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Pediatric Hyperkalemia Clinical Presentation

  • Author: Michael J Verive, MD, FAAP; Chief Editor: Timothy E Corden, MD  more...
Updated: Jan 08, 2016


History for a previously well child with acute hyperkalemia should focus on how the blood sample was obtained, potassium intake or recent blood product transfusion, risk factors for transcellular shift of potassium (acidosis) or tissue death/necrosis, medication use (by the child, other family members, pets, etc) associated with hyperkalemia, and presence or signs of renal insufficiency.

Specific questions may be focused on the following:

  • Urine output (last void or number of wet diapers) and fluid intake
  • Cola-colored urine (which may indicate acute glomerulonephritis)
  • Bloody stool (which may indicate hemolytic-uremic syndrome [HUS])
  • Presence of drugs in the household (or used by recent visitors), such as potassium preparations, digoxin, and diuretics
  • Any history of trauma (crush injuries) or thermal injury (burns)

Medical history, family history, and review of systems should be explored for any of the following:

  • Acute or chronic renal failure
  • Hypertension
  • Diabetes
  • Adrenogenital syndromes
  • Malignancy (tumor lysis syndrome)

Family history (hyperkalemic periodic paralysis, miscarriages, deaths of very young siblings) may include the following conditions:

  • Neuromuscular disorders
  • Malignant hyperthermia


High potassium levels interfere with repolarization of the cellular membrane following completion of the action potential. Findings depend on the degree of hyperkalemia and primarily relate to the deleterious effects of elevated plasma potassium levels on cardiac conduction. Children with hyperkalemia can present with cardiac arrest due to wide-complex tachycardia or ventricular fibrillation.

Symptoms short of circulatory collapse/cardiac arrest include respiratory failure and weakness that progresses to paralysis. Patients may report nausea, vomiting, and paresthesias (eg, tingling). Most often, patients with hyperkalemia are asymptomatic, with the first clinical manifestation of the condition either ECG changes (peaked T waves) or sudden cardiac arrest.

Nonspecific findings can include muscle weakness (skeletal, respiratory), fatigue, ileus with hypoactive or absent bowel sounds, and depression.



Although the etiology of hyperkalemia can be multifactorial, differential diagnoses include fictitious hyperkalemia and hyperkalemia due to increased potassium intake, transcellular potassium shift, or decreased potassium excretion.

Fictitious hyperkalemia may be caused by the following:

  • Hemolysis, tissue lysis, or tissue ischemia during phlebotomy
  • Contamination of blood sample with potassium-containing fluids
  • Thrombocytosis or leukocytosis (affects serum K + but not plasma K +)

Hyperkalemia due to increased K+ intake may be due to the following:

  • Blood transfusion (increasing risk with increased duration of cell storage) [10]
  • Intravenous (IV) or oral potassium
  • Maintenance K+ in IV or oral solutions combined with decreased renal function

Hyperkalemia due to transcellular K+ shift may be caused by the following:

  • Metabolic acidosis
  • Beta-adrenergic blockade [11, 12]
  • Acute tubular necrosis
  • Electrical burns
  • Thermal burns
  • Cell depolarization
  • Head trauma
  • Rhabdomyolysis
  • Digitalis toxicity
  • Fluoride toxicity [13]
  • Cyclosporin A [14]
  