Lecture on Hyperosmolar Hyperglycemic State (HHS)

Introduction

• Topic: Hyperosmolar Hyperglycemic State (HHS)
• Outline:
  • Pathophysiology
  • Symptoms
  • Lab values and treatment

Pathophysiology of HHS

• Definition: A life-threatening medical emergency in type 2 diabetes patients.
• Key Features:
  • Restricted fluid intake
  • Severe dehydration
  • Hyperosmolarity
• Comparison:
  • Unlike diabetic ketoacidosis, HHS has minimal or no ketone body formation, hence no ketoacidosis.
• Mechanism:
  • Insulin Levels: Low insulin levels favor glucose function.
  • Stress Response: Production of catecholamines increases glucagon production.
  • Liver Activity:
    • Increases glucose production
    • Increases glycogenolysis
    • Decreases glucose utilization
  • Result: Raises blood glucose levels.
  • Fluid Intake: Restricted fluid intake alongside hyperglycemia increases blood osmolarity.
  • Ketone Bodies: Minimal insulin prevents ketone body formation, differentiating from diabetic ketoacidosis.

Symptoms of HHS

• Glycosuria: Glucose filtered out by kidneys into urine, pulling water and causing dehydration.
• Dehydration: Worsens the HHS.
• Central Nervous System:
  • Hyperosmolarity in bloodstream pulls water out of CNS.
  • Causes altered mental status, potentially progressing to coma.

Laboratory Findings

• Blood Glucose Levels: Very high, typically > 600 mg/dL.
• pH Levels: > 7.3 (no acidosis occurs).
• Ketones: Absent in urine and blood.
• Anion Gap: < 12.
• Serum Osmolarity: > 320 mOsm/kg.
• Key Focus:
  • Glucose levels > 600 mg/dL.
  • Serum osmolarity > 320 mOsm/kg.

Treatment of HHS

• Goals:
  • Reduce high glucose levels with insulin administration.
  • Manage hyperosmolarity with IV fluids.
• Insulin Caution:
  • Potential for hypokalemia due to intracellular shift of potassium when insulin is administered.
  • Mechanism: Insulin stimulates sodium-potassium pump, exchanging extracellular potassium for intracellular sodium.
  • Prevention: Add potassium to IV fluids a few hours after starting therapy.

Conclusion

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