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Hypoglycemia (Hpg) is a metabolic brain disorder caused by critically low blood glucose levels, leading to neuronal dysfunction and potential irreversible damage if untreated. It manifests as acute neurological impairment ranging from confusion to coma.

Hypoglycemia (Hpg)

Hypoglycemic encephalopathy is a metabolic brain disorder caused by critically low blood glucose levels, leading to neuronal dysfunction and potential irreversible damage if untreated. It manifests as acute neurological impairment ranging from confusion to coma.

Hypoglycemia (Hpg): Overview, Diagnosis, and Management

Hypoglycemia (Hpg) is a metabolic brain disorder caused by critically low blood glucose levels, leading to neuronal dysfunction and potential irreversible damage if untreated. It manifests as acute neurological impairment ranging from confusion to coma.

Causes and Pathophysiology

Hypoglycemia occurs when blood glucose falls below 70 mg/dL, disrupting cerebral energy metabolism. Key mechanisms include:

  1. Neuronal Energy Depletion: Glucose is the brain’s primary fuel; deficiency triggers ATP depletion, lactic acidosis, and oxidative stress13.
  2. Excitotoxicity: Glutamate release and NMDA receptor activation cause neuronal injury13.
  3. Inflammation: Hypoglycemia-induced cytokine release exacerbates brain damage13.

Risk Factors:

Clinical Presentation

Symptoms progress rapidly and correlate with glucose levels:

StageSymptoms
EarlyTremor, sweating, tachycardia, hunger, irritability, confusion.
IntermediateSlurred speech, ataxia, dizziness, blurred vision, loss of consciousness.
AdvancedSeizures, coma, decerebrate posturing, permanent brain injury (if prolonged)

Key Signs:

  • Autonomic instability: Tachycardia, diaphoresis.
  • Focal deficits: Rare; suggests secondary causes (e.g., stroke)13.

Diagnosis

Laboratory Tests:

  • Confirmatory: Blood glucose <70 mg/dL (critical <40 mg/dL)13.
  • Exclude: Electrolyte imbalances, hepatic/renal dysfunction, drug toxicity.

Imaging:

  • CT/MRI: Non-specific; may show edema or infarction in severe cases13.
  • EEG: Generalized slowing or triphasic waves in advanced stages13.

Differential Diagnosis:

  • Metabolic encephalopathies: Hepatic, uremic, or hyperosmolar states.
  • Structural causes: Stroke, intracranial hemorrhage.
  • Psychogenic: Factitious hypoglycemia13.

Treatment

Immediate Intervention:

  1. Glucose administration:
    • Conscious patients: Oral glucose (15–20 g).
    • Unconscious patients: IV dextrose (25–50 g) or glucagon (1 mg IM)13.
  2. Recurrent hypoglycemia: Address underlying causes (e.g., insulin dose adjustment).

Supportive Care:

  • Seizure control: Benzodiazepines or levetiracetam if refractory13.
  • Monitor: Serial glucose checks, neurological exams.

Prognosis

  • Reversible: Prompt treatment prevents permanent damage.
  • Poor outcomes: Delayed therapy leads to cerebral edema, coma, or death13.

Key Considerations

  • Prevention: Educate diabetic patients on glucose monitoring and hypoglycemia recognition.
  • Critical care: Continuous glucose monitoring in ICU settings for early detection13.

Consult with Our Team of Experts Now!
At DrStemCellsThailand (DRSCT)‘s Anti-Aging and Regenerative Medicine Center of Thailand, we emphasize comprehensive evaluations and personalized treatment plans of Cellular Therapy and Stem Cells for managing various health conditions. If you have questions about Hypoglycemia or would like more information on our services, consult with our experts today!

Consult with Our Team of Experts Now!

References

Radiopaedia: Hypoglycemic Encephalopathy
DOI: 10.5334/pr.1
LinkRadiopaedia Hypoglycemic Encephalopathy

Cleveland Clinic: Hypoglycemia
DOI: 10.7326/0003-4819-146
LinkCleveland Clinic Hypoglycemia


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