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

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Term Occurence Count Dictionary
hyperglycemia 63 endocrinologydiseases
hyperinsulinemia 1 endocrinologydiseases
hypoglycemia 4 endocrinologydiseases
lactic acidosis 2 endocrinologydiseases
Insulin 1 endocrinologydiseasesdrugs
cortisol 1 endocrinologydiseasesdrugs
diabetes mellitus 2 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 18366 includes both intravenous glucose and enteral feeding with low carbohydrates [[76]–[78]].Glucose control Insulin increases glucose utilization and reduces the damage of hyperglycemia to brain cells [[79]]. Owing to
cortisol 7099 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
Select Disease Character Offset Disease Term Instance
diabetes mellitus 9445 potential to be an independent predictor of poor outcome and mortality after TBI [[38], [39]]. Latent diabetes mellitus may be particularly problematic, especially in elderly patients. The symptoms of DM can be exacerbated
diabetes mellitus 22548 the mechanisms leading to hyperglycemia after TBI, including stress response, inflammatory response, diabetes mellitus , pituitary and/or hypothalamic dysfunction, surgery, and anaesthesia. TBI patients with hyperglycemia
hyperglycemia 52 Title: OncotargetReview: Traumatic brain injury and hyperglycemia , a potentially modifiable risk factorJia ShiBo DongYumin MaoWei GuanJiachao CaoRongxing ZhuSuinuan Wang1
hyperglycemia 546 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
hyperglycemia 702 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,
hyperglycemia 2247 mainly ischemic in nature [[8]], and include hypoxemia[[8]][[9]], hypotension, hypertension [[8]], hyperglycemia , and hypoglycemia [[10]]. Among these secondary complications, hyperglycemia (both peak glucose and
hyperglycemia 2324 hypotension, hypertension [[8]], hyperglycemia, and hypoglycemia [[10]]. Among these secondary complications, hyperglycemia (both peak glucose and persistent hyperglycemia) in TBI patients is one of the most common and correlates
hyperglycemia 2372 hypoglycemia [[10]]. Among these secondary complications, hyperglycemia (both peak glucose and persistent hyperglycemia ) in TBI patients is one of the most common and correlates with the severity of the injury and clinical
hyperglycemia 2541 correlates with the severity of the injury and clinical outcome [[11], [12]]. Furthermore, the link between hyperglycemia and poor prognosis is also observed in ischemic stroke, subarachnoid hemorrhage, and intracerebral hemorrhage
hyperglycemia 2711 subarachnoid hemorrhage, and intracerebral hemorrhage [[13]–[15]]. Importantly, as treatments for hyperglycemia become available, blood glucose control has attracted significant attention as a promising intervention
hyperglycemia 2907 promising intervention for reducing the complications of TBI.Previous studies have demonstrated that hyperglycemia plays a causative role in promoting poor clinical outcomes in TBI. In this review, we summarize the
hyperglycemia 3053 promoting poor clinical outcomes in TBI. In this review, we summarize the potential causes and effects of hyperglycemia in TBI patients and attempt to address the pathological mechanisms that might explain the association
hyperglycemia 3172 TBI patients and attempt to address the pathological mechanisms that might explain the association of hyperglycemia with poor clinical outcomes. Furthermore, we perform a systematic review of research studying glycemic
hyperglycemia 5646 TBI had greater admission blood glucose levels compared to those with mild TBI [[27]]. This initial hyperglycemia was associated with increased mortality (37% in the hyperglycemia group versus 8% in the normoglycemia
hyperglycemia 5712 with mild TBI [[27]]. This initial hyperglycemia was associated with increased mortality (37% in the hyperglycemia group versus 8% in the normoglycemia group), indicating a close relationship between TBI and glucose
hyperglycemia 5891 relationship between TBI and glucose levels [[28]]. Thus, exploring the underlying causes leading to hyperglycemia after TBI may provide new treatment options. The following sections address a number of mechanisms by
