Cerebral metabolic effects of strict versus conventional glycaemic targets following severe traumatic brain injury

Plummer, Mark P.; Notkina, Natalia; Timofeev, Ivan; Hutchinson, Peter J.; Finnis, Mark; Gupta, Arun Kumar

doi:10.1186/s13054-017-1933-5

Cited by 16 publications

(75 citation statements)

References 28 publications

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“…However, intensive insulin therapy was associated with markers of neurotoxicity and metabolic distress, such as higher glutamate (p < 0.01) and LPR (p < 0.03) and lower brain glucose (p < 0.05) (Vespa et al, 2006). Similar findings from observational and comparative studies later confirmed the increased risk of brain metabolic distress and reduced brain glucose related to aggressive insulin treatment and tight glycemic control (Vespa et al, 2006;Oddo et al, 2008;Schlenk et al, 2008;Meierhans et al, 2010;Plummer et al, 2018).…”

Section: Systemic and Brain Glucosementioning

confidence: 61%

Nutrition Therapy, Glucose Control, and Brain Metabolism in Traumatic Brain Injury: A Multimodal Monitoring Approach

Kurtz

Rocha²

2020

Front. Neurosci.

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The goal of neurocritical care in patients with traumatic brain injury (TBI) is to prevent secondary brain damage. Pathophysiological mechanisms lead to loss of body mass, negative nitrogen balance, dysglycemia, and cerebral metabolic dysfunction. All of these complications have been shown to impact outcomes. Therapeutic options are available that prevent or mitigate their negative impact. Nutrition therapy, glucose control, and multimodality monitoring with cerebral microdialysis (CMD) can be applied as an integrated approach to optimize systemic immune and organ function as well as adequate substrate delivery to the brain. CMD allows real-time bedside monitoring of aspects of brain energy metabolism, by measuring specific metabolites in the extracellular fluid of brain tissue. Sequential monitoring of brain glucose and lactate/pyruvate ratio may reveal pathologic processes that lead to imbalances in supply and demand. Early recognition of these patterns may help individualize cerebral perfusion targets and systemic glucose control following TBI. In this direction, recent consensus statements have provided guidelines and recommendations for CMD applications in neurocritical care. In this review, we summarize data from clinical research on patients with severe TBI focused on a multimodal approach to evaluate aspects of nutrition therapy, such as timing and route; aspects of systemic glucose management, such as intensive vs. moderate control; and finally, aspects of cerebral metabolism. Research and clinical applications of CMD to better understand the interplay between substrate supply, glycemic variations, insulin therapy, and their effects on the brain metabolic profile were also reviewed. Novel mechanistic hypotheses in the interpretation of brain biomarkers were also discussed. Finally, we offer an integrated approach that includes nutritional and brain metabolic monitoring to manage severe TBI patients.

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Section: Systemic and Brain Glucosementioning

confidence: 61%

Nutrition Therapy, Glucose Control, and Brain Metabolism in Traumatic Brain Injury: A Multimodal Monitoring Approach

Kurtz

Rocha²

2020

Front. Neurosci.

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“…A network meta‐analysis was performed using 35 RCTs. 366 , 620 , 677 , 678 , 679 , 680 , 681 , 682 , 683 , 684 , 685 , 686 , 687 , 688 , 689 , 690 , 691 , 692 , 693 , 694 , 695 , 696 , 697 , 698 , 699 , 700 , 701 , 702 , 703 , 704 , 705 , 706 , 707 , 708 , 709 We divided target blood glucose levels into less than 110 mg/dL, 110–144 mg/dL, 144–180 mg/dL, and > 180 mg/dL. The results showed that the estimated values of mortality were as follows: when compared to < 110 mg/dL, a range of 110–144 mg/dL yielded a RD of 40 fewer per 1,000 (95%CI: 100 fewer to 30 more) (1 RCT, n = 90), a range of 144–180 mg/dL yielded an RD of 27 fewer per 1,000 (95%CI: 45 fewer to 8 fewer) (5 RCTs, n = 7,323), and a range > 180 mg/dL yielded an RD of 4 more per 1,000 (95%CI: 22 fewer to 35 more) (12 RCTs, n = 8,027).…”

Section: Methods Used For Creating This Guidelinementioning

confidence: 99%

The Japanese Clinical Practice Guidelines for Management of Sepsis and Septic Shock 2020 (J‐SSCG 2020)

