Systemic Glucose and Brain Energy Metabolism after Subarachnoid Hemorrhage

Helbok, Raimund; Schmidt, J. Michael; Kurtz, Pedro; Hanafy, Khalid A.; Fernández, Luís; Stuart, R. Morgan; Presciutti, Mary; Ostapkovich, Noeleen; Connolly, E. Sander; Lee, Ki-Won; Badjatia, Neeraj; Mayer, Stephan A.; Claassen, Jan

doi:10.1007/s12028-009-9327-4

Cited by 72 publications

(40 citation statements)

References 30 publications

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“…324 Nevertheless, even serum glucose levels within the normal range may be associated with brain energy metabolic crisis and lactate-pyruvate ratio elevation in patients with poor-grade aSAH. 325 Anemia is common after aSAH and may compromise brain oxygen delivery. 326 Transfusion of red blood cells in anemic patients with aSAH results in a significant rise in cerebral oxygen delivery and a reduction in oxygen extraction ratio.…”

Section: Management Of Medical Complications Associated With Asahmentioning

confidence: 99%

Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage

Connolly¹,

Rabinstein²,

Carhuapoma³

et al. 2012

Stroke

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2,957

1,375

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Purpose— The aim of this guideline is to present current and comprehensive recommendations for the diagnosis and treatment of aneurysmal subarachnoid hemorrhage (aSAH). Methods— A formal literature search of MEDLINE (November 1, 2006, through May 1, 2010) was performed. Data were synthesized with the use of evidence tables. Writing group members met by teleconference to discuss data-derived recommendations. The American Heart Association Stroke Council's Levels of Evidence grading algorithm was used to grade each recommendation. The guideline draft was reviewed by 7 expert peer reviewers and by the members of the Stroke Council Leadership and Manuscript Oversight Committees. It is intended that this guideline be fully updated every 3 years. Results— Evidence-based guidelines are presented for the care of patients presenting with aSAH. The focus of the guideline was subdivided into incidence, risk factors, prevention, natural history and outcome, diagnosis, prevention of rebleeding, surgical and endovascular repair of ruptured aneurysms, systems of care, anesthetic management during repair, management of vasospasm and delayed cerebral ischemia, management of hydrocephalus, management of seizures, and management of medical complications. Conclusions— aSAH is a serious medical condition in which outcome can be dramatically impacted by early, aggressive, expert care. The guidelines offer a framework for goal-directed treatment of the patient with aSAH.

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Section: Management Of Medical Complications Associated With Asahmentioning

confidence: 99%

Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage

Connolly¹,

Rabinstein²,

Carhuapoma³

et al. 2012

Stroke

Self Cite

2,957

1,375

View full text Add to dashboard Cite

show abstract

“…Hence, in these situations the brain can become acidotic even with blood glucose concentrations within the ''normal'' range [61,64]. Furthermore, neuroglycopenia per se (even in the absence of increased brain lactate levels) has been found to correlate with poor delayed functional outcome in at least one study of patients with severe TBI [65].…”

Section: The Perils Of Hypoglycemia For the Acutely Injured Brainmentioning

confidence: 99%

Treating Hyperglycemia in Neurocritical Patients: Benefits and Perils

Godoy

Napoli²,

Rabinstein

2010

Neurocrit Care

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There is growing debate over the value of intensive insulin therapy (IIT) in critically ill patients. Available trials have been performed in general medical or surgical intensive care units, and the results may not be directly applicable to patients with severe acute brain disease because these patients may have heightened susceptibility to hyperglycemia (HyperG) and hypoglycemia. Our objective was to review the pathophysiology and effects of HyperG and hypoglycemia in neurocritical patients and to analyze the potential role of IIT in this population. Source data were obtained from a PubMed search of the medical literature combining the terms HyperG, hypoglycemia, insulin, stroke, intracerebral hemorrhage (ICH), subarachnoid hemorrhage (SAH), traumatic brain injury (TBI), spinal cord injury (SCI), and related diagnoses. Brain metabolism is highly dependent on constant supply of glucose. As a consequence, the acutely injured brain is particularly sensitive to hypoglycemia, which can induce a state of energy failure (metabolic crisis). Meanwhile, neurocritical patients have a high prevalence of HyperG, and its occurrence is associated with poor outcome after acute ischemic stroke, ICH, SAH, and TBI. It is unclear whether this association is due to direct detrimental effects exerted by HyperG or simply represents a marker of severe brain injury. Insulin has been shown to have various potentially pleiotropic neuroprotective properties in experimental models. However, the safety and efficacy of IIT in patients with critical brain disease have not been well studied. Available results do not support the use of IIT to maintain strict normoglycemia in this population. Patients with critical brain disease should have frequent glucose monitoring because severe HyperG and even modest hypoglycemia may be detrimental. Careful use of insulin infusion protocols appears advisable, but maintenance of strict normoglycemia cannot be recommended. Rigorous studies must be conducted to assess the value of insulin therapy and to determine the optimal blood glucose targets in patients with the most common acute vascular and traumatic brain insults.

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“…In patients with poor-grade subarachnoid hemorrhage the acute reductions in serum glucose, even to levels within the normal range, could generate brain energy metabolic crisis and lactate/pyruvate ratio elevation (82). When the brain's metabolism autoregulation is altered, there ares parts of them specially more susceptible than others (83)(84)(85)(86), when could be thoughtful glucose level as "sufficient" in a patient whith acute brain lesion this might be insuffient and even deleterious.…”

Section: Hypoglucemia and The Schimentioning

confidence: 99%

Glycemia in Spontaneous Intracerebral Hemorrhage: Clinical Implications

Alvis-Miranda¹,

Alcalá-Cerra²,

Moscote-Salazar³

2014

Romanian Neurosurgery

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Spontaneous cerebral hemorrhage or intracranial hemorrhage accounts for 10-15% of all strokes. Intracranial hemorrhage is much less common than ischemic stroke, but has higher mortality and morbidity, one of the leading causes of severe disability. Various alterations, among these the endocrine were identified when an intracerebral hemorrhage, these stress-mediated mechanisms exacerbate secondary injury. Deep knowledge of the injuries which are directly involved alterations of glucose, offers insight as cytotoxicity, neuronal death and metabolic dysregulations alter the prognosis of patients with spontaneous intracerebral hemorrhage.

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Systemic Glucose and Brain Energy Metabolism after Subarachnoid Hemorrhage

Abstract: Acute reductions in serum glucose, even to levels within the normal range, may be associated with brain energy metabolic crisis and LPR elevation in poor-grade SAH patients.

Cited by 72 publications

References 30 publications

Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage

Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage

Treating Hyperglycemia in Neurocritical Patients: Benefits and Perils

Glycemia in Spontaneous Intracerebral Hemorrhage: Clinical Implications

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