On this page


AKA: hypokalaemia, hypopotassemia, hypopotassaemia

Evaluation and management of low blood potassium in pediatric patients


  • Decreased potassium intake
    • E.g., feeding intolerance

Kidney potassium loss

  • Excess mineralocorticoid activity
    • Mineralocorticoid disorder
    • Renal artery stenosis
    • Liddle syndrome
  • Potassium-wasting diuretics
    • Loop diuretics
    • Thiazide diuretics
  • Tubulopathy
    • Bartter syndrome, Gitelman syndrome
    • Fanconi syndrome
    • Potassium wasting due to hypomagnesemia
      • Mechanism: magnesium inhibits renal outer medullary potassium (ROMK) channel on the apical membrane of the thick ascending limb of the loop of Henle and the principal cells in the collecting duct; lack of magnesium results in enhanced ROMK activity and increased potassium secretion

Gastrointestinal (GI) potassium loss

  • Diarrhea
    • Laxative abuse
  • Vomiting
    • Nasogastric/orogastric (NG/OG) suction

Intracellular shifts (movement of potassium into cells)

  • Alkalosis
  • Insulin
  • β-agonists (e.g., albuterol)
  • Hypokalemic periodic paralysis (AKA: PP, hypoKPP, hypoPP)
    • Incidence of 1:100000
      • May be inherited (autosomal dominant) or acquired (thyrotoxicosis)
    • Defect in muscle ion channels
    • Attacks of generalized weakness precipitated by events that ↑ epinephrine or insulin (e.g., fasting, stress, exercise, carbohydrate load)
      • Can last several hours and occur a few times per week

Signs and symptoms

  • Usually asymptomatic
  • Muscle cramps, weakness
  • Cardiac arrhythmias (esp., ventricular tachycardia, ventricular fibrillation)
  • Can decrease ability to concentrate urine


  • If hypertension present, consider evaluation for mineralocorticoid disorder, renal artery stenosis, Liddle’s syndrome, etc.
  • Laboratory workup:
    • Evaluate for other electrolyte derangements, esp. hypomagnesemia
    • Alkalosis
  • ECG (EKG) if severe (consider if <2.5 mEq/L, esp. if <2 mEq/L)


  • Treat underlying cause
    • If hypomagnesemia present (e.g., due to diarrhea, diuretics, other medications), will be difficult to correct hypokalemia without correcting hypomagnesemia


  • Supplementation is generally indicated if symptoms or ECG (EKG) changes are present
  • Enteral potassium replacement is easiest and safest for mild hypokalemia (3-3.5 mEq/L)
    • KCl is the default choice given better K retention compared to other formulations
      • Preferred for patients with hypochloremia and metabolic alkalosis due to diuretics or vomiting
      • KCl 1 to 1.5 mEq/kg/dose (max 40 mEq/dose)
    • KPhos is reasonable if hypophosphatemia is present (e.g., proximal RTA/Fanconi syndrome)
    • Other formulations available depending on clinical context: bicarbonate, citrate, gluconate
    • Serial monitoring of potassium level to ensure normalization
  • IV repletion for severe symptoms (cardiac arrhythmias, extreme muscle weakness, respiratory distress) or if unable to tolerate PO
    • IV KCl 0.5 mEq/kg (max 20-40 mEq/dose), given over 1-2 hours depending on symptom severity
      • Can be associated with pain, phlebitis if given peripherally
      • High doses can be given centrally
    • Continuous cardiac monitoring during repletion
    • Repeat potassium level 1 hour after dose is given
    • Once potassium level stabilizes, transition to enteral supplements

Hypokalemic periodic paralysis

  • Short term treatment is usually with enteral potassium
    • IV repletion reserved for potentially life threatening cases
  • Incrementally increase dose until potassium level normalizes
    • Start with KCl 10-40 mEq