg; n = 7) and those with inconsistent/lower PbtO2 scores (< 28 mmHg; n = 8). Standard student t-tests were used to find potential statistical differences between the groups (α = 0.05).ResultsThere were seven patients in the consistently high PbtO2 category (≥ 28 mmHg) and eight patients in the inconsistent/low PbtO2 category (<28 mmHg). The average maximum and minimum PbtO2 for the group displaying worse outcomes (as defined by GCS/GOS) was 23.0 mmHg and 14 mmHg, respectively. Those with consistent Day 2 PbtO2 scores of ≥ 28 mmHg had significantly higher GCS scores at discharge/end of medical care (p < 0.05). Average GCS for the patient group with >28 mmHg PbtO2 averaged over Days 2-5 group was 11.4 (n=7). Average GCS for the <28 group was 7.0 (n=8). The GCS for the >28 group was 63% higher than found in the <28 group (p = 0.03). GOS scores were significantly higher in those with consistently higher PbtO2 (≥ 28) than those with lower PbtO2 scores (< 28). The averages were 3.5 in the higher PbtO2 group as compared to 2 in the lower PbtO2 group.ConclusionAlong with ICP monitors and monitoring in the assessment of CPP, brain tissue oxygenation allows yet another metric by which to optimize treatment in TBI patients. At our institution, a PbtO2 level of ≥ 28 mmHg is targeted in order to facilitate a good functional outcome in TBI patients. Keeping patients at this level improves GCS and GOS at discharge/end of medical treatment.

Mild and Moderate Traumatic Brain Injury and Gender-Based Critical Care Outcomes.

Traumatic brain injury (TBI) is a major contributor to death and complications. Previous studies have identified gender disparities among trauma patients. This study aims to examine the association between gender and outcomes in TBI patients. Review of our trauma registry: Patients were classified into groups according to their gender. Demographics extracted from the registry included age, injury severity score (ISS), Glasgow Coma Score (GCS), head abbreviated injury score (AIS), and the presence of an epidural hematoma (EDH). The primary outcome was mortality; secondary outcomes included ICU length of stay (ICU-LOS), craniotomy rate, ventilator-associated pneumonia (VAP), and readmission rates. Significance was defined as p < 0.05. Nine hundred and thirty-five patients with TBI were studied: 62.1% (n = 581) were male and 37.9% (n = 354) were female. There were no differences in GCS, ISS, and head AIS. Males were younger [53 (IQR 30-77) vs. 76 (IQR 49.25-84), p < 0.05] and were more likely to have an EDH (9.6% vs. 4.8%, p = 0.007). Males also had a longer median ICU-LOS [4days (IQR 2-8) vs. 3days (IQR 0-5), p < 0.05] and were significantly more likely to require a craniotomy (44.6% vs. 19.2%, p < 0.001). In addition, males were more likely to develop VAP (4.1% vs. 0.8%, p = 0.004). Predicted survival (79.2% vs. 72.9%) and actual mortality rates (4.5% vs. 4.5%) were similar in both genders (p > 0.05). In the context of our study, male patients with TBI were significantly younger, were more likely to sustain an EDH, and were also more likely to require a craniotomy, but mortality rates between both genders were similar. The male gender was also associated with a significantly increased ICU-LOS and VAP.

Aberrant ER Stress Induced Neuronal-IFNβ Elicits White Matter Injury Due to Microglial Activation and T-Cell Infiltration after TBI.

