POST-STROKE HYPERGLYCEMIA AS A MARKER OF STROKE SEVERITY AND PROGNOSIS
Ahmed Mostafa Abd El Fattah Kassab;
Abstract
A stroke is defined as rapidly developing clinical symptoms and/or signs of focal, and at times global (applied to patients in deep coma and to those with subarachnoid hemorrhage) loss of brain function, with symptoms lasting more than 24-hours or leading to death, with no apparent cause other than that of vascular origin.(Hatano 1976)
Worldwide, according to the World Health Organization (WHO) stroke has remained the second major killer during the past decade.(WHO 2014) In the past two decades globally, noticeable increases took place in the absolute numbers of people with incident stroke (a 68% increase), stroke survivors (84%), stroke-related deaths (26%), and disability-adjusted life year(DALYs) lost (12%). The most striking increases in the number of stroke survivors (113%),DALYs lost (31%), and stroke-related deaths (36%) were in people aged 75 years and older.(Feigin et al. 2014)
Stroke is also the leading cause of disability in adults. Of the hundreds of thousands of stroke survivors each year, approximately 30% require assistance with activities of daily living, 20% require assistance with ambulation, and 16% require institutional care.(Daroff et al. 2012)
It is accepted that 85% of strokes are due to cerebral infarction, 10% due to primary intracerebral hemorrhage (ICH) and 5% due to subarachnoid hemorrhage. The risk of recurrent stroke is 26% within 5 years of a first stroke and 39% by 10 years.(Mohan et al. 2011)
Hyperglycemia and insulin resistance are common in critically ill patients with or without a history of diabetes.(Gearhart & Parbhoo 2006)
In addition, hyperglycemia is a risk factor for poor clinical outcomes in the same population.(DiNardo et al. 2004)
The documented adverse effects associated with hyperglycemia are altered fluid balance, increased rates of infection and renal failure, morbidity after acute myocardial infarction, increased risk of congestive heart failure, increased severity of disability after an acute cerebral vascular event, and an increased overall mortality.(DiNardo et al. 2004)
Patients with acute stroke frequently present with hyperglycemia, with its incidence estimates varying and depending on the frequency of glucose measurements and the criteria used to define hyperglycemia.(Lees 2009)
The incidence of post-stroke hyperglycemia was approximately 45% in studies with frequent glucose measurements and a cut-off of 126 mg/dl to define hyperglycemia.(Allport et al. 2006)
In a systematic review, it was found that even though the elevation of blood glucose levels is moderate in stroke patients, hyperglycemia is associated with mortality and poor functional recovery compared with lower glucose levels.(Capes et al. 2001)
Interestingly, non-diabetic ischemic stroke patients have an increased risk of mortality if their blood glucose levels are > 110 mg/dl at early time points following the acute phase of ischemic stroke onset.(Vriesendorp et al. 2009)
In a recent study, Rosso et al. reported that infarct growth was greater in patients with high blood glucose levels than in patients with low blood glucose levels after ischemic stroke.(Rosso et al. 2011)
Several mechanisms underlying hyperglycemia after ischemic stroke have been proposed.(Guyomard et al. 2009) Specifically, ischemic stroke–related cytokines have been shown to activate the hypothalamus–pituitary–adrenal axis, leading to increased serum glucocorticoid levels and the activation of the sympathetic autonomic nervous system leading to catecholamine release, resulting in excessive glucose production and insulin resistance.(Chan et al. 2005)
However, in clinical practice, not all patients with hyperglycemia presenting during the acute phase of ischemic stroke show a significantly elevated catecholamine, suggesting that the hyperglycemia observed during the acute phase of ischemic stroke cannot be explained by increased catecholamines alone.(Harada et al. 2012)
Possible mechanisms by which hyperglycemia would damage brain include poor blood flow to the ischemic penumbra, intracellular acidification, reactive oxygen species (ROS) accumulation, blood brain barrier (BBB) disruption, inflammatory response induction, and axonal degradation.(Suarez 2006)
Clinical research has shown that normalization of blood glucose levels (from 135 to 81 mg/dl of FBG) during the first 48 h of hospitalization appears to confer
Worldwide, according to the World Health Organization (WHO) stroke has remained the second major killer during the past decade.(WHO 2014) In the past two decades globally, noticeable increases took place in the absolute numbers of people with incident stroke (a 68% increase), stroke survivors (84%), stroke-related deaths (26%), and disability-adjusted life year(DALYs) lost (12%). The most striking increases in the number of stroke survivors (113%),DALYs lost (31%), and stroke-related deaths (36%) were in people aged 75 years and older.(Feigin et al. 2014)
Stroke is also the leading cause of disability in adults. Of the hundreds of thousands of stroke survivors each year, approximately 30% require assistance with activities of daily living, 20% require assistance with ambulation, and 16% require institutional care.(Daroff et al. 2012)
It is accepted that 85% of strokes are due to cerebral infarction, 10% due to primary intracerebral hemorrhage (ICH) and 5% due to subarachnoid hemorrhage. The risk of recurrent stroke is 26% within 5 years of a first stroke and 39% by 10 years.(Mohan et al. 2011)
Hyperglycemia and insulin resistance are common in critically ill patients with or without a history of diabetes.(Gearhart & Parbhoo 2006)
In addition, hyperglycemia is a risk factor for poor clinical outcomes in the same population.(DiNardo et al. 2004)
The documented adverse effects associated with hyperglycemia are altered fluid balance, increased rates of infection and renal failure, morbidity after acute myocardial infarction, increased risk of congestive heart failure, increased severity of disability after an acute cerebral vascular event, and an increased overall mortality.(DiNardo et al. 2004)
Patients with acute stroke frequently present with hyperglycemia, with its incidence estimates varying and depending on the frequency of glucose measurements and the criteria used to define hyperglycemia.(Lees 2009)
The incidence of post-stroke hyperglycemia was approximately 45% in studies with frequent glucose measurements and a cut-off of 126 mg/dl to define hyperglycemia.(Allport et al. 2006)
In a systematic review, it was found that even though the elevation of blood glucose levels is moderate in stroke patients, hyperglycemia is associated with mortality and poor functional recovery compared with lower glucose levels.(Capes et al. 2001)
Interestingly, non-diabetic ischemic stroke patients have an increased risk of mortality if their blood glucose levels are > 110 mg/dl at early time points following the acute phase of ischemic stroke onset.(Vriesendorp et al. 2009)
In a recent study, Rosso et al. reported that infarct growth was greater in patients with high blood glucose levels than in patients with low blood glucose levels after ischemic stroke.(Rosso et al. 2011)
Several mechanisms underlying hyperglycemia after ischemic stroke have been proposed.(Guyomard et al. 2009) Specifically, ischemic stroke–related cytokines have been shown to activate the hypothalamus–pituitary–adrenal axis, leading to increased serum glucocorticoid levels and the activation of the sympathetic autonomic nervous system leading to catecholamine release, resulting in excessive glucose production and insulin resistance.(Chan et al. 2005)
However, in clinical practice, not all patients with hyperglycemia presenting during the acute phase of ischemic stroke show a significantly elevated catecholamine, suggesting that the hyperglycemia observed during the acute phase of ischemic stroke cannot be explained by increased catecholamines alone.(Harada et al. 2012)
Possible mechanisms by which hyperglycemia would damage brain include poor blood flow to the ischemic penumbra, intracellular acidification, reactive oxygen species (ROS) accumulation, blood brain barrier (BBB) disruption, inflammatory response induction, and axonal degradation.(Suarez 2006)
Clinical research has shown that normalization of blood glucose levels (from 135 to 81 mg/dl of FBG) during the first 48 h of hospitalization appears to confer
Other data
| Title | POST-STROKE HYPERGLYCEMIA AS A MARKER OF STROKE SEVERITY AND PROGNOSIS | Other Titles | إستخدام إرتفاع نسبة السكر بالدم فيما بعد السكتة الدماغية كمؤشر للتكهن بشدة السكتة الدماغية ونتائجها | Authors | Ahmed Mostafa Abd El Fattah Kassab | Issue Date | 2015 |
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