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Pediatric Hypokalemia Clinical Presentation

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


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 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.



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
Contributor Information and Disclosures

Michael J Verive, MD, FAAP Pediatrician, UP Health System Portage

Michael J Verive, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, Society for Pediatric Sedation

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami Leonard M Miller School of Medicine/ Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Director, Palliative Care Team, Holtz Children's Hospital; Medical Manager, FEMA, South Florida Urban Search and Rescue, Task Force 2

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

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Prominent U waves after T waves in hypokalemia.
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