Hyperglycaemia and the ischaemic brain: continuous glucose monitoring and implications for therapy.
Hyperglycaemia following acute stroke is both common and prolonged, regardless of diabetes status. A substantial body of evidence, derived from animal and human literature, has demonstrated that post-stroke hyperglycaemia has a deleterious effect upon clinical and radiological stroke outcomes. Whether intensive glycaemic manipulation positively influences the fate of ischaemic tissue remains to be shown. This article provides an overview of the prevalence, aetiology, and mechanisms of tissue injury arising as a result of post-stroke hyperglycaemia, as well as exploring the evidence from glucose-lowering treatment trials to date. Additionally, novel insights into post-stroke hyperglycaemia derived from continuous glucose monitoring are discussed. Stroke is a leading cause of death worldwide and the commonest cause of long-term disability amongst adults. Increasing evidence suggests that disordered physiological variables following acute ischaemic stroke adversely affect outcomes. Of these, post-stroke hyperglycaemia (PSH) is the most frequently recognised abnormality and is documented in up to 50% of patients at the time of stroke presentation. Importantly, a significant proportion of hyperglycaemic acute stroke patients (approximately 50%) have undiagnosed disorders of glucose metabolism, including diabetes. Animal and human data have repeatedly demonstrated that PSH negatively impacts upon the fate of ischaemic brain tissue, with greater infarct growth, higher mortality and more severe disability being consistent findings amongst hyperglycaemic stroke subjects. For these reasons, PSH represents an attractive physiological target for acute stroke therapies with potential application across broad time windows, stroke subtypes and stroke severity. In addition to providing an overview of the adverse effects of hyperglycaemia following acute ischaemic stroke, this article aims to summarise the evidence from current glucose-lowering treatment trials as well as exploring continuous glucose monitoring and the implications for future glycaemic manipulation.
Allport
Louise E
LE
Department of Neurology, Royal Melbourne Hospital, Parkville, Vic 3050, Australia.
Baird
Tracey A
TA
Davis
Stephen M
SM
D000328:Adult; D000818:Animals; D001786:Blood Glucose / Q000032:analysis* / Q000378:metabolism; D001921:Brain / Q000473:pathology; D002545:Brain Ischemia / Q000097:blood* / Q000150:complications / Q000473:pathology; D006233:Persons with Disabilities; D006801:Humans; D006943:Hyperglycemia / Q000097:blood* / Q000453:epidemiology / Q000503:physiopathology; D023421:Models, Animal; D018670:Monitoring, Ambulatory / Q000379:methods*; D020521:Stroke / Q000097:blood / Q000150:complications / Q000473:pathology
D001786:Blood Glucose