Persistent endoplasmic reticulum (ER) stress in neurons is associated with activation of inflammatory cells and subsequent neuroinflammation following traumatic brain injury (TBI); however, the underlying mechanism remains elusive. We found that induction of neuronal-ER stress, which was mostly characterized by an increase in phosphorylation of a protein kinase R-like ER kinase (PERK) leads to release of excess interferon (IFN)β due to atypical activation of the neuronal-STING signaling pathway. IFNβ enforced activation and polarization of the primary microglial cells to inflammatory M1 phenotype with the secretion of a proinflammatory chemokine CXCL10 due to activation of STAT1 signaling. The secreted CXCL10, in turn, stimulated the T-cell infiltration by serving as the ligand and chemoattractant for CXCR3+ T-helper 1 (Th1) cells. The activation of microglial cells and infiltration of Th1 cells resulted in white matter injury, characterized by impaired myelin basic protein and neurofilament NF200, the reduced thickness of corpus callosum and external capsule, and decline of mature oligodendrocytes and oligodendrocyte precursor cells. Intranasal delivery of CXCL10 siRNA blocked Th1 infiltration but did not fully rescue microglial activation and white matter injury after TBI. However, impeding PERK-phosphorylation through the administration of GSK2656157 abrogated neuronal induction of IFNβ, switched microglial polarization to M2 phenotype, prevented Th1 infiltration, and increased Th2 and Treg levels. These events ultimately attenuated the white matter injury and improved anxiety and depressive-like behavior following TBI.SIGNIFICANCE STATEMENT A recent clinical study showed that human brain trauma patients had enhanced expression of type-1 IFN; suggests that type-1 IFN signaling may potentially influence clinical outcome in TBI patients. However, it was not understood how TBI leads to an increase in IFNβ and whether induction of IFNβ has any influence on neuroinflammation, which is the primary reason for morbidity and mortality in TBI. Our study suggests that induction of PERK phosphorylation, a characteristic feature of ER stress is responsible for an increase in neuronal IFNβ, which, in turn, activates microglial cells and subsequently manifests the infiltration of T cells to induce neuroinflammation and subsequently white matter injury. Blocking PERK phosphorylation using GSK2656157 (or PERK knockdown) the whole cascade of neuroinflammation was attenuated and improved cognitive function after TBI.

Midline Shift vs. Mid-Surface Shift: Correlation with Outcome of Traumatic Brain Injuries.

Traumatic brain injury (TBI) is a major health and socioeconomic problem globally that is associated with a high level of mortality. Early and accurate diagnosis and prognosis of TBI is important in patient management and preventing any secondary injuries. Computer tomography (CT) imaging assists physicians in diagnosing injury and guiding treatment. One of the clinical parameters extracted from CT images is midline shift, a measure of linear displacement in brain structure, which is correlated with TBI patient outcomes. However, only a tiny fraction of the overall tissue displacement is quantified through this parameter. In this paper, a novel measurement of overall mid-surface shift is proposed that quantifies the total volume of brain tissue shifted across the midline. When compared to traditional midline shift, mid-surface shift has a stronger correlation with TBI patient outcomes.

Determination of serum tissue kallikrein levels after traumatic brain injury

BackgroundTissue kallikrein (TK) plays an important role in the kallikrein-kinin system. Its protective role has been demonstrated in traumatic brain injury (TBI). We attempted to determine relationship between serum TK levels and trauma severity in addition to clinical outcome in TBI. MethodsWe recruited 112 patients with severe TBI (Glasgow coma scale score < 9) and 112 controls. We configured 2 multivariate models to assess the relationship between serum TK levels and 30-day death. Its prognostic predictive ability was analyzed under receiver operating characteristic curve. ResultsTK levels were significantly lower in patients than in controls (median 0.148 mg/l, the upper - lower quartiles 0.121–0.185 vs. median 0.258 mg/l, the upper - lower quartiles 0.207–0.342, P < 0.001). TK levels were closely and positively correlated with Glasgow coma scale score (r = 0.550). TK levels <0.148 mg/l independently predicted 30-day mortality with odds ratio value of 4.752 (95% confidence interval (CI), 1.166–19.367) and 30-day overall survival with hazard ratio value of 3.698 (95% CI, 1.026–13.333). TK levels significantly discriminated 30-day mortality with area under curve of 0.822 (95% CI, 0.738–0.887). ConclusionsSerum TK can represent a potential predictor of clinical outcome in TBI patients.