hyperglycemia 6013 TBI may provide new treatment options. The following sections address a number of mechanisms by which hyperglycemia is induced following TBI.Stress responseThere are several explanations for high glucose levels after
hyperglycemia 6179 several explanations for high glucose levels after TBI, and one of the most studied is stress-induced hyperglycemia . During a 4-year study, a total of 626 patients were enrolled with severe TBI defined by GCS score from
hyperglycemia 6338 patients were enrolled with severe TBI defined by GCS score from 3 to 8. Among 184 patients admitted with hyperglycemia , 152 (82.6%) were diagnosed with stress-induced hyperglycemia (SIH) and 32 patients (17.4%) were diagnosed
hyperglycemia 6400 to 8. 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
hyperglycemia 6473 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,
hyperglycemia 6568 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
hyperglycemia 7936 a systemic inflammatory response syndrome (SIRS), in which there may be two mechanisms that lead to hyperglycemia . First, during the inflammatory response, several cytokines are released, including TNF-α, IL-6, and
hyperglycemia 8284 genes and increasing levels of preadipocyte-specific genes, contributing to insulin resistance and hyperglycemia [[36]]. Second, inflammatory responses increase the level of corticotrophin-releasing hormone (CRH)
hyperglycemia 8741 pathways that lead to the release of corticosterone from the adrenal gland, and finally results in hyperglycemia . [[37]]. While not still understood, the interaction between inflammatory response and hyperglycemia
hyperglycemia 8842 hyperglycemia. [[37]]. While not still understood, the interaction between inflammatory response and hyperglycemia is clearly important and warrants further investigation.Diabetes mellitus (DM)Diabetes mellitus (DM)
hyperglycemia 8978 and warrants further investigation.Diabetes mellitus (DM)Diabetes mellitus (DM) is another source of hyperglycemia in this setting. Severe TBI with DM has a higher mortality (14%) compared to severe TBI without DM (8.2%),
hyperglycemia 10387 Pituitary dysfunction directly leads to impaired glucose metabolism and may act as a potential cause of hyperglycemia [[43]]. In addition, injury of the pituitary leads to disorders of neuroendocrine function [[44], [45]],
hyperglycemia 10745 glucose metabolism [[46]]. Thus, pituitary/hypothalamic dysfunction may contribute significantly to hyperglycemia in TBI patients.Iatrogenic factorsThere are several other explanations of hyperglycemia induced by TBI.
hyperglycemia 10833 significantly to hyperglycemia in TBI patients.Iatrogenic factorsThere are several other explanations of hyperglycemia induced by TBI. Surgery,anaesthesia, treatment strategies (including too high a dosage of hyperosmotic
hyperglycemia 11032 dosage of hyperosmotic glucose or a high calorie substance), and psychological factors, may also lead to hyperglycemia in TBI patients, especially in severe TBI [[47], [48]].In conclusion, an elevated stress and inflammatory
hyperglycemia 11192 [[47], [48]].In conclusion, an elevated stress and inflammatory response seem to be the major causes of hyperglycemia after TBI. Preexisting hyperglycemia does not seem to have a predominant role in TBI patients, and a
hyperglycemia 11229 stress and inflammatory response seem to be the major causes of hyperglycemia after TBI. Preexisting hyperglycemia does not seem to have a predominant role in TBI patients, and a relationship between pituitary and/or
hyperglycemia 11395 patients, and a relationship between pituitary and/or hypothalamic dysfunction, iatrogenic factors, and hyperglycemia is plausible.HYPERGLYCEMIA AND CLINICAL OUTCOMES AFTER TRAUMATIC BRAIN INJURYDuring one study, a total
hyperglycemia 11988 high blood glucose levels and poor outcome after TBI appears to be more pronounced with persistent hyperglycemia (PH) than solely hyperglycemia on admission [[49]]. One study showed that PH was an independent predictor
hyperglycemia 12019 poor outcome after TBI appears to be more pronounced with persistent hyperglycemia (PH) than solely hyperglycemia on admission [[49]]. One study showed that PH was an independent predictor of clinical outcome in severe
