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Background
Elevated blood glucose levels in stroke patients are considered hyperglycemia when over 140 mg/dL.
High blood sugar in acute stroke patients without diabetes. Cortisol and catecholamines release due to stress raise blood glucose.
Stroke increases brain energy demand and high glucose leads to lactic acid production, acidosis, and neuronal harm.
Accelerated atherosclerosis affects vessels in many distributions including both small and large vessels with potential cardiac involvement.
Hypoglycemia is defined as abnormal low blood glucose levels when less than 70 mg/dL. Excessive use of oral hypoglycemic agents or insulin causes low glucose levels.
Brain primarily uses glucose for oxidative metabolism. Cerebral cortex and basal ganglia have highest metabolic demands.
Less demand for substrate in cerebellum and subcortical white matter may cause focal deficits.
Epidemiology
Diabetes is a risk factor for stroke and can lead to strokes at younger ages in high diabetes prevalence groups.
30% to 40% of acute stroke patients have hyperglycemia at time of hospital admission. Prevalence increases to 60% in diabetes history patients.
Hyperglycemia is common in ischemic strokes and hemorrhagic strokes to cause worse outcomes in stroke patients.
Hypoglycemia rare in stroke patients compared to hyperglycemia affects 2% to 5% of acute cases.
Anatomy
Pathophysiology
Hormones raise blood glucose, promote gluconeogenesis, glycogenolysis, and decrease insulin sensitivity.
Anaerobic metabolism in ischemic brain causes lactic acid buildup to worsen acidosis.
High glucose level causes overproduction of reactive oxygen species and damage to cellular structures.
Hypoglycemia causes ATP shortage in cells to impair function and energy failure.
Neuronal membrane depolarization from excess glutamate leads to excitotoxicity, calcium influx, and cell death pathway activation.
Etiology
The causes for Hyperglycemia and Hypoglycemia are:
Stress-Induced Hyperglycemia
Acute Stress Response
Pre-existing Diabetes Mellitus
Type 1 and Type 2 Diabetes
Obesity and Metabolic Syndrome
Diabetes-Related Causes
Insulin or Oral Hypoglycemic Agents
Poor Nutritional Intake
Adrenal Insufficiency
Genetics
Prognostic Factors
Acute high blood sugar upon admission leads to worse outcomes. Studies link higher glucose levels to more severe strokes and increased mortality.
Prolonged high blood sugar in hospital indicates worse outcomes and higher complication risk.
Inflammation and high blood sugar suggest poor neurological prognosis risk.
Long-lasting low blood sugar heightens danger of irreversible brain damage and negative results due to lack of glucose.
Hypoglycemia in stroke patients can worsen neurological deficits to long-term issues if not promptly addressed.
Clinical History
Clinical History:
Collect details including patient history and presenting symptoms to understand clinical history of patient.
Physical Examination
Body assessment
Neurological Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Acute symptoms are:
Increased thirst, frequent urination, fatigue, confusion, seizures, and loss of consciousness, sudden weakness, numbness, difficulty speaking, consciousness
Differential Diagnoses
Hemorrhagic Stroke
Ischemic Stroke
Diabetic Ketoacidosis
Meningitis
Hypernatremia
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Regularly check blood sugar after stroke onset to manage common hyperglycemia promptly for care.
Ideal blood glucose in stroke’s target range is 140-180 mg/dL to prevent imbalances.
Continuous IV insulin given with frequent monitoring and adjustments based on levels.
Transition IV insulin to subcutaneous or oral agents based on regimen and glucose control.
Give conscious patient oral glucose tablets, juice, or snack to quickly treat hypoglycemia.
Intensive insulin therapy in DCCT delays onset and slows progression of retinopathy, nephropathy, and neuropathy in diabetes.
Neurologists avoid giving glucose fluids without thiamine to prevent acute Wernicke encephalopathy.
Patient with hypoglycemia from illness or malnutrition susceptible to vitamin deficiency.