Preinjury Statins Are Associated With Improved Survival in Patients With Traumatic Brain Injury

BackgroundStatins have been shown to improve outcomes in traumatic brain injury (TBI) in animal models. The aim of our study was to determine the effect of preinjury statins on outcomes in TBI patients. MethodsWe performed a 4-y (2014-2017) review of our TBI database and included all patients aged ≥18 y with severe isolated TBI. Patients were stratified into those who were on statins and those who were not and were matched (1:2 ratio) using propensity score matching. The primary outcome was in-hospital mortality. The secondary outcomes were skilled nursing facility disposition, Glasgow Outcome Scale–extended score, and hospital and intensive care unit length of stay (LOS). ResultsWe identified 1359 patients, of which 270 were matched (statin: 90, no-statin: 180). Mean age was 55 ± 8y, median Glasgow Coma Scale was 10 (8-12), and median head–abbreviated injury scale was 3 (3-5). Matched groups were similar in age, mechanism of injury, Glasgow Coma Scale, Injury Severity Score, neurosurgical intervention, type and size of intracranial hemorrhage, and preinjury anticoagulant or antiplatelet use. The overall in-hospital mortality rate was 18%. Patients who received statins had lower rates of in-hospital mortality (11% versus 21%, P = 0.01), skilled nursing facility disposition (19% versus 28%; P = 0.04), and a higher median Glasgow Outcome Scale–extended (11 [9-13] versus 9 [8-10]; P = 0.04). No differences were found between the two groups in terms of hospital LOS (6 [4-9] versus 5 [3-8]; P = 0.34) and intensive care unit LOS (3 [3-6] versus 4 [3-5]; P = 0.09). ConclusionsPreinjury statin use in isolated traumatic brain injury patients is associated with improved outcomes. This finding warrants further investigations to evaluate the potential beneficial role of statins as a therapeutic drug in a TBI. Level of evidenceLevel III Therapeutic.

A retrospective study of the effect of fibrinogen levels during fresh frozen plasma transfusion in patients with traumatic brain injury.

The association between traumatic brain injury (TBI) and coagulopathy is well established. While coagulopathy prophylaxis in TBI involves replenishing coagulation factors with fresh frozen plasma (FFP), its effectiveness is controversial. We investigated the relationship between plasma fibrinogen concentration 3h after initiating FFP transfusion and outcomes and evaluated the correlation with D-dimer levels at admission. We retrospectively examined data from 380 patients with severe isolated TBI with blood samples collected a maximum of 1h following injury. Plasma fibrinogen and D-dimer concentrations were obtained at admission, and plasma fibrinogen concentration was again assessed 3-4h following injury. The patients were divided into two groups based on whether or not they received FFP transfusion. Patients were also divided into subgroups according their fibrinogen level: ≥ 150mg/dL (high-fibrinogen subgroup) or < 150mg/dL (low-fibrinogen subgroup) 3h after injury. Demographic, clinical, radiological and laboratory data were compared between these subgroups. Glasgow Outcome Scale (GOS) scores at discharge and 3months after injury were significantly lower in the FFP transfusion group than in the FFP non-transfusion group. Among patients who received FFP, GOS scores at discharge and 3months after injury were significantly higher in the high-fibrinogen subgroup than in the low-fibrinogen subgroup. Elevated admission D-dimer predicted subsequent fibrinogen decrease. In FFP transfusion, fibrinogen level ≥ 150mg/dL 3h after injury was associated with better outcomes in TBI patients. Assessing the admission D-dimer and tracking the fibrinogen are crucial for optimal coagulopathy prophylaxis in TBI patients.

Is The Combination of Glasgow Coma Scale and Transcranial Doppler Pulsatility Index Improving The Prediction of Outcome in Traumatic Brain Injury Patients?

Background: Glasgow coma scale (GCS) is a familiar scoring system with a standard statistical association with neurological outcome, it has many limitations that minimize its ability in prediction of Traumatic brain injury (TBI) patients' outcome. Transcranial Doppler (TCD) is a noninvasive aid in this field that can improve outcome prediction. Objective: This study aims to explore the effect of combination of GCS and Pulsatility Index (PI) in the prediction of outcome of TBI patients. Patients and Method: This study was performed in Zagazig University Hospital (ZUH). 103 traumatic brain injured patients were engaged in the investigations with hospital days of 1, 2, 3, and 7 or until patient discharge. The study was performed by TCD along with GCS recordings. Prognosis was also assessed by the Glasgow outcome scale (GOS). Results: The sensitivity and negative predictive value of PI was more than GCS in TBI patients (GCS 3-15), as they were (67.5% versus 50%) and (81.1% versus 74.3%), respectively. The combination of both PI and GCS increased the sensitivity and the negative predictive value up to 70% and 83.3%, respectively. PI had higher sensitivity, positive and negative predictive values than GCS in the identification of secondary neurologic deterioration (SND) in mild and moderate TBI patients (73.3% versus 40.0%, 61.1% versus 50.0%, and 92.0% versus 83.9%, respectively), while the combined value of both PI and GCS increased both sensitivity and positive predictive value up to 76.7% and 66.7%, respectively. Conclusion: The combination of GCS and PI would improve the prediction of outcome.

