Impact of tight glycemic control on cerebral glucose metabolism after severe brain injury: A microdialysis study*

Oddo, Mauro; Schmidt, J. Michael; Carrera, Emmanuel; Badjatia, Neeraj; Connolly, E. Sander; Presciutti, Mary; Ostapkovich, Noeleen; Levine, Joshua M.; Roux, Peter Le; Mayer, Stephan A.

doi:10.1097/ccm.0b013e31818f4026

Cited by 364 publications

(221 citation statements)

References 45 publications

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“…The threshold to begin insulin therapy was not well-determined, but some evidence suggests that the association of HG with poor outcomes starts at a level of 150 to 160 mg/dL (8.29 to 8.84 mmol/L) 4,18,19,25 . Hence, treatment of HG should be performed cautiously in these patients using validated insulin infusion protocols based on frequent glucose monitoring.…”

Section: Discussionmentioning

confidence: 99%

“…In fact, studies using cerebral microdialysis in patients with traumatic brain injuries have documented "metabolic crises", which are characterized by the increase in glutamate, and lactate/pyruvate ratio (markers of cellular distress and impending energy failure), along with reduction in the extracellular level of glucose in patients treated with IIT -target blood glucose of 90 to 120 mg/dL (4.97 to 6.63 mmol/L) -, even in the absence of serum hypoglycemia 18,19 .…”

Section: Discussionmentioning

confidence: 99%

“…Modest degrees of hypoglycemia or even low-normal blood glucose levels induce the production of markers of cerebral metabolic failure 18,19 .…”

mentioning

confidence: 99%

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Hyperglycemia in nondiabetic patients during the acute phase of stroke

Godoy¹,

Soler²,

Videtta³

et al. 2012

Arq. Neuro-Psiquiatr.

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OBJECTIVE: To determine patterns of hyperglycemic (HG) control in acute stroke. METHODS: Anonymous survey through Internet questionnaire. Participants included Latin-American physicians specialized in neurocritical care. RESULTS: The response rate was 74%. HG definition varied widely. Fifty per cent considered it when values were >140 mg/dL (7.8 mmol/L). Intravenous (IV) regular insulin was the drug of choice for HG correction. One fifth of the respondents expressed adherence to a protocol. Intensive insulin therapy (IIT) was used by 23%. Glucose levels were measured in all participants at admission. Routine laboratory test was the preferred method for monitoring. Reactive strips were more frequently used when monitoring was intensive. Most practitioners (56.7%) monitored glucose more than two times daily throughout the Intensive Care Unit stay. CONCLUSIONS: There is considerable variability and heterogeneity in the management of elevated blood glucose during acute phase of stroke by the surveyed Latin-American physicians.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Hyperglycemia in nondiabetic patients during the acute phase of stroke

Godoy¹,

Soler²,

Videtta³

et al. 2012

Arq. Neuro-Psiquiatr.

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“…However, cerebral hypoperfusion might have occurred in elderly patients with TBI. Cerebral extracellular glucose is a good indicator of the prognosis, 24) and levels of extracellular cerebral glucose are significantly less in patients with TBI who had poor outcome. 33) These findings together suggest that persistent cerebral hypoperfusion may underlay the persistent lower glucose concentration and poor outcome in elderly patients.…”

Section: Discussionmentioning

confidence: 99%

Lower Extracellular Glucose Level Prolonged in Elderly Patients With Severe Traumatic Brain Injury: A Microdialysis Study

Yokobori

Watanabe

Matsumoto

et al. 2011

Neurol. Med. Chir.(Tokyo)

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Age may be an independent predictor of outcomes in traumatic brain injury (TBI), but the causes of the poor outcomes in elderly patients remain unclear. To clarify the differences between elderly and young patients with TBI, brain metabolism parameters were monitored with the microdialysis method in 30 patients with severe TBI (Glasgow Coma Scale scores 3-8). The microdialysis probe was inserted in the penumbra area of the brain and extracellular levels of glucose, glutamate, glycerol, lactate, and pyruvate were measured hourly for the initial 168 hours (7 days) after operation. The lactate/pyruvate ratio, which is considered to be a good indicator of neuronal ischemia, was also calculated. The patients were divided into the elderly group aged 65 years or older and the young group aged less than 65 years, and the biochemical markers were compared daily between these two groups. The value of extracellular glucose concentration was significantly lower in the elderly group than in the young group, and continued until the 7th day after injury. Moreover, the lactate/pyruvate ratio peaked on the 5th day after injury in the elderly group, later than in the young group. We concluded that neural vulnerability persisted longer in elderly patients than in young patients with TBI, and this should be considered to prevent the occurrence of additional secondary brain injury.

