Pediatric Hypokalemia 

Updated: Nov 11, 2015
Author: Michael J Verive, MD, FAAP; Chief Editor: Timothy E Corden, MD 

Overview

Background

Potassium is the most abundant intracellular cation and is necessary for maintaining a normal charge difference between intracellular and extracellular environments. Potassium homeostasis is integral to normal cellular function and is tightly regulated by specific ion-exchange pumps, primarily by cellular, membrane-bound, sodium-potassium adenosine triphosphatase (ATPase) pumps. Derangements of potassium regulation may lead to neuromuscular, GI, and cardiac conduction abnormalities.

Hypokalemia is generally defined as a serum potassium level of less than 3.5 mEq/L in children, although exact values for reference ranges of serum potassium are age-dependent, and vary among laboratories. It is frequently present in pediatric patients who are critically ill and reflects a total body deficiency of potassium or, more commonly, reflects conditions that promote the shift of extracellular potassium into the intracellular space.

Pathophysiology

Hypokalemia may be due to a total body deficiency of potassium, which may result from prolonged inadequate intake or excessive losses (including but not limited to, long-term diuretic or laxative use, and chronic diarrhea, hypomagnesemia, or hyperhidrosis). Acute causes of potassium depletion include diabetic ketoacidosis,[1] severe GI losses due to vomiting and diarrhea, dialysis, and diuretic therapy.

Hypokalemia may also be the manifestation of large potassium shifts from the extracellular to intracellular space, as seen with alkalosis, insulin, catecholamines (including albuterol and other commonly-used beta2-adrenergic agonists), sympathomimetics, and hypothermia.

Other recognizable causes include renal tubular disorders, such as distal renal tubular acidosis, Bartter syndrome,[2] and Gitelman syndrome, periodic hypokalemic paralysis, hyperthyroidism, and hyperaldosteronism.

Other mineralocorticoid excess states that may cause hypokalemia include cystic fibrosis (with hyperaldosteronism from severe chloride and volume depletion), Cushing syndrome, and exogenous steroid administration. Excessive natural licorice consumption can also cause or exacerbate potassium loss due to inhibition of 11-betahydoxysteroid dehydrogenase, which leads to elevated endogenous mineralocorticoid activity.[3]

Epidemiology

Mortality/Morbidity

With adequate control of potassium levels and resolution of any predisposing condition, the prognosis is excellent.

Morbidity/mortality

Mortality is rare, except when hypokalemia is severe or occurs following cardiac surgery, when accompanied by arrhythmia, or in patients who have underlying heart disease and require digoxin therapy.

Short-term morbidity is common and may include GI hypomotility or ileus; cardiac dysrhythmia; QT prolongation; appearance of U waves that may mimic atrial flutter, T-wave flattening, or ST-segment depression; and muscle weakness or cramping.

Mortality and morbidity can also be related to treatment for hypokalemia with potassium supplementation, particularly if potassium is given in large doses or rapidly. Because of the risk associated with potassium replacement, alleviation of the cause of hypokalemia may be preferable to treatment, especially if hypokalemia is mild, asymptomatic, or transient and is likely to resolve without treatment.

Complications

Complications of hypokalemia include the following:

  • Hyperkalemia due to excessive/rapid potassium replacement

  • Cardiac dysrhythmia

  • Gastric erosions

  • Strictures

Race

Racial differences may be present in predisposing conditions such as Bartter syndrome, Gitelman syndrome, Conn syndrome (ie, hyperaldosteronism), Cushing syndrome, and familial hypokalemic paralysis. In addition, significant hypokalemia and hypokalemic paralysis develop in 2-8% of Asians with hyperthyroidism.

Sex

No known sex predilection has been noted.

Age

Viral GI infections tend to be more common in infants and younger children. Younger children with emesis or diarrhea are at an increased risk of hypokalemia because the depletion of fluid volume and electrolytes from GI loss is relatively higher than that found in older children and adults.

Insulin-dependent diabetes mellitus that results in diabetic ketoacidosis (with its inherent fluid and potassium loss) is more common in children. Excessive corticosteroid and mineralocorticoid secretion, as in Cushing syndrome and Conn syndrome, is a less common cause of hypokalemia in the pediatric patient. Periodic hypokalemic paralysis may appear in childhood or young adulthood, precipitated by rest after strenuous exercise, physical or metabolic stress (eg, exposure to cold, alcohol ingestion), a high-carbohydrate meal, or exposure to exogenous insulin or catecholamines (eg, epinephrine and albuterol). Hypokalemia due to hyperthyroidism is generally observed in adults.