hyperglycemia 12278 mortality rates in patients with severe TBI [[50]]. These studies beg the question: How exactly does hyperglycemia affect outcomes after traumatic brain injury? (Figure 2) Here we show that hyperglycemia may increase
hyperglycemia 12367 exactly does hyperglycemia affect outcomes after traumatic brain injury? (Figure 2) Here we show that hyperglycemia may increase the damage of nerve function and brain structure in a number of ways.Figure 2Figure illustrating
hyperglycemia 12516 function and brain structure in a number of ways.Figure 2Figure illustrating hypothetical mechanisms: hyperglycemia in patients with traumatic brain injury (upper panel); and explaining a detrimental effect of hyperglycemia
hyperglycemia 12624 hyperglycemia in patients with traumatic brain injury (upper panel); and explaining a detrimental effect of hyperglycemia on clinical outcome (lower panel)BBB, blood-brain barrier.Lactic acidosisIn the early stages after severe
hyperglycemia 12824 stages after severe TBI, local blood flow decreases [[51]]. During ischemic and hypoxic conditions, hyperglycemia inhibits the tricarboxylic acid cycle (TCA) and promotes anaerobic glycolysis, contributing to the accumulation
hyperglycemia 13103 support of a detrimental function of lactic acid is the discovery that in patients with severe TBI, hyperglycemia is associated with both intracellular acidosis and disruption of BBB, eventually leading to ischemia,
hyperglycemia 15428 with the severity and bad outcome of TBI patients [[65]]. An in vitro experiment demonstrated that hyperglycemia induced by walnut oil increased the release of pro-inflammatory cytokines, which led to reduced antioxidant
hyperglycemia 16105 outcomes [[68]].Other effectsHyperglycemia can affect clinical outcomes in other ways. For instance, hyperglycemia can directly cause increased blood viscosity and diffuse small vessel disorders, resulting in ischemia
hyperglycemia 16277 small vessel disorders, resulting in ischemia and hypoxia in the brain tissues [[69]]. Additionally, hyperglycemia exacerbates edema of endothelial cells, impairs glial cells, and can induce the rupture of the BBB [[70],
hyperglycemia 16520 also has the potential to accelerate cerebral vasospasm [[72]]. Thus, the causal relationship between hyperglycemia and poor clinical outcome in TBI patients may be multifactorial. In the sequence of insults that occur
hyperglycemia 16648 clinical outcome in TBI patients may be multifactorial. In the sequence of insults that occur after TBI, hyperglycemia may play a detrimental role by elevating secondary complications such as dysregulated energy metabolism,
hyperglycemia 16909 intracranial hypertension.MANAGEMENT OF HYPERGLYCEMIA IN PATIENTS WITH TRAUMATIC BRAIN INJURYAs discussed, hyperglycemia may manifest poor outcomes after TBI through several responses. Besides lowering blood glucose with
hyperglycemia 17244 relevant in this setting. Current thinking suggests that comprehensive measures should be taken to address hyperglycemia after TBI.Nutritional supportPatients with severe TBI are usually in catabolic and hyperglycemic states,
hyperglycemia 18430 carbohydrates [[76]–[78]].Glucose controlInsulin increases glucose utilization and reduces the damage of hyperglycemia to brain cells [[79]]. Owing to insulin resistance after TBI, most studies use exogenous insulin and
hyperglycemia 18596 after TBI, most studies use exogenous insulin and dynamically monitor blood glucose to fight against hyperglycemia after TBI [[79]]. In 2001, intensive insulin therapy (IIT) was implemented in intensive care units (ICUs)
hyperglycemia 22157 saline administration are effective ways of decreasing hyperpermeability and raised ICP induced by hyperglycemia after severe TBI [[89], [90]].CONCLUSIONSHyperglycemia (both peak glucose and persistent hyperglycemia)
hyperglycemia 22260 hyperglycemia after severe TBI [[89], [90]].CONCLUSIONSHyperglycemia (both peak glucose and persistent hyperglycemia ) is one of the most common secondary complications of severe TBI and is associated with poor clinical
hyperglycemia 22473 clinical outcomes after this type of injury. In this review, we have summarized the mechanisms leading to hyperglycemia after TBI, including stress response, inflammatory response, diabetes mellitus, pituitary and/or hypothalamic
