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      Neuropsychiatric Disease and Treatment (submit here)

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      Cerebral Salt Wasting in Traumatic Brain Injury Is Associated with Increased Morbidity and Mortality

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          Abstract

          Introduction

          In the setting of cerebral injury, cerebral salt wasting (CSW) is a potential cause of hyponatremia, which contributes to adverse effects and mortality.

          Objective

          The primary objective of this study was to evaluate the clinical outcomes of severe traumatic brain injury (TBI) patients complicated by CSW.

          Methods

          A retrospective data analysis was performed on data collected from patients with TBI with an abbreviated injury scale (AIS) greater than 3. Data was divided into 2 groups of patients with CSW and those without. The primary endpoint was incidence of adverse effects of CSW in regard to injury severity score (ISS), hospital length of stay (HLOS), ventilator days, ICU length of stay (ICU LOS) and survival to discharge. Data was analyzed using a one-way analysis of variance (ANOVA).

          Results

          A total of 310 consecutive patients with severe head injury (anatomic injury score 3 or greater) were evaluated over a 3-year period. A total of 125 of the 310 patients (40%) were diagnosed with cerebral salt wasting as defined by hyponatremia with appropriate urinary output and salt replacement. Patients with CSW had poorer outcomes in regard to ISS (21.8 vs 14.2, p<0.0001), HLOS (14.1 vs 3.5, p<0.0001), ventilator days (5.0 vs 0.45, p<0.0001), ICU LOS (8.5 vs 1.6, p<0.0001), and survival to discharge (88% vs 99%, p<0.0001).

          Discussion

          Common adverse effects of CSW were noted in this study. Patients with TBI have a predilection towards development of CSW and consequently have poorer outcomes including increased morbidity and mortality. Data is sparse on the duration of CSW and degree of hyponatremia over time. Larger, comparative studies need to be performed to investigate the hyponatremic patient population and the clinical outcomes of those who present with CSW.

          Most cited references10

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          Brain networks under attack: robustness properties and the impact of lesions.

          A growing number of studies approach the brain as a complex network, the so-called 'connectome'. Adopting this framework, we examine what types or extent of damage the brain can withstand-referred to as network 'robustness'-and conversely, which kind of distortions can be expected after brain lesions. To this end, we review computational lesion studies and empirical studies investigating network alterations in brain tumour, stroke and traumatic brain injury patients. Common to these three types of focal injury is that there is no unequivocal relationship between the anatomical lesion site and its topological characteristics within the brain network. Furthermore, large-scale network effects of these focal lesions are compared to those of a widely studied multifocal neurodegenerative disorder, Alzheimer's disease, in which central parts of the connectome are preferentially affected. Results indicate that human brain networks are remarkably resilient to different types of lesions, compared to other types of complex networks such as random or scale-free networks. However, lesion effects have been found to depend critically on the topological position of the lesion. In particular, damage to network hub regions-and especially those connecting different subnetworks-was found to cause the largest disturbances in network organization. Regardless of lesion location, evidence from empirical and computational lesion studies shows that lesions cause significant alterations in global network topology. The direction of these changes though remains to be elucidated. Encouragingly, both empirical and modelling studies have indicated that after focal damage, the connectome carries the potential to recover at least to some extent, with normalization of graph metrics being related to improved behavioural and cognitive functioning. To conclude, we highlight possible clinical implications of these findings, point out several methodological limitations that pertain to the study of brain diseases adopting a network approach, and provide suggestions for future research.
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            Prognostic value of admission laboratory parameters in traumatic brain injury: results from the IMPACT study.