Egi

Ogura

Yatabe

et al. 2021

Acute Medicine & Surgery

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The Japanese Clinical Practice Guidelines for Management of Sepsis and Septic Shock 2020 (J‐SSCG 2020), a Japanese‐specific set of clinical practice guidelines for sepsis and septic shock created as revised from J‐SSCG 2016 jointly by the Japanese Society of Intensive Care Medicine and the Japanese Association for Acute Medicine, was first released in September 2020 and published in February 2021. An English‐language version of these guidelines was created based on the contents of the original Japanese‐language version. The purpose of this guideline is to assist medical staff in making appropriate decisions to improve the prognosis of patients undergoing treatment for sepsis and septic shock. We aimed to provide high‐quality guidelines that are easy to use and understand for specialists, general clinicians, and multidisciplinary medical professionals. J‐SSCG 2016 took up new subjects that were not present in SSCG 2016 (e.g., ICU‐acquired weakness [ICU‐AW], post‐intensive care syndrome [PICS], and body temperature management). The J‐SSCG 2020 covered a total of 22 areas with four additional new areas (patient‐ and family‐centered care, sepsis treatment system, neuro‐intensive treatment, and stress ulcers). A total of 118 important clinical issues (clinical questions, CQs) were extracted regardless of the presence or absence of evidence. These CQs also include those that have been given particular focus within Japan. This is a large‐scale guideline covering multiple fields; thus, in addition to the 25 committee members, we had the participation and support of a total of 226 members who are professionals (physicians, nurses, physiotherapists, clinical engineers, and pharmacists) and medical workers with a history of sepsis or critical illness. The GRADE method was adopted for making recommendations, and the modified Delphi method was used to determine recommendations by voting from all committee members. As a result, 79 GRADE‐based recommendations, 5 Good Practice Statements (GPS), 18 expert consensuses, 27 answers to background questions (BQs), and summaries of definitions and diagnosis of sepsis were created as responses to 118 CQs. We also incorporated visual information for each CQ according to the time course of treatment, and we will also distribute this as an app. The J‐SSCG 2020 is expected to be widely used as a useful bedside guideline in the field of sepsis treatment both in Japan and overseas involving multiple disciplines.

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“…Human insulin (Wan-Bang Biochemical Medicine Ltd., XuZhou, JiangSu, China) was instilled intravenously at 1IU/ml at the speed of 2-20 IU/h within 2-4 h via microinfusing pump (MP-30, Medcaptain, Shenzhen, China). The target conventional glycemic level is maintained at 8.0-10.0 mmol/L [33,62]. During insulin infusion, glucose levels were measured repeatedly on xed time points between 1 and 2 h after the last glucose measurement [61].…”

Section: Intensive Insulin Therapymentioning

confidence: 99%

“…The substrate of NO synthase, L-arginine, its transport was diminished in platelets from obese and metabolic syndrome patients, and correlated negatively with insulin resistance [32] . TBI, as a severe stress, could provoke critical hyperglycemia [33,34] and central insulin resistance in human [35] and in mice [36], possibly due to central glutamate excitotoxicity [37] and endoplasmic reticulum stress to elevate sympathetic nerve tone [38], or through adipose-derived monocyte chemoattractant protein-1 (MCP-1) to increase coagulation factors [39]. Hence, peripheral insulin resistance following TBI in either human [40] or in mice [41,42] was an independent predictor of the mortality [40].…”

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confidence: 99%

Prognostic Significance of Plasma Insulin Level for Deep Venous Thrombosis in Patients with Severe Traumatic Brain Injury in Critical Care

Zhang

Tang

et al. 2022

Neurocrit Care

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Background:Whether insulin resistance is underlying the deep venous thrombosis (DVT) development in patients with traumatic brain injury (TBI) is elusive. To associate kinetics of plasma insulin level in patients with TBI with developing DVT in ICU. Methods:A prospective observational study of 73 patients with TBI who had measurements of insulin, glucose, glucagon-like peptide 1 (GLP-1), in ammatory factors, and hematological pro le within 4 preset time periods during the 14 days after TBI. Ultrasonic surveillance of DVT was tracked weekly for time-to-event analyses. Two-way ANOVA analysis was applied to determine whether the above factors could discriminate between patients with and without DVT, or with and without insulin therapy. Partial correlations of insulin level with all the variables were carried out separately in patients with or without DVT. Factors associated with DVT were analyzed by multivariable logistic regression. Neurological outcome 6 months after TBI was assessed for Glasgow Outcome Scale (GOS).Results:Among patients with an average (SD) age of 53±16 years, DVT developed in 20 (27%) on mean (median) TBI day 10±8. The 14-day insulin levels were higher in patients with DVT (P=0.01). Platelet pro le discriminated signi cantly between patients with and without DVT. Surprisingly, none of other factors differed between the two groups. Patients with insulin therapy had signi cant higher insulin (P=0.006), glucose (P<0.001) and GLP-1 (P=0.01) levels, and were more likely to develop DVT (60% vs. 15%, P<0.001) with concomitant platelet depletion. Insulin levels correlated with glucose, GLP-1 levels, and platelet count exclusively in patients without DVT. Conversely, in patients with DVT, insulin correlated negatively with GLP-1 level (r=-0.297, P=0.016). Age (P=0.01) and elevated insulin level at day 4-7 (P=0.04) were independently associated with DVT. Patients with insulin therapy also showed worse GOS (P=0.001). Conclusions:Elevated insulin level in the rst 14 days after TBI may present insulin resistance in TBI, which was associated with consistent platelet activation, thus increasing risk of DVT. Our data suggest that insulin resistance index may be a predictive biomarker for DVT.

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Cerebral metabolic effects of strict versus conventional glycaemic targets following severe traumatic brain injury

Cited by 16 publications

References 28 publications

Nutrition Therapy, Glucose Control, and Brain Metabolism in Traumatic Brain Injury: A Multimodal Monitoring Approach

Nutrition Therapy, Glucose Control, and Brain Metabolism in Traumatic Brain Injury: A Multimodal Monitoring Approach

The Japanese Clinical Practice Guidelines for Management of Sepsis and Septic Shock 2020 (J‐SSCG 2020)

Prognostic Significance of Plasma Insulin Level for Deep Venous Thrombosis in Patients with Severe Traumatic Brain Injury in Critical Care

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