Hyperglycemia and Hypoglycemia in Stroke

Updated: September 27, 2024

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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

Metformin:

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

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Hyperglycemia and Hypoglycemia in Stroke

Updated : September 27, 2024

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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

Metformin:

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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