 

Presentation

History

Hypokalemia due to excessive loss is usually accompanied by a history of GI loss (emesis or diarrhea), urinary output, or sweating. This may be exacerbated by inadequate oral intake.

Query about current or recent treatment with medications and herbal products (especially natural licorice), including insulin, albuterol or other beta2-sympathomimetics, corticosteroids, diuretics, laxatives, enemas, or bowel-prep solutions. A complete and up-to-date medication and supplement list is essential, especially if the patient is taking new medications or may have had medication substitutions.

The patient may have had similar episodes in the past. Familial historical data may include surgery for pituitary or adrenal tumors or acute intermittent episodes of paralysis, with or without association with hyperthyroidism.

Physical

Physical examination findings may frequently be within the reference range. Occasionally, muscle weakness is evident.

Cardiac arrhythmias and acute respiratory failure from muscle paralysis are life-threatening complications that require immediate diagnosis.

Cardiovascular examination findings may also be within normal limits. Occasionally, tachycardia with irregular beats may be heard. Severe hypokalemia may manifest as bradycardia with cardiovascular collapse.

Hypoactive bowel sounds may suggest hypokalemic gastric hypomotility or ileus.

Causes

Hypokalemia may be due to a total body deficit of potassium, which may occur chronically with the following:

  • Prolonged diuretic use

  • Inadequate potassium intake

  • Laxative use

  • Diarrhea (including congenital chloride diarrhea)[4]

  • Hyperhidrosis

  • Hypomagnesemia

  • Renal tubular losses (including Fanconi syndrome,[5] Bartter syndrome, Gitelman syndrome, and others)

  • Dengue syndrome[6]

Acute causes of potassium depletion include the following:

  • Diabetic ketoacidosis

  • Severe GI losses from vomiting and diarrhea

  • Dialysis and diuretic therapy

  • Alcohol intoxication/overdose[7]

Hypokalemia may also be due to excessive potassium shifts from the extracellular to the intracellular space, as seen with the following:

  • Alkalosis

  • Insulin use

  • Catecholamine use

  • Sympathomimetic use

  • Use of sodium bicarbonate, especially during therapeutic alkalinization (commonly used to treat salicylate and cyclic antidepressant overdoses, tumor lysis syndrome, rhabdomyolysis, etc)

  • Use of sodium polystyrene sulfonate to treat transient hyperkalemia

  • Hypothermia

Other recognizable causes of hypokalemia include the following:

  • Renal tubular disorders, such as Bartter syndrome and Gitelman syndrome

  • Type I or classic distal tubular acidosis

  • Periodic hypokalemic paralysis

  • Hyperaldosteronism

  • Celiac disease[8]

Other states of mineralocorticoid excess that may cause hypokalemia include the following:

  • Cystic fibrosis with hyperaldosteronism from severe chloride and volume depletion

  • Cushing syndrome

  • Exogenous steroid administration, including fludrocortisone and other mineralocorticoids

  • Excessive licorice consumption[3]

Other conditions that may cause hypokalemia include acute myelogenous, monomyeloblastic, or lymphoblastic leukemia.

Drugs that may commonly cause hypokalemia include the following:

  • Furosemide, bumetanide, and other loop diuretics

  • Methylxanthines (theophylline, aminophylline, caffeine)

  • Verapamil (with overdose)

  • Amphotericin B, micafungin[9]

  • Quetiapine (particularly in overdose)

  • Ampicillin, carbenicillin, high-dose penicillins[10]

  • Sirolimus[11]

  • Drugs associated with magnesium depletion, such as aminoglycosides, amphotericin B, and cisplatin

 

DDx

Diagnostic Considerations

Important considerations

Adequately communicate the risks of treatment to the caregivers and/or patient.

Monitor patients receiving potassium supplementation for complications, especially patients with renal failure or patients receiving potassium-sparing diuretics or angiotensin-converting enzyme inhibitors.

Follow serum potassium and other electrolyte concentrations during or after therapy.

Ensure adequate precautions against treating a patient on the basis of a low serum potassium value that is false because of a sampling or laboratory error. However, do not fail to treat a patient with symptoms of actual hypokalemia because of an elevated serum potassium value that is false because of a sampling or laboratory error.