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“…In contrast to oxygen based modalities, cerebral microdialysis measures extracellular markers of metabolism. Increased lactate, excitatory amino acids, and glycerol with concomitant decreases in glucose and pyruvate are suggestive of metabolic stress [5]. The use of these monitoring methods must be approached with caution, as it remains unclear whether treatment directed at improving PbrO 2 , jugular venous saturation, or metabolic substrates leads to better outcomes.…”

mentioning

confidence: 99%

State of the Art in Cerebral Trauma: A Neurosurgeon’s Perspective

Hsu

Keen

2011

Transl. Stroke Res.

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CommentaryNeurosurgery has always played an integral role in the management of cerebral trauma but, historically, treatments were limited and mortality and morbidity high. While cerebral trauma remains a leading cause of death worldwide, advancements in basic science injury models, pharmacology, and prevention strategies over the past several decades have resulted in a better understanding of injury mechanisms and have lead to improved outcomes in certain groups. The elucidation of the pathophysiology of secondary brain injury has lead to more targeted therapies; and the establishment of evidence-based guidelines has systematized the management of cerebral trauma, spawning the growth of neurocritical care, multimodal neuromonitoring, and the resurgence of surgical management.Cerebral trauma consists of a heterogeneous group of primary injuries with different causes, presentations, severity, and outcomes, but the final common pathway that leads to the most deleterious effects is that of secondary injury, which involves complex biomechanical and biochemical-triggered cascades that lead to cerebral ischemia, metabolic derangements, inflammation, edema, and cell death. Once cerebral blood flow, and therefore oxygenation, is diminished, neurons depolarize and release excitatory neurotransmitters, such as glutamate, that act at NMDA and AMPA receptors to permit massive influxes of sodium and calcium. The influx of calcium, in particular, activates multiple self-digesting mechanisms that lead to membrane damage, DNA degradation, and ultimately cell death [1]. These processes will often propagate until diffuse ischemia, inflammation, and edema lead to brain herniation and death, unless there is prompt intervention.The goal of neurocritical care is to anticipate the evolution of secondary injury and intervene early. Traditionally, this has been accomplished by measuring intracranial pressure (ICP) with external ventricular drains and parenchymal monitors to derive cerebral perfusion pressure (CPP) by subtracting ICP from mean arterial pressure. The goal has been to keep CPP above an acceptable threshold to ensure adequate cerebral perfusion and oxygenation. While consensus exists for treating ICP greater than 20 mmHg, CPP management has been less straightforward. Some studies have demonstrated improved outcomes with CPP >70 mmHg, whereas several others have not and revealed high rates of pulmonary complications [2]. Currently, the recommended threshold below which CPP should not fall is 50 mmHg, but artificially driving CPP higher than 70 mmHg has fallen out of favor [3]. The difficulty with an ICP and CPP management strategy is that some individuals may benefit from higher or lower CPP values depending upon the nature of their injury. Another complicating factor is that focal injury causing regional metabolic derangements may not be detected by more globally oriented monitoring techniques, such as intracranial pressure monitoring, whereas focal monitoring may not detect the presence of larger areas of injury if the devi...

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Impact of tight glycemic control on cerebral glucose metabolism after severe brain injury: A microdialysis study*

Cited by 364 publications

References 45 publications

Hyperglycemia in nondiabetic patients during the acute phase of stroke

Hyperglycemia in nondiabetic patients during the acute phase of stroke

Lower Extracellular Glucose Level Prolonged in Elderly Patients With Severe Traumatic Brain Injury: A Microdialysis Study

State of the Art in Cerebral Trauma: A Neurosurgeon’s Perspective

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