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AKA: hyperkalaemia, hyperpotassemia, hyperpotassaemia

Evaluation and management of elevated blood potassium in pediatric patients


Decreased renal potassium excretion

  • ACE inhibitors, ARBs, aldosterone antagonists (e.g., spironolactone)
  • Pseudohypoaldosteronism or true hypoaldosteronism
    • Urinary tract obstruction (with or without pyelonephritis) can decrease responsiveness to aldosterone
      • Excretion of potassium is regulated by epithelial sodium channel (ENaC) of the principal cells in the collecting tubules and cortical collecting ducts
        • Sodium absorption creates a negative charge in the tubular lumen, which stimulates potassium secretion from the principal cells
        • Stimulation of ENaC with aldosterone or increased sodium delivery will increase potassium excretion
  • Congenital adrenal hyperplasia
  • Kidney failure

Excessive potassium intake

  • Generally occurs in setting of comorbid disorder (e.g., kidney insufficiency) as kidney can usually handle large potassium load
  • IV fluids
  • Hyperalimentation
  • PRBC transfusions
  • High-potassium foods, drugs, nutritional supplements

Extracellular shifts (movement of potassium out of cells)

  • Acidosis
  • Hemolysis, tumor lysis, rhabdomyolysis (e.g., burn injury)
  • Hypoinsulinemia, diabetic ketoacidosis
  • β-blockers


  • Hemolysis
    • Capillary stick (finger/heel stick) technique
    • Specimen sitting for too long before testing
    • Shaking test tube, transporting in pneumatic tube

Signs and symptoms

  • Usually asymptomatic
  • Muscle weakness, paralysis
  • ECG (EKG) changes
    • Shortened QT interval
    • Widened PR interval
    • Widened QRS
  • Cardiac arrhythmia (ventricular fibrillation, asystole)


  • Ensure quality specimen (ideally venipuncture)
  • ECG to evaluate for electrocardiographic changes
  • Transtubular potassium gradient (TTKG) sometimes used if concern for kidney potassium retention
    • Should be ≥7 if hyperkalemic; low value suggests hypoaldosteronism
    • However, TTKG has limited supporting evidence for its use in evaluation of hyperkalemia, and may be more useful in evaluating response to mineralocorticoid therapy
  • Urine electrolytes before and after fludrocortisone to evaluate responsiveness to mineralocorticoid
  • Serum cortisol, aldosterone levels (to assess for CAH)


  • Treat underlying cause
  • Stabilize:
    • Calcium
    • Insulin + glucose: shift potassium intracellularly by stimulating Na⁺/K⁺-ATPase
    • β-agonists (e.g., albuterol, epinephrine): shift potassium intracellularly by stimulating Na⁺/K⁺-ATPase
    • Sodium bicarbonate (NaHCO₃): stimulates release of H⁺ from cells in exchange for K⁺ via H⁺-K⁺ exchanger to maintain electroneutrality
  • Remove excess potassium (definitive therapy):
    • Sodium chloride
    • Diuretics
      • Thiazide diuretics
      • Loop diuretics
      • Diuretics will increase in urinary sodium losses resulting in a decrease in circulating volume, which may be undesirable
        • Can be counteracted with saline administration
    • Sodium polystyrene sulfonate (SPS, Kayexalate®)
      • Ion exchange resin - exchanges Na⁺ for K⁺
        • Large sodium load, can cause hypernatremia
        • In vivo, 1 g of SPS delivers ~33 mg (1.4 mEq) Na⁺ and binds ~1 mEq of K⁺
          • In vitro, 1 g SPS contains ~100 mg (4.1 mEq) Na and will bind 2-3.1 mEq K⁺
      • Given orally or rectally
        • Risk of bowel obstruction, perforation or necrosis
    • Dialysis
      • Treatment of choice for severe, life-threatening hyperkalemia