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There are two lines of evidence that drove the evolution of these guidelines: (1) The weight of arguments that suggest an association between high glucose levels and detrimental outcome has substantially increased in the last few years. Observational studies, both naturalistic [8, 9] and trialassociated [10–12] , have reported higher morbidity and mortality in patients with initial hyperglycaemia. (Note that there is neither consensus as to what actually defines ‘initial’ – is it a 1-measurement baseline, continuously elevated levels within the first 24 h or other timelines? – nor is there a clear definition of when hyperglycaemia necessitates treatment [13] .) Moreover, experimental data have underlined the association. Early neuropathological animal studies provided evidence that hyperglycaemia augments morphological brain damage in acute stroke [14, 15] . Imaging studies in hyperglycaemic animals subjected to ischaemic stroke corroborated these findings: hyperglycaemia is associated with enhanced MRI diffusion-weighted imaging alterations [16] and reduced hemispheric cerebral blood volume [17] . Importantly, equivalent correlations have been established in MRI studies in human subjects. Acute hyperglycaemia is associated with reduced salvage of perfusion-impaired tissue and larger final infarct size [18, 19] . This is also true for patients treated with intravenous tissue plasminogen Hyperglycaemia is a common phenomenon after cerebral ischaemia (for that matter, after most acute medical or surgical conditions), and clinicians have certainly been itching to treat. But should we? The devil is in the details. Continuous assessment of blood glucose levels and qualified treatment are often noted to be core components of specialized stroke care [1] . Expert statements have taken a somewhat sinusoidal course when discussing the matter. In 1994, the Stroke Council of the American Heart Association said that it may be a good idea to treat hyperglycaemia in patients with stroke just as one would treat hyperglycaemia in ‘other persons with elevated blood glucose’ [2] . The guideline was substantiated in 2003, with treatment then being warranted should blood glucose levels exceed 16.6 mmol/l (300 mg/dl) [3] . Europeans were more stringent, finding that a cut-off of 10 mmol/l (180 mg/dl) would be optimal [4, 5] . The American Stroke Association followed this lead and in 2007 revised its suggestions and noted that treatment should begin above 11.1 mmol/l (200 mg/dl), possibly as low as 7.8 mmol/l (140 mg/dl) [6] . In 2008, instead of continuing on the downward track and effectively postulating fasting normoglycaemia below 5.5 mmol/l (99 mg/dl), the European Stroke Organization retained its previous recommendation of 10 mmol/l (180 mg/dl) [7] . Received: August 26, 2009 Accepted: August 26, 2009 Published online: March 30, 2010

cerebrovascular diseases

Sugar and NICE – Aggressive Hyperglycaemic Control in Ischaemic Stroke and What Can We Learn from Non-Neurological Intensive Glucose Control Trials in the Critically Ill?