Hyperkalemia

Causes

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

Artifact

• 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)

Evaluation

• 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)

Treatment

• 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