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
use-of-non-pharmacological-approach-for-hyperglycemia-and-hypoglycemia-in-stroke
Close monitoring of hyperglycemic stroke patients in hospital settings allows for timely intervention for dangerously high blood glucose levels.
Maintain a comfortable room temperature to avoid an extra stress on the body.
Home space should be modified for better dietary habits with low-glycemic foods and regular mealtimes.
Regular physical activity can improve insulin sensitivity and blood glucose control.
Proper awareness about Hyperglycemia and Hypoglycemia in Stroke should be provided and its related causes with management strategies.
Appointments with a neurologist and preventing recurrence of disorder is an ongoing life-long effort.
Use of insulin therapy
Dextrose:
It releases energy in glycolysis, citric cycle, and phosphorylation in cells.
Use of oral hypoglycemic agents
It blocks liver sugar production and glucagon due to impaired cAMP signalling pathways.
use-of-intervention-with-a-procedure-in-treating-hyperglycemia-and-hypoglycemia-in-stroke
Mechanical thrombectomy is indicated as the standard procedure for acute ischemic stroke with large occlusion.
Feeding tubes placed for post-stroke patients with severe dysphagia to prevent hypoglycemia from poor oral intake.
use-of-phases-in-managing-hyperglycemia-and-hypoglycemia-in-stroke
In acute phase (0 to 72 hours) rapidly assess blood glucose levels upon presentation of stroke symptoms.
In subacute phase (72 hours to 2 weeks) switch IV insulin to subcutaneous or oral agents carefully.
Pharmacologic therapy is effective in the treatment phase as it includes use of insulin therapy and oral hypoglycemic agents.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies.
The regular follow-up visits with the neurologist are scheduled to check the improvement of patients along with treatment response.
Medication
Future Trends
Elevated blood glucose levels in stroke patients are considered hyperglycemia when over 140 mg/dL.
High blood sugar in acute stroke patients without diabetes. Cortisol and catecholamines release due to stress raise blood glucose.
Stroke increases brain energy demand and high glucose leads to lactic acid production, acidosis, and neuronal harm.
Accelerated atherosclerosis affects vessels in many distributions including both small and large vessels with potential cardiac involvement.
Hypoglycemia is defined as abnormal low blood glucose levels when less than 70 mg/dL. Excessive use of oral hypoglycemic agents or insulin causes low glucose levels.
Brain primarily uses glucose for oxidative metabolism. Cerebral cortex and basal ganglia have highest metabolic demands.
Less demand for substrate in cerebellum and subcortical white matter may cause focal deficits.
Diabetes is a risk factor for stroke and can lead to strokes at younger ages in high diabetes prevalence groups.
30% to 40% of acute stroke patients have hyperglycemia at time of hospital admission. Prevalence increases to 60% in diabetes history patients.
Hyperglycemia is common in ischemic strokes and hemorrhagic strokes to cause worse outcomes in stroke patients.
Hypoglycemia rare in stroke patients compared to hyperglycemia affects 2% to 5% of acute cases.
Hormones raise blood glucose, promote gluconeogenesis, glycogenolysis, and decrease insulin sensitivity.
Anaerobic metabolism in ischemic brain causes lactic acid buildup to worsen acidosis.
High glucose level causes overproduction of reactive oxygen species and damage to cellular structures.
Hypoglycemia causes ATP shortage in cells to impair function and energy failure.
Neuronal membrane depolarization from excess glutamate leads to excitotoxicity, calcium influx, and cell death pathway activation.
The causes for Hyperglycemia and Hypoglycemia are:
Stress-Induced Hyperglycemia
Acute Stress Response
Pre-existing Diabetes Mellitus
Type 1 and Type 2 Diabetes
Obesity and Metabolic Syndrome
Diabetes-Related Causes
Insulin or Oral Hypoglycemic Agents
Poor Nutritional Intake
Adrenal Insufficiency
Acute high blood sugar upon admission leads to worse outcomes. Studies link higher glucose levels to more severe strokes and increased mortality.
Prolonged high blood sugar in hospital indicates worse outcomes and higher complication risk.
