Electrolyte Changes in Diabetes

Diabetic Ketoacidosis (DKA)

• Pathophysiology: Absolute insulin deficiency leads to hyperglycemia, ketogenesis (metabolic acidosis), and osmotic diuresis. This results in profound water and electrolyte loss.
• Key Electrolyte Changes:
  • Potassium (K⁺):
    • Serum K⁺: Can be normal or elevated on presentation despite a total body K⁺ deficit.
    • Mechanism of Hyperkalemia: Lack of insulin (which normally drives K⁺ into cells) and extracellular shift of K⁺ in exchange for H⁺ during acidosis.
    • Total Body Deficit: Caused by significant urinary losses from osmotic diuresis.
    • Clinical Pearl: Tx with insulin will drive K⁺ back into cells, causing a rapid drop in serum levels and potentially life-threatening hypokalemia. K⁺ replacement is critical, and insulin should be held if initial K⁺ is <3.3 mEq/L.
  • Sodium (Na⁺):
    • Serum Na⁺: Usually low (pseudohyponatremia) due to the osmotic effect of hyperglycemia drawing water into the extracellular space, diluting the sodium.
    • Correction Formula: For every 100 mg/dL increase in glucose above 100 mg/dL, add ~1.6 mEq/L to the measured Na⁺ to estimate the corrected value.
  • Phosphate (PO₄^3-):
    • Serum PO₄^3-: Often elevated initially due to extracellular shifts but reflects a total body deficit from urinary losses.
    • Clinical Pearl: Insulin therapy drives phosphate back into cells, which can lead to severe hypophosphatemia, impairing muscle function (including respiratory muscles) and ATP production.
  • Bicarbonate (HCO₃^-):
    • Serum HCO₃^-: Low (<18 mEq/L) due to titration by ketoacids, resulting in a high anion gap metabolic acidosis.

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Hyperosmolar Hyperglycemic State (HHS)

• Pathophysiology: Relative insulin deficiency allows for extreme hyperglycemia but is sufficient to prevent significant ketosis. The primary issue is profound dehydration from osmotic diuresis.
• Key Electrolyte Changes:
  • Potassium (K⁺):
    • Similar to DKA, patients have a total body K⁺ deficit due to massive urinary losses.
    • Initial serum K⁺ can be normal or even high due to extracellular shifts from insulin deficiency and hyperosmolality.
  • Sodium (Na⁺):
    • Can be low, normal, or high.
    • Pseudohyponatremia is common due to extreme hyperglycemia.
    • However, if water loss exceeds sodium loss (which is typical in HHS), hypernatremia can occur.
  • Phosphate (PO₄^3-) & Magnesium (Mg²⁺):
    • Total body stores are depleted due to prolonged osmotic diuresis.
  • Bicarbonate (HCO₃^-):
    • Usually normal or only mildly decreased (>15 mEq/L) as significant ketoacidosis is absent.

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Effects of Insulin Therapy

• Mechanism: Insulin activates the Na⁺/K⁺-ATPase pump, driving potassium into cells.
• Key Effects:
  • ↓ Serum K⁺: Insulin administration is a primary treatment for hyperkalemia but is the reason for iatrogenic hypokalemia during DKA/HHS treatment.
  • ↓ Serum PO₄^3- & Mg²⁺: Insulin also promotes the intracellular shift of phosphate and magnesium.
• Refeeding Syndrome:
  • Relevant in malnourished patients (including those with uncontrolled DM) upon initiation of nutrition/insulin.
  • Insulin release stimulates the cellular uptake of glucose, K⁺, PO₄^3-, and Mg²⁺ from the already depleted extracellular space.
  • This can lead to severe hypophosphatemia, hypokalemia, and hypomagnesemia, causing cardiac arrhythmias, muscle weakness, and respiratory failure.