Stress-induced hyperglycemia is associated with higher mortality in severe traumatic brain injury

Bosarge, Patrick L.; Shoultz, Thomas; Griffin, Russell; Kerby, Jeffrey D.

doi:10.1097/ta.0000000000000716

Cited by 79 publications

(80 citation statements)

References 43 publications

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“…In humans and flies, the probability of mortality following TBI is associated with age and blood/hemolymph glucose level, which is influenced by diet (Susman et al 2002; Hukkelhoven et al 2003; Griesdale et al 2009; Dhandapani et al 2012; Katzenberger et al 2013, 2015a; Wang et al 2013; Borsage et al 2015; Chong et al 2015). Furthermore, studies of repetitive primary injuries in mammals and flies indicate that the time between primary injuries can affect the probability of mortality (Kanayama et al 1996; Friess et al 2009; Meehan et al 2012; Huang et al 2013; Weil et al 2014; Bolton Hall et al 2016) (Figure 1 and Figure 3).…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, reducing glucose levels in the hemolymph by feeding flies water rather than molasses food following primary injuries reduces the MI 24 . Hyperglycemia is not only associated with mortality following TBI in flies but also in humans, suggesting that mechanisms underlying hyperglycemia-mediated secondary injuries are evolutionarily conserved (Griesdale et al 2009; Borsage et al 2015; Chong et al 2015). …”

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confidence: 99%

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Age and Diet Affect Genetically Separable Secondary Injuries that Cause Acute Mortality Following Traumatic Brain Injury in Drosophila

Katzenberger

Ganetzky

Wassarman

2016

G3 Genes|Genomes|Genetics

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Outcomes of traumatic brain injury (TBI) vary because of differences in primary and secondary injuries. Primary injuries occur at the time of a traumatic event, whereas secondary injuries occur later as a result of cellular and molecular events activated in the brain and other tissues by primary injuries. We used a Drosophila melanogaster TBI model to investigate secondary injuries that cause acute mortality. By analyzing mortality percentage within 24 hr of primary injuries, we previously found that age at the time of primary injuries and diet afterward affect the severity of secondary injuries. Here, we show that secondary injuries peaked in activity 1–8 hr after primary injuries. Additionally, we demonstrate that age and diet activated distinct secondary injuries in a genotype-specific manner, and that concurrent activation of age- and diet-regulated secondary injuries synergistically increased mortality. To identify genes involved in secondary injuries that cause mortality, we compared genome-wide mRNA expression profiles of uninjured and injured flies under age and diet conditions that had different mortalities. During the peak period of secondary injuries, innate immune response genes were the predominant class of genes that changed expression. Furthermore, age and diet affected the magnitude of the change in expression of some innate immune response genes, suggesting roles for these genes in inhibiting secondary injuries that cause mortality. Our results indicate that the complexity of TBI outcomes is due in part to distinct, genetically controlled, age- and diet-regulated mechanisms that promote secondary injuries and that involve a subset of innate immune response genes.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Age and Diet Affect Genetically Separable Secondary Injuries that Cause Acute Mortality Following Traumatic Brain Injury in Drosophila

Katzenberger

Ganetzky

Wassarman

2016

G3 Genes|Genomes|Genetics

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“…Among 184 patients admitted with hyperglycemia, 152 (82.6%) were diagnosed with stress-induced hyperglycemia (SIH) and 32 patients (17.4%) were diagnosed with diabetic hyperglycemia (DH). Patients with SIH had a 50% increased mortality as compared to nondiabetic hyperglycemia patients, whereas DH patients did not have a significant increase in mortality [29]. During TBI, the hypothalamic-pituitary-adrenal axis and the sympathetic autonomic nervous system are activated, resulting in increased levels of neuro-hormonal factors and insulin resistance.…”