Interleukin-1 in cerebrospinal fluid for evaluating the neurological outcome in traumatic brain injury.

Objective Severe traumatic brain injury (TBI) is associated with unfavorable outcomes secondary to injury from activation of the inflammatory cascade, the release of excitotoxic neurotransmitters, and changes in the reactivity of cerebral vessels, causing ischemia. Inflammation induced by TBI is complex, individual-specific, and associated with morbidity and mortality. The aim of the present study was to discover the differentially expressed cerebrospinal fluid (CSF) proteins and identify which can improve the clinical outcomes in TBI patients.Methods In the present study, we reported 145 patients with TBI and found the change in patients’ leukocytes in serum and interleukin-1 (IL-1) in CSF, which strongly correlated with the neurological outcome. In terms of results of leukocytes in blood and IL-1 in CSF, we retained the patient’s CSF specimens and conducted a proteomic analysis.Results A total of 119 differentially expressed proteins were detected between samples of TBI and the normal, which were commonly expressed in all samples, indicating the differentially expressed proteins. When the patients’ Glasgow outcome score (GOS) improved, IL-1 was down-regulated, and when the patients’ GCS score deteriorated, IL-1 was up-regulated accompanied with the progression in TBI.Conclusion The differentially expressed proteins in CSF may be the novel therapeutic targets for TBI treatment. The leukocytes in blood samples and the IL-1 in CSF may be two important indicators for predicting the prognosis of TBI patients.

Dietary Energy Restriction Ameliorates Cognitive Impairment in a Mouse Model of Traumatic Brain Injury.

Traumatic brain injury (TBI) is one of the most common causes of neurological damage in young people. It was previously reported that dietary restriction, by either intermittent fasting (IF) or daily caloric restriction (CR), could protect neurons against dysfunction and degeneration in animal models of stroke and Parkinson's disease. Recently, several studies have shown that the protein Sirtuin 1 (SIRT1) plays a significant role in the induced neuroprotection following dietary restriction. In the present study, we found a significant reduction of SIRT1 levels in the cortex and hippocampus in a mouse model of mild weight-drop closed head TBI. This reduction was prevented in mice maintained on IF (alternate day fasting) and CR initiated after the head trauma. Hippocampus-dependent learning and memory (measured using a novel object recognition test) was impaired 30days post-injury in mice fed ad libitum, but not in mice in the IF and CR groups. These results suggest a clinical potential for IF and/or CR as an intervention to reduce brain damage and improve functional outcome in TBI patients.

Temporal Delays Along the Neurosurgical Care Continuum for Traumatic Brain Injury Patients at a Tertiary Care Hospital in Kampala, Uganda.

BACKGROUNDSignificant care continuum delays between acute traumatic brain injury (TBI) and definitive surgery are associated with poor outcomes. Use of the “3 delays” model to evaluate TBI outcomes in low- and middle-income countries has not been performed.OBJECTIVETo describe the care continuum, using the 3 delays framework, and its association with TBI patient outcomes in Kampala, Uganda.METHODSProspective data were collected for 563 TBI patients presenting to a tertiary hospital in Kampala from 1 June to 30 November 2016. Four time intervals were constructed along 5 time points: injury, hospital arrival, neurosurgical evaluation, computed tomography (CT) results, and definitive surgery. Time interval differences among mild, moderate, and severe TBI and their association with mortality were analyzed.RESULTSSignificant care continuum differences were observed for interval 3 (neurosurgical evaluation to CT result) and 4 (CT result to surgery) between severe TBI patients (7 h for interval 3 and 24 h for interval 4) and mild TBI patients (19 h for interval 3 and 96 h for interval 4). These postarrival delays were associated with mortality for mild (P = .05) and moderate TBI (P = .03) patients. Significant hospital arrival delays for moderate TBI patients were associated with mortality (P = .04).CONCLUSIONDelays for mild and moderate TBI patients were associated with mortality, suggesting that quality improvement interventions could target current triage practices. Future research should aim to understand the contributors to delays along the care continuum, opportunities for more effective resource allocation, and the need to improve prehospital logistical referral systems.