Other considerations

Pseudohypokalemia may be seen with sampling errors, particularly if a blood sample is taken upstream of an infusion of saline, dextrose, or other fluids that contain little or no potassium. Clues to sampling errors include other serum level abnormalities that reflect sampling of a mixture of blood and the fluid that is infused. Additionally, the new onset of hypokalemia in otherwise stable patients without known risk factors may reflect the use of different equipment/methods used for blood analysis, and this diagnosis should be confirmed using alternative methods prior to initiating treatment.

Differential Diagnoses

 

Workup

Laboratory Studies

The following studies are indicated in patients with hypokalemia:

  • Serum electrolyte tests: Screen for concurrent electrolyte abnormalities, which may affect treatment.

  • Blood gas analysis: Assess acid-base status; alkalosis may induce hypokalemia, and treatment of acidosis may worsen existing hypokalemia.

  • Drug screen (serum or urine): Amphetamines and other sympathomimetic stimulants can cause hypokalemia; other drugs that can cause hypokalemia include verapamil (with overdose), theophylline, amphotericin B, aminoglycosides, and cisplatin.

  • Serum adrenocorticotropic hormone (ACTH), cortisol, renin activity, and aldosterone tests: Evaluate for suspected Cushing, Conn, or adrenal hyperplasia syndromes, including 11-beta-hydroxylase deficiency.

  • Simultaneous serum insulin and C-peptide tests: Because hyperinsulinism can cause transient hypokalemia, elevated serum insulin without appropriately elevated C-peptide suggests exogenous insulin administration, which may represent M√ľnchhausen-by-proxy syndrome.

Imaging Studies

Magnetic resonance imaging

Perform brain magnetic resonance imaging (MRI) if a brain or pituitary tumor is suspected as a cause of hypercortisolism.

Ultrasonography and computed tomography scanning

Perform abdominal ultrasonography or computed tomography (CT) scanning if an adrenal tumor or hyperplasia is suspected.

Electrocardiography

Although ECG changes may be helpful if present, their absence should not be taken as reassurance of normal cardiac conduction.[12] The ECG in hypokalemia may appear normal or may have only subtle findings immediately before clinically significant dysrhythmias.

ECG findings may include the following (see the image below):

  • Ventricular dysrhythmia

  • Prolongation of QT interval

  • ST-segment depression

  • T-wave flattening

  • Appearance of U waves

    Prominent U waves after T waves in hypokalemia. Prominent U waves after T waves in hypokalemia.

During therapy, monitor for changes associated with overcorrection and hyperkalemia, including a prolonged QRS, peaked T waves, bradyarrhythmia, sinus node dysfunction, and asystole.

 

Treatment

Medical Care

Note the following:

  • The treatment of hypokalemia depends on severity and etiology.

  • 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.

Transfer

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

Surgical Care

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

Consultations

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.

Diet

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.

Activity

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.

 

Medication

Medication Summary

Medical therapy is aimed at potassium supplementation by the enteral (ie, oral or through feeding tubes) or parenteral route. Transient, asymptomatic, or mild hypokalemia may resolve spontaneously, or it may be treated using enteral potassium supplements. Symptomatic or severe hypokalemia should be corrected with intravenous potassium preparations.

Potassium supplements

Class Summary

These agents are used to restore body potassium storage. Electrolytes are used to correct disturbances in fluid and electrolyte homoeostasis or acid-base balance and to reestablish osmotic equilibrium of specific ions.

Potassium chloride (also citrate, acetate, bicarbonate, gluconate)

Potassium chloride is the preferred salt for patients with preexisting alkalosis. First choice for IV therapy. Essential for transmission of nerve impulses; contraction of cardiac muscle; and maintenance of intracellular tonicity, skeletal and smooth muscles, and normal renal function. Gradual potassium depletion occurs via renal excretion, through GI loss, or because of low intake. Depletion may result from diuretic therapy, primary or secondary hyperaldosteronism, diabetic ketoacidosis, severe diarrhea, vomiting, or inadequate replacement during prolonged parenteral nutrition.

 

Follow-up

Further Outpatient Care

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.

Inpatient & Outpatient Medications

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

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.

Deterrence/Prevention

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.

Patient Education

Patients should be educated in terms of predisposing conditions. The importance and risks involved with potassium supplementation and the warning signs of hypokalemia or overtreatment must be emphasized upon discharge from the hospital.

Knowledge of cardiopulmonary resuscitation and education on timely access to emergency medical services may prevent morbidity or mortality.

Ongoing communication is essential for reducing the risks and in therapy, especially in patients with chronic conditions associated with hypokalemia.

For patient education resources, see the Thyroid and Metabolism Center, as well as Low Potassium.