Hypokalemia

Causes

• 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

Evaluation

• 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)

Treatment

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

Supplementation

• 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