Pediatric Hypokalemia Treatment & Management

Updated: Jan 06, 2021
  • Author: Michael J Verive, MD, FAAP; Chief Editor: Timothy E Corden, MD  more...
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Approach Considerations

Other than potassium supplementation as described above, no additional medications are required.

Because many medications (particularly loop diuretics, mineralocorticoids, catecholamines, methylxanthines, alkalinizing agents) may be responsible for hypokalemia, eliminating or reducing the doses of these medications may be helpful in preventing or minimizing hypokalemia.

If current medications are responsible for hypokalemia, substitution of potassium-sparing alternatives may help reduce degree of hypokalemia and may help minimize requirements for potassium supplementation.

If the condition is expected to persist beyond inpatient care, patients should receive follow-up medical care for home treatment. Additional medical follow-up must be obtained for associated medical conditions.

Patients with severe or symptomatic hypokalemia require transfer to an ICU for intravenous potassium supplementation and continuous electrocardiographic monitoring.

Except for excision of tumors leading to hypokalemia, management is nonsurgical.


Medical Care

The treatment of hypokalemia depends on severity and etiology. Note the following:

  • Unlike hyponatremia, in which the total body sodium deficit can be readily estimated, serum potassium may not accurately reflect total body stores. Indeed, during diabetic ketoacidosis, serum potassium levels are usually initially elevated, even in the face of severe depletion of total body potassium. Correction of acidosis in diabetic ketoacidosis may cause a precipitous drop in serum potassium levels.

  • Treatment of hypokalemia should be directed at the etiology of hypokalemia as well as its correction, as treatment of hypokalemia carries with it a significant risk of iatrogenic hyperkalemia.

  • Transient, asymptomatic, or mild hypokalemia may spontaneously resolve or may be treated with enteral potassium supplements.

  • Symptomatic or severe hypokalemia should be corrected with a solution of intravenous potassium.

  • Whenever practical, treatment of hypokalemia should be performed in a monitored setting with medications and personnel available to intervene in the event that treatment results in symptomatic hyperkalemia.

After the initial phase of hypokalemia therapy is completed, focus further inpatient care on matching potassium intake to losses, periodic testing of serum potassium levels, and electrocardiographic monitoring for hypokalemia or hyperkalemia due to therapy.

Alleviation of aggravating conditions, simplification of medication administration, and patient education form the basis of ongoing patient health and safety.

Dasgupta et al reported the case of a 31-week gestation premature male infant with congestive heart failure due to a left-to-right shunt who failed to respond to typical treatment and developed hyperaldosteronism and severe hypokalemia secondary to activation of the renin angiotensin aldosterone system. The patient’s hypokalemia was unresponsive to intravenous potassium chloride supplementation and induced digoxin toxicity despite a relatively normal level of digoxin; the patient’s earliest signs of digoxin toxicity were junctional rhythm and bradycardia, demonstrating that serum digoxin level alone may fail as an independent guide in the diagnosis of digoxin toxicity. Based upon their ultimate success in treating this patient by discontinuing digoxin, administering digoxin specific immunoglobulin fragments (Fab), and adding spironolactone (an aldosterone antagonist), the investigators concluded that in premature infants with congestive heart failure and hypokalemia, healthcare providers should consider the addition of an aldosterone antagonist. [19]

In a multicenter phase 2B study, Lemonnier et al found evidence that bumetanide improves the core symptoms of autism spectrum disorder (ASD) in children, but that one of the most frequent adverse events is hypokalemia. Eighty-eight patients with ASD (2-18 years old) were divided into four age groups and randomized to receive bumetanide (0.5, 1.0, or 2.0 mg twice daily) or placebo for 3 months. The adverse event of hypokalemia occurred primarily at the start of the treatment at the 1.0 and 2.0 mg twice-daily doses, and it improved gradually with the intake of oral potassium supplements. [20]



After resolution, consultation with subspecialists (including, but not limited to, endocrinologist, nephrologist, pulmonologist, gastroenterologist, geneticist, or specialist in metabolic disease) may be necessary to diagnose and manage predisposing conditions.

Consultation with a dietitian may be helpful in cases of hypokalemia due to inadequate dietary intake.

Consultation with mental health professionals may be necessary for ongoing treatment of hypokalemia secondary to anorexia and/or bulimia.



Dietary modification may be necessary for patients with excessive potassium losses (eg, diuretic or laxative use) or patients with hypokalemia who are at increased risk, such as those receiving digoxin.

Avoidance of specific foods (eg, licorice) may also be necessary for high-risk individuals. [5]



Patients with hypokalemic periodic paralysis may need to modify exercise regimens to avoid periods of strenuous exercise.

Patients at risk of hypokalemia from sweat losses should have adequate potassium and fluid available during activities likely to result in significant sweating and should be given anticipatory guidance regarding symptoms of hypokalemia.