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Hyperglycemia and cerebral glucose in aneurysmal subarachnoid hemorrhage

Objective To determine whether hyperglycemia exerts deleterious effects via cerebral energy metabolism and to illuminate the effects of cerebral high/low glucose in patients with aneurysmal subarachnoid hemorrhage. Design and setting Prospective, nonrandomized single-center study over a 2-year perio...

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Bibliographic Details
Published in:Intensive care medicine 2008-07, Vol.34 (7), p.1200-1207
Main Authors: Schlenk, Florian, Nagel, Alexandra, Graetz, Daniela, Sarrafzadeh, Asita S.
Format: Article
Language:English
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Summary:Objective To determine whether hyperglycemia exerts deleterious effects via cerebral energy metabolism and to illuminate the effects of cerebral high/low glucose in patients with aneurysmal subarachnoid hemorrhage. Design and setting Prospective, nonrandomized single-center study over a 2-year period in an intensive care unit at a primary-level university hospital. Patients 28 subarachnoid hemorrhage patients (age 53 ± 10 years, WFNS grade 2.8 ± 1.5) classified as asymptomatic ( n  = 5) or symptomatic with acute focal or delayed ischemic neurological deficits ( n  = 23). Measurements and results Hyperglycemia (> 7.8 mmol/l; > 140 mg/dl) was more frequent in symptomatic patients and was reflected in higher glycerol concentrations than in asymptomatic patients. In all patients a microdialysis catheter was inserted into the tissue at risk; dialysates were collected hourly for 10 days. Cerebral low-glucose episodes ( 2.6 mmol/l) occurred independently of blood glucose levels. During high-glucose episodes cerebral microdialysate levels were normal, while cerebral low glucose, occurring more frequently in symptomatic patients, was associated with severe cellular distress (increase in lactate/pyruvate ratio, glutamate, glycerol) and with unfavorable outcome if combined with hyperglycemia. Conclusions Although hyperglycemia was more frequent in symptomatic patients and associated with high glycerol levels, hyperglycemia was not related to cerebral high glucose. It appears that the association of adverse outcome with acute-phase hyperglycemia is not mediated by cerebral glucose metabolism. Cerebral low glucose was associated with severe metabolic distress and may present a target for therapy to improve clinical outcome.
ISSN:0342-4642
1432-1238
DOI:10.1007/s00134-008-1044-5