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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.

We report our management of a patient presenting with concomitant cortical stroke and pulmonary embolism. Stroke symptoms and respiratory distress were present for 2 h at the time of initial assessment. The patient was treated with intravenous tissue plasminogen activator (tPA). Intravenous unfractionated heparin was given 24 h after treatment with tPA. The patient's neurological and respiratory status both improved following thrombolysis. The treatment options and potential dilemmas are discussed.

Background and Purpose: Acute poststroke hyperglycemia has been associated with larger infarct volumes and a cortical location, regardless of diabetes status. Stress hyperglycemia has been attributed to activation of the hypothalamic-pituitary-adrenal axis but never a specific cortical location. We tested the hypothesis that damage to the insular cortex, a site with autonomic connectivity, results in hyperglycemia reflecting sympathoadrenal dysregulation., Methods: Diffusion-weighted MRI, glycosylated hemoglobin (HbA1c), and blood glucose measurements were obtained in 31 patients within 24 hours of ischemic stroke onset. Acute diffusion-weighted imaging (DWI) lesion volumes were measured, and involvement of the insular cortex was assessed on T2-weighted images., Results: Median admission glucose was significantly higher in patients with insular cortical ischemia (8.6 mmol/L; n=14) compared with those without (6.5 mmol/L; n=17; P=0.006). Multivariate linear regression demonstrated that insular cortical ischemia was a significant independent predictor of glucose level (P=0.001), as was pre-existing diabetes mellitus (P=0.008). After controlling for the effect of insular cortical ischemia, DWI lesion volume was not associated with higher glucose levels (P=0.849). There was no association between HbA1c and glucose level (P=0.737)., Conclusions: Despite the small sample size, insular cortical ischemia appeared to be associated with the production of poststroke hyperglycemia. This relationship is independent of pre-existing glycemic status and infarct volume. Neuroendocrine dysregulation after insular ischemia may be 1 aspect of a more generalized acute stress response. Future studies of poststroke hyperglycemia should account for the effect of insular cortical ischemia.