Hyperglycaemia after acute stroke

Several aspects of physiology, notably blood pressure, body temperature, blood glucose, and blood oxygen saturation, may be altered after an ischemic stroke and intracerebral hemorrhage. Generally, blood pressure and temperature rise acutely after a stroke, before returning to normal. Blood glucose and oxygen levels may be abnormal in individuals, but they do not follow a set pattern. Several aspects of these physiological alterations remain unclear, including their principal determinants - whether they genuinely affect prognosis (as opposed to merely representing underlying processes such as inflammation or a stress response), whether these effects are adaptive or maladaptive, whether the effects are specific to certain subgroups (e.g. lacunar stroke) and whether modifying physiology also modifies its prognostic effect. Hypertension and hyperglycemia may be helpful or harmful, depending on the perfusion status after an ischemic stroke; the therapeutic response to their lowering may be correspondingly variable. Hypothermia may provide benefits, in addition to preventing harm through protection from hyperthermia. Hypoxia is harmful, but normobaric hyperoxia is unhelpful or even harmful in normoxic patients. Hyperbaric hyperoxia, however, may be beneficial, though this remains unproven. The above-mentioned uncertainties necessitate generally conservative measures for physiology management, although there are notably specific recommendations for thrombolysis-eligible patients. Stroke unit care is associated with better outcome, possibly through better management of poststroke physiology. Stroke units can also facilitate research to clarify the relationship between physiology and prognosis, and to subsequently clarify management guidelines.

show abstract

“…[120] A neuroendocrine stress response[121] and an inflammatory response[122] may also play a role in generating hyperglycemia.…”

Section: Glucosementioning

confidence: 99%

Early changes in physiological variables after stroke

Wong

Read

2008

Ann Indian Acad Neurol

View full text Add to dashboard Cite

show abstract

“…The possible pathogenesis of hyperglycemia in acute ischemic stroke is stress response or pre-existing impaired glucose intolerance in patients without history of diabetes 9 , 10 , although there is no sufficient evidence regarding the management of hyperglycemia in these patients. Furthermore, the studies regarding hyperglycemia in lacunar stroke have reported inconclusive findings, and one meta-analysis of 1375 patients with ischemic stroke from two placebo-controlled trials reported that hyperglycemia did not harm patients with lacunar stroke, and that moderate hyperglycemia (> 8mmol/L) might even be beneficial 11 .…”

Section: Introductionmentioning

confidence: 99%

The Influence of Acute Hyperglycemia in an Animal Model of Lacunar Stroke That Is Induced by Artificial Particle Embolization

et al. 2016

View full text Add to dashboard Cite

Animal and clinical studies have revealed that hyperglycemia during ischemic stroke increases the stroke's severity and the infarct size in clinical and animal studies. However, no conclusive evidence demonstrates that acute hyperglycemia worsens post-stroke outcomes and increases infarct size in lacunar stroke. In this study, we developed a rat model of lacunar stroke that was induced via the injection of artificial embolic particles during full consciousness. We then used this model to compare the acute influence of hyperglycemia in lacunar stroke and diffuse infarction, by evaluating neurologic behavior and the rate, size, and location of the infarction. The time course of the neurologic deficits was clearly recorded from immediately after induction to 24 h post-stroke in both types of stroke. We found that acute hyperglycemia aggravated the neurologic deficit in diffuse infarction at 24 h after stroke, and also aggravated the cerebral infarct. Furthermore, the infarct volumes of the basal ganglion, thalamus, hippocampus, and cerebellum but not the cortex were positively correlated with serum glucose levels. In contrast, acute hyperglycemia reduced the infarct volume and neurologic symptoms in lacunar stroke within 4 min after stroke induction, and this effect persisted for up to 24 h post-stroke. In conclusion, acute hyperglycemia aggravated the neurologic outcomes in diffuse infarction, although it significantly reduced the size of the cerebral infarct and improved the neurologic deficits in lacunar stroke.

show abstract

“…Acute hyperglycemia also increased the risk of a poor functional recovery in non-diabetic stroke survivors with a relative risk of 1.4. Other studies have not found hyperglycemia to be an independent predictor of stroke outcome and have suggested that hyperglycemia simply reflects a catecholamine-based stress response to a more severe stroke [62,63,64]. …”

Section: Control Of Glycemiamentioning

confidence: 99%

Non-Pharmacological Neuroprotection: Role of Emergency Stroke Management

Leira¹,

Blanco²,

Rodríguez‐Yáñez³

et al. 2006

Cerebrovasc Dis

View full text Add to dashboard Cite

Acute stroke should be considered a medical emergency, where actions taken in the first hours are fundamental for achieving recovery of the damaged cerebral tissue and a better prognosis for the patient. Recanalization and neuroprotective treatment has been used with mixed results. The effectiveness observed in the first hours with thrombolytic drug treatment is only applicable to a small percentage of patients, and attempts to widen this treatment window have not yet proved fruitful. Pharmacological neuroprotective treatment has not yet demonstrated the clinical effectiveness observed in experimental models. The concept of neuroprotection in cerebral ischemia also involves a series of mechanisms that take place at the cerebral level following vascular occlusion. In this context, it should be borne in mind that a series of physiological functions usually involved in the cerebral metabolism (control of blood pressure, of temperature, of glycemia and of arterial oxygen saturation) play a key role in modulation of the ischemic process. Changes in the control of these mechanisms may aggravate the process of cerebral damage in the first hours of ischemic stroke. In this work we review the prognostic importance of the main mechanisms that may influence the acute phase of cerebral ischemic stroke, as well as their therapeutic management and control in the clinical situation.

show abstract

Hyperglycaemia after acute stroke

Abstract: GD, Dyker AG, Lees KR. Is hyperglycaemia an independent predictor of poor outcome after acute stroke? Results of a long term follow up study.

Cited by 16 publications

References 1 publication

Early changes in physiological variables after stroke

Early changes in physiological variables after stroke

The Influence of Acute Hyperglycemia in an Animal Model of Lacunar Stroke That Is Induced by Artificial Particle Embolization

Non-Pharmacological Neuroprotection: Role of Emergency Stroke Management

Contact Info

Product

Resources

About