hyperglycemia 22654 diabetes mellitus, pituitary and/or hypothalamic dysfunction, surgery, and anaesthesia. TBI patients with hyperglycemia possess an increased risk of poor outcome and an increased mortality rate, which is more pronounced
hyperglycemia 22784 increased risk of poor outcome and an increased mortality rate, which is more pronounced with persistent hyperglycemia (PH) than hyperglycemia on admission [[49]]. Some of the direct effects of hyperglycemia may be attributed
hyperglycemia 22808 outcome and an increased mortality rate, which is more pronounced with persistent hyperglycemia (PH) than hyperglycemia on admission [[49]]. Some of the direct effects of hyperglycemia may be attributed to lactic acidosis,
hyperglycemia 22873 persistent hyperglycemia (PH) than hyperglycemia on admission [[49]]. Some of the direct effects of hyperglycemia may be attributed to lactic acidosis, electrolyte disturbances, inflammation, vessel disorders, rupture
hyperglycemia 23084 rupture of the BBB, and hyperpermeability. At present, the treatments of secondary brain injury with hyperglycemia may include nutritional support, glucose control, moderated hypothermia, naloxone, and mannitol. Although
hyperglycemia 23229 support, glucose control, moderated hypothermia, naloxone, and mannitol. Although the relationship between hyperglycemia and severe TBI has made great progress in recent years, there are still many treatment limitations and
hyperglycemia 24191 significantly, research should focus on examining the relationship between brain cell metabolism and hyperglycemia after severe TBI.There is not widespread agreement on the best way to approach glycemic control in patients
hyperglycemia 24525 convincing proof of glucose control in future treatments. As previously mentioned, the therapy of IIT for hyperglycemia post TBI remains controversial to date, and the treatment comes at the cost of an increased risk of
hyperglycemia 24947 severe TBI patients. Multidisciplinary teams should play a role in providing individual treatments for hyperglycemia in TBI patients, including diabetic and TBI experts to facilitate the implementation of glucose control
hyperglycemia 25283 monitoring of blood glucose and frequent adjustment of insulin is strongly recommended [[93]].In conclusion, hyperglycemia is one of the most common and serious secondary complications of severe TBI. Future studies are needed
hyperglycemia 25582 of blood glucose control and to further research the relationship between brain cell metabolism and hyperglycemia after severe TBI
hyperinsulinemia 7769 catecholamines can inhibit glucose transport via inhibition of insulin binding, leading to IR with hyperinsulinemia [[34]].Inflammatory responseTBI is accompanied by a systemic inflammatory response syndrome (SIRS),
hypoglycemia 2266 nature [[8]], and include hypoxemia[[8]][[9]], hypotension, hypertension [[8]], hyperglycemia, and hypoglycemia [[10]]. Among these secondary complications, hyperglycemia (both peak glucose and persistent hyperglycemia)
hypoglycemia 19096 of 81-108 mg/dL (4.5-6 mmol/L)) was in fact associated with an increased risk of mortality and even hypoglycemia (glucose<40 mg/dL (2.2 mmol/L)), which may be due to the effects of IIT on cerebral glucose homeostasis
hypoglycemia 24639 post TBI remains controversial to date, and the treatment comes at the cost of an increased risk of hypoglycemia (glucose < 2.2 mmol/L). Therefore, methods to improve IIT without inducing secondary complications should
hypoglycemia 24828 secondary complications should be investigated, and attention should also focus on the prevention of hypoglycemia in severe TBI patients. Multidisciplinary teams should play a role in providing individual treatments
lactic acidosis 13783 in nerve cells.Electrolyte disturbancesWithin minutes after TBI, dysfunctional energy metabolism and lactic acidosis lead to increased intracellular Ca2+, causing cellular toxicity and the accumulation of free fatty acid
lactic acidosis 22908 hyperglycemia on admission [[49]]. Some of the direct effects of hyperglycemia may be attributed to lactic acidosis , electrolyte disturbances, inflammation, vessel disorders, rupture of the BBB, and hyperpermeability.

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