Patient-specific management of severe TBI depending on age and cerebrovascular autoregulation status

Determination of proper choice of patient-specific management methodology is crucial for patients with traumatic brain injury (TBI). The treatment outcomes of TBI patients depend on cerebral blood flow autoregulation impairments which can also be affected by patients’ age, brain injury grade or pharmacological influences (anaesthetics, sedation, etc.). The objective of the prospective study was to explore the influence of various factors (dynamics of cerebrovascular autoregulation (CA) status, cerebral perfusion pressure (CPP) declination from optimal CPP value (ΔCPPopt), TBI severity, age, glucose level in blood, etc.) on the TBI patients' outcome. Multimodal ABP, ICP, CPP and CA monitoring of 81 TBI patients has been performed in Republic Vilnius University Hospital (Lithuania). ICM+ software (Cambridge, UK) was used for continuous CA status assessment by calculating Pressure Reactivity Index (PRx) and for identification of patient-specific optimal CPP (optCPP). The post-hoc analysis of associations between the patients' outcome and complex influence monitored parameters was performed by creating multifactorial model of predicting TBI patient's outcome and determining the most important factors affecting outcome. The multifactorial logistic regression model showed that the most significant factors affecting TBI patient's outcome are age, Glasgow Coma Scale (GCS), glucose level in blood serum samples (determined within 24 hours after admission), Helsinki CT (HCT) score and duration of longest CA impairment when PRx(t) > 0.5 within 24 hours after admission. The modelled accuracies for mortality and unfavorable outcome prediction were 82% and 86% respectively. The age > 45 years (P = 0.034, χ2 = 17.48) and HCT > 7 (P = 0.14, χ2 = 15.13) were found statistically significantly associated with unfavorable outcome or mortality. OptCPP-targeted management was found statistically significantly associated with better outcome for younger patients (age 0.36 and duration of LCAI > 100 min (P = 0.043, χ2 = 18.00) were found associated with mortality for younger patients group ( 0.26 (P = 0.005, χ2 = 7.80) and duration of LCAI > 61 min (P = 0.019, χ2 = 5.44) were founded associated with mortality for elderly patients group (> 45 years). The main factors affecting TBI treatment outcomes are patient's age, HCT, GCS, blood glucose level and the CA status during first day after patient admission. The optCPP-targeted patient-specific management is useful for stabilizing CA in severe TBI patients as well as for improving outcome for younger patients with age

Biomarkers in acute brain trauma: A narrative review

Biomarkers have been used to diagnose, prognose, evaluate, and identify the severity and outcomes in traumatic brain injury (TBI) patients. This study explored if it is possible to predict the outcome of TBI patients by estimating the biomarkers in cerebrospinal fluid and serum. We searched data bases and literature about biomarkers, and found forty epidemiologic studies from 92 potentially relevant articles. However, limited data are available about postanoxic encephalopathy. It showed that presently, neurofilament, S100B, glial fibrillary acidic protein, and ubiquitin carboxyl terminal hydrolase-L1 seemed to have the best potential as diagnostic biomarkers for distinguishing focal and diffuse injury, whereas C-Tau, neuron-specific enolase, S100B, glial fibrillary acidic protein, and spectrin breakdown products appear to be candidates for reflective biomarkers of TBI. Point-of-care biomarkers are needed in TBI which is one of the most important additional risk factors in road traffic injuries. In a holistic approach, more researches about biomarkers of TBI are required. These biomarkers are very useful for treatment of patients with TBI.