Endocrine System: DKA vs. HHS

Introduction

• Lecturer: Eddie Watson
• Channel: ICU Advantage
• Topic: Differences between Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS)
• Audience: Critical care students/professionals

Overview of DKA and HHS

• Both are hyperglycemic emergencies requiring quick intervention and ICU monitoring.
• Similarities involve acute hyperglycemia in decompensated diabetic patients.

Diabetic Ketoacidosis (DKA)

Key Characteristics

• Primarily occurs in Type 1 diabetics (rare in Type 2).
• Defined by:
  • Hyperglycemia: Glucose > 300 mg/dL
  • Hypovolemia
  • Ketoneemia and Ketonuria (ketones in blood and urine)
  • Anion gap metabolic acidosis

Lab Values

• Glucose: > 300 mg/dL
• Bicarb: < 15 mEq/L (can go < 10 in moderate, < 5 in severe)
• pH: < 7.3 (can go < 7.2 in moderate, < 7.1 in severe)
• Ketoneemia & Ketonuria

Causes

• Newly diagnosed Type 1 diabetes
• Insufficient insulin administration
• Stressful events: infection, trauma, surgery, pregnancy, alcohol intoxication

Pathophysiology

• Develops in < 24 hours
• Trigger: Insufficient or absent insulin levels
• Results:
  • Increased fatty acid metabolism → ketones production
  • Increased liver gluconeogenesis → glucose from proteins/amino acids
  • Secretion of counter-regulatory hormones (glucagon, catecholamines, cortisol, growth hormone)
  • Higher blood glucose but cellular glucose deprivation

Components

1. Fluid Volume Deficit & Electrolyte Imbalance:
   • Osmotic pressure increase → fluid shift to extracellular space → osmotic diuresis
   • Loss of water, sodium, magnesium, calcium, and phosphorus
   • Risk of hypovolemic shock, decreased GFR, dehydration of brain cells (neurological symptoms)
2. Acid-Base Imbalance:
   • Cellular starvation → fats & proteins metabolism → ketone acids → metabolic acidosis
   • Tissue hypoperfusion → anaerobic metabolism → lactic acid → worsened metabolic acidosis
   • Increased anion gap
   • Respiratory compensation: increased respiration rate & tidal volume
   • Intracellular potassium shift → potential hypokalemia

Signs and Symptoms

• Acetone Breath: Fruity smell
• Kussmaul Respirations: Rapid deep breathing
• **Abdominal Pain, Nausea, Vomiting
• Altered mental status: Paresthesia, paresis, aphasia
• Other Symptoms: Tachycardia, polyuria, polydipsia, lethargy, stupor, unconsciousness

Hyperosmolar Hyperglycemic State (HHS)

Key Characteristics

• Mostly seen in Type 2 diabetics
• Severe hyperglycemia (600-2000 mg/dL, typically ~1100)
• Profound dehydration, hyperosmolality, absence of ketosis
• Progressive onset (weeks to months)

Pathophysiology

• Partially functional insulin prevents lipolysis & ketones production
• Higher osmotic pressure → higher diuresis → profound dehydration (9-10 liters deficit)
• Less obvious symptoms delay treatment
• Elevated glucose leads to osmotic diuresis and dehydration, but pH generally normal
• Risk of lactic acid buildup due to hypoperfusion

Signs and Symptoms

• CNS Dysfunction & Higher Mortality: Due to severe dehydration, often in chronically ill patients
• Risks: Cardiac respiratory center depression, cerebral edema, cardiovascular collapse, renal shutdown, vascular embolism

Treatment for DKA and HHS

• Similarities
  • Fluid replacement
  • Treating hyperglycemia
  • Electrolyte replacement
  • Treating underlying disorder

Fluid Replacement

• Priority: Prevent cardiovascular collapse
• Initial rapid bolus of 0.9% normal saline (1-3 liters in the first hour)
• Continue fluids until volume restored
• Switch to D5 half NS as glucose normalizes to avoid hypoglycemia
• For DKA: Switch at glucose ~250 mg/dL; for HHS, higher to avoid cerebral edema

Hyperglycemia Treatment

• IV insulin
• Goal: Decrease glucose by 50-70 per hour
• Continue insulin until normal pH to avoid intracellular hypokalemia
• Monitor frequently (requires ICU care)

Electrolyte Replacement

• Frequent monitoring of potassium, magnesium, calcium, and phosphorus
• Hypokalemia risk: due to potassium shift and insulin administration
• Replace based on serum levels
• Monitor for signs of electrolyte imbalance

Underlying Disorder Treatment

• Determine and treat precipitating event (often infection)

Summary

• Understanding distinctions between DKA and HHS is crucial for effective treatment.
• Focus on fluid replacement, hyperglycemia management, electrolyte balance, and root cause treatment.
• Proper intervention can significantly improve patient outcomes and reduce mortality.

Conclusion

• This concludes the lesson on DKA vs. HHS.
• Upcoming lessons will cover differences between DI (Diabetes Insipidus) and SIADH (Syndrome of Inappropriate Antidiuretic Hormone).
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