            Abnormalities in laboratory parameters are frequent following traumatic brain injury (TBI), but few studies have investigated their predictive value. We aimed to describe and quantify the relation between laboratory parameters that are routinely determined on admission and final outcome following TBI. Individual patient data were available in the IMPACT database from six Phase III randomized controlled trials and one observational study in TBI. We studied glucose (N = 4834), sodium ( N = 5270), pH ( N = 3398), hemoglobin (Hb, N = 3875), platelet count ( N = 1629), and prothrombin time (PT; N = 840) for their associations with outcome at 6 months (Glasgow Outcome Scale [GOS]). We used logistic regression models with linear, quadratic, and restricted cubic spline functions. The strength of the associations was expressed as an unadjusted odds ratio, calculated over the shift in outcome between the 25th and 75th percentiles. Proportional odds methodology was further applied to quantify the strength of the associations across the full range of the GOS. All parameters were consistently associated with outcome in a continuous relationship: glucose and prothrombin time showed a positive linear relation to outcome (i.e., increasing values associated with poorer outcome) and Hb, platelets, and pH an inverse linear relation (i.e., low values associated with poorer outcome). Sodium demonstrated a U-shaped relation to outcome, with low levels being more strongly related to poorer outcome. Effects were strongest for increasing levels of glucose (odds ratio 1.7; 95% CI 1.54-1.83) and decreasing levels of Hb (odds ratio 0.7; CI 0.60-0.78). Higher glucose values were associated with increasing age, but on adjusted analysis, the strength of the association with outcome remained. Whether treatment of abnormal values may improve outcome needs further rigorous study.
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              Harbingers of poor outcome the day after severe brain injury: hypothermia, hypoxia, and hypoperfusion.

              Traumatic brain injury (TBI) can be compounded by physiologic derangements that produce secondary brain injury. The purpose of this study is to elucidate the frequency with which physiologic factors that are associated with secondary brain injury occur in patients with severe closed head injuries and to determine the impact of these factors on outcome. The records of 81 adult blunt trauma patients with Glasgow Coma Scale scores < or = 8 and transport times < 2 hours to a Level I trauma center were retrospectively reviewed searching for the following 11 secondary brain injury factors (SBIFs) in the first 24 hours postinjury: hypotension, hypoxia, hypercapnia, hypocapnia, hypothermia, hyperthermia, metabolic acidosis, seizures, coagulopathy, hyperglycemia, and intracranial hypertension. We recorded the worst SBIF during six time periods: hours 1, 2, 3, 4, 5 to 14, and 16 to 24. Occurrence of each SBIF was then correlated with outcome. Hypocapnia, hypotension, and acidosis occurred more frequently than other SBIFs (60-80%). Hypotension, hyperglycemia, and hypothermia were associated with increased mortality rate. Patients with episodes of hypocapnia, acidosis, and hypoxia had significantly longer intensive care unit length of stay (LOS). These three SBIFs and hyperglycemia related to longer hospital LOS as well. Hypotension and acidosis were associated with discharge to a rehabilitation facility rather than home. Finally, multivariate regression analysis revealed that hypotension, hypothermia, and Abbreviated Injury Scale score of the head were independently related to mortality, whereas other SBIFs, age, Injury Severity Score, and Glasgow Coma Scale score were not. Metabolic acidosis and hypoxia were related to longer intensive care unit and hospital LOS. Our early management of head-injured patients stresses avoidance and correction of SBIFs at all costs. Nonetheless, SBIFs occur frequently in the first 24 hours after traumatic brain injury. Six of the 11 factors studied are associated with significantly worse outcomes. Hypotension and hypothermia are independently related to mortality. Because these SBIFs are potentially preventable, protocols could be developed to decrease their frequency.
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                Author and article information

                Journal
                Neuropsychiatr Dis Treat
                Neuropsychiatr Dis Treat
                NDT
                neurodist
                Neuropsychiatric Disease and Treatment
                Dove
                1176-6328
                1178-2021
                25 March 2020
                2020
                : 16
                : 801-806
                Affiliations
                [1 ]Department of Surgery, Richmond University Medical Center , Staten Island, NY, USA
                [2 ]Department of Surgery, SUNY Downstate Medical Center , Brooklyn, NY, USA
                Author notes
                Correspondence: Akella Chendrasekhar Email achendrasekhar@rumcsi.org
                Article
                233389
                10.2147/NDT.S233389
                7104213
                38e15d5d-66f5-4a3b-af8d-6fda459332e3
                © 2020 Chendrasekhar et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                : 04 October 2019
                : 11 February 2020
                Page count
                Figures: 6, References: 11, Pages: 6
                Categories
                Original Research

                Neurology
                hyponatremia,hypovolemia,natriuresis,traumatic brain injury,neurosurgery
                Neurology
                hyponatremia, hypovolemia, natriuresis, traumatic brain injury, neurosurgery

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