Section: Mechanisms Of Hyperglycemia After Traumatic Brain Injury (Fimentioning

confidence: 99%

“…After TBI, the activation of the hypothalamic-pituitary-adrenal axis and the sympathetic autonomic nervous system induce elevated blood levels of catecholamine, cortisol, glucagon and growth hormone, which enhance glycogenolysis and hypermetabolism and lead to excessive glucose production [29, 30]. By functioning on islet beta cells' alpha 2 receptor, catecholamines also increase glucagon production and decrease insulin secretion [31, 32].…”

Section: Mechanisms Of Hyperglycemia After Traumatic Brain Injury (Fimentioning

confidence: 99%

Review: Traumatic brain injury and hyperglycemia, a potentially modifiable risk factor

et al. 2016

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Hyperglycemia after severe traumatic brain injury (TBI) occurs frequently and is associated with poor clinical outcome and increased mortality. In this review, we highlight the mechanisms that lead to hyperglycemia and discuss how they may contribute to poor outcomes in patients with severe TBI. Moreover, we systematically review the proper management of hyperglycemia after TBI, covering topics such as nutritional support, glucose control, moderated hypothermia, naloxone, and mannitol treatment. However, to date, an optimal and safe glycemic target range has not been determined, and may not be safe to implement among TBI patients. Therefore, there is a mandate to explore a reasonable glycemic target range that can facilitate recovery after severe TBI.

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“…However, these studies included all hyperglycemic patients without considering the patients’ history of diabetes. Bosarge et al found that SIH was associated with higher mortality after severe TBI than diabetic hyperglycemia4). However, diabetic hyperglycemic patients might have some degree of stress response invoking their hyperglycemia.…”

Section: Discussionmentioning

confidence: 99%

Radiologic Findings and Patient Factors Associated with 30-Day Mortality after Surgical Evacuation of Subdural Hematoma in Patients Less Than 65 Years Old

Han

Ryu

Kim

et al. 2017

J Korean Neurosurg Soc

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ObjectiveThe purpose of this study is to evaluate the associations between 30-day mortality and various radiological and clinical factors in patients with traumatic acute subdural hematoma (SDH). During the 11-year study period, young patients who underwent surgery for SDH were followed for 30 days. Patients who died due to other medical comorbidities or other organ problems were not included in the study population.MethodsFrom January 1, 2004 to December 31, 2014, 318 consecutive surgically-treated traumatic acute SDH patients were registered for the study. The Kaplan–Meier method was used to analyze 30-day survival rates. We also estimated the hazard ratios of various variables in order to identify the independent predictors of 30-day mortality.ResultsWe observed a negative correlation between 30-day mortality and Glasgow coma scale score (per 1-point score increase) (hazard ratio [HR], 0.60; 95% confidence interval [CI], 0.52–0.70; p<0.001). In addition, use of antithrombotics (HR, 2.34; 95% CI, 1.27–4.33; p=0.008), history of diabetes mellitus (HR, 2.28; 95% CI, 1.20–4.32; p=0.015), and accompanying traumatic subarachnoid hemorrhage (hazard ratio, 2.13; 95% CI, 1.27–3.58; p=0.005) were positively associated with 30-day mortality.ConclusionWe found significant associations between short-term mortality after surgery for traumatic acute SDH and lower Glasgow Coma Scale scores, use of antithrombotics, history of diabetes mellitus, and accompanying traumatic subarachnoid hemorrhage at admission. We expect these findings to be helpful for selecting patients for surgical treatment of traumatic acute SDH, and for making accurate prognoses.

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Stress-induced hyperglycemia is associated with higher mortality in severe traumatic brain injury

Abstract: Prognostic/epidemiologic study, leve III.

Cited by 79 publications

References 43 publications

Age and Diet Affect Genetically Separable Secondary Injuries that Cause Acute Mortality Following Traumatic Brain Injury in Drosophila

Age and Diet Affect Genetically Separable Secondary Injuries that Cause Acute Mortality Following Traumatic Brain Injury in Drosophila

Review: Traumatic brain injury and hyperglycemia, a potentially modifiable risk factor

Radiologic Findings and Patient Factors Associated with 30-Day Mortality after Surgical Evacuation of Subdural Hematoma in Patients Less Than 65 Years Old

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