Inflammation and high blood sugar suggest poor neurological prognosis risk.
Long-lasting low blood sugar heightens danger of irreversible brain damage and negative results due to lack of glucose.
Hypoglycemia in stroke patients can worsen neurological deficits to long-term issues if not promptly addressed.
Clinical History:
Collect details including patient history and presenting symptoms to understand clinical history of patient.
Body assessment
Neurological Examination
Acute symptoms are:
Increased thirst, frequent urination, fatigue, confusion, seizures, and loss of consciousness, sudden weakness, numbness, difficulty speaking, consciousness
Hemorrhagic Stroke
Ischemic Stroke
Diabetic Ketoacidosis
Meningitis
Hypernatremia
Regularly check blood sugar after stroke onset to manage common hyperglycemia promptly for care.
Ideal blood glucose in stroke’s target range is 140-180 mg/dL to prevent imbalances.
Continuous IV insulin given with frequent monitoring and adjustments based on levels.
Transition IV insulin to subcutaneous or oral agents based on regimen and glucose control.
Give conscious patient oral glucose tablets, juice, or snack to quickly treat hypoglycemia.
Intensive insulin therapy in DCCT delays onset and slows progression of retinopathy, nephropathy, and neuropathy in diabetes.
Neurologists avoid giving glucose fluids without thiamine to prevent acute Wernicke encephalopathy.
Patient with hypoglycemia from illness or malnutrition susceptible to vitamin deficiency.
Neurology
Close monitoring of hyperglycemic stroke patients in hospital settings allows for timely intervention for dangerously high blood glucose levels.
Maintain a comfortable room temperature to avoid an extra stress on the body.
Home space should be modified for better dietary habits with low-glycemic foods and regular mealtimes.
Regular physical activity can improve insulin sensitivity and blood glucose control.
Proper awareness about Hyperglycemia and Hypoglycemia in Stroke should be provided and its related causes with management strategies.
Appointments with a neurologist and preventing recurrence of disorder is an ongoing life-long effort.
Neurology
Dextrose:
It releases energy in glycolysis, citric cycle, and phosphorylation in cells.
Neurology
It blocks liver sugar production and glucagon due to impaired cAMP signalling pathways.
Neurology
Mechanical thrombectomy is indicated as the standard procedure for acute ischemic stroke with large occlusion.
Feeding tubes placed for post-stroke patients with severe dysphagia to prevent hypoglycemia from poor oral intake.
Neurology
In acute phase (0 to 72 hours) rapidly assess blood glucose levels upon presentation of stroke symptoms.
In subacute phase (72 hours to 2 weeks) switch IV insulin to subcutaneous or oral agents carefully.
Pharmacologic therapy is effective in the treatment phase as it includes use of insulin therapy and oral hypoglycemic agents.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies.
The regular follow-up visits with the neurologist are scheduled to check the improvement of patients along with treatment response.
Elevated blood glucose levels in stroke patients are considered hyperglycemia when over 140 mg/dL.
High blood sugar in acute stroke patients without diabetes. Cortisol and catecholamines release due to stress raise blood glucose.
Stroke increases brain energy demand and high glucose leads to lactic acid production, acidosis, and neuronal harm.
Accelerated atherosclerosis affects vessels in many distributions including both small and large vessels with potential cardiac involvement.
Hypoglycemia is defined as abnormal low blood glucose levels when less than 70 mg/dL. Excessive use of oral hypoglycemic agents or insulin causes low glucose levels.
Brain primarily uses glucose for oxidative metabolism. Cerebral cortex and basal ganglia have highest metabolic demands.
Less demand for substrate in cerebellum and subcortical white matter may cause focal deficits.
Diabetes is a risk factor for stroke and can lead to strokes at younger ages in high diabetes prevalence groups.
30% to 40% of acute stroke patients have hyperglycemia at time of hospital admission. Prevalence increases to 60% in diabetes history patients.
Hyperglycemia is common in ischemic strokes and hemorrhagic strokes to cause worse outcomes in stroke patients.
Hypoglycemia rare in stroke patients compared to hyperglycemia affects 2% to 5% of acute cases.
Hormones raise blood glucose, promote gluconeogenesis, glycogenolysis, and decrease insulin sensitivity.
Anaerobic metabolism in ischemic brain causes lactic acid buildup to worsen acidosis.
High glucose level causes overproduction of reactive oxygen species and damage to cellular structures.
Hypoglycemia causes ATP shortage in cells to impair function and energy failure.
Neuronal membrane depolarization from excess glutamate leads to excitotoxicity, calcium influx, and cell death pathway activation.
The causes for Hyperglycemia and Hypoglycemia are:
Stress-Induced Hyperglycemia
Acute Stress Response
Pre-existing Diabetes Mellitus
Type 1 and Type 2 Diabetes
Obesity and Metabolic Syndrome
Diabetes-Related Causes
Insulin or Oral Hypoglycemic Agents
Poor Nutritional Intake
Adrenal Insufficiency
Acute high blood sugar upon admission leads to worse outcomes. Studies link higher glucose levels to more severe strokes and increased mortality.
Prolonged high blood sugar in hospital indicates worse outcomes and higher complication risk.
Inflammation and high blood sugar suggest poor neurological prognosis risk.
Long-lasting low blood sugar heightens danger of irreversible brain damage and negative results due to lack of glucose.
Hypoglycemia in stroke patients can worsen neurological deficits to long-term issues if not promptly addressed.
Clinical History:
Collect details including patient history and presenting symptoms to understand clinical history of patient.
Body assessment
Neurological Examination
Acute symptoms are:
Increased thirst, frequent urination, fatigue, confusion, seizures, and loss of consciousness, sudden weakness, numbness, difficulty speaking, consciousness
Hemorrhagic Stroke
Ischemic Stroke
Diabetic Ketoacidosis
Meningitis
Hypernatremia
Regularly check blood sugar after stroke onset to manage common hyperglycemia promptly for care.
Ideal blood glucose in stroke’s target range is 140-180 mg/dL to prevent imbalances.
Continuous IV insulin given with frequent monitoring and adjustments based on levels.
Transition IV insulin to subcutaneous or oral agents based on regimen and glucose control.
Give conscious patient oral glucose tablets, juice, or snack to quickly treat hypoglycemia.
Intensive insulin therapy in DCCT delays onset and slows progression of retinopathy, nephropathy, and neuropathy in diabetes.
Neurologists avoid giving glucose fluids without thiamine to prevent acute Wernicke encephalopathy.
Patient with hypoglycemia from illness or malnutrition susceptible to vitamin deficiency.
Neurology
Close monitoring of hyperglycemic stroke patients in hospital settings allows for timely intervention for dangerously high blood glucose levels.
Maintain a comfortable room temperature to avoid an extra stress on the body.
Home space should be modified for better dietary habits with low-glycemic foods and regular mealtimes.
Regular physical activity can improve insulin sensitivity and blood glucose control.
Proper awareness about Hyperglycemia and Hypoglycemia in Stroke should be provided and its related causes with management strategies.
Appointments with a neurologist and preventing recurrence of disorder is an ongoing life-long effort.
Neurology
Dextrose:
It releases energy in glycolysis, citric cycle, and phosphorylation in cells.
Neurology
It blocks liver sugar production and glucagon due to impaired cAMP signalling pathways.
Neurology
Mechanical thrombectomy is indicated as the standard procedure for acute ischemic stroke with large occlusion.
Feeding tubes placed for post-stroke patients with severe dysphagia to prevent hypoglycemia from poor oral intake.
Neurology
In acute phase (0 to 72 hours) rapidly assess blood glucose levels upon presentation of stroke symptoms.
In subacute phase (72 hours to 2 weeks) switch IV insulin to subcutaneous or oral agents carefully.
Pharmacologic therapy is effective in the treatment phase as it includes use of insulin therapy and oral hypoglycemic agents.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies.
The regular follow-up visits with the neurologist are scheduled to check the improvement of patients along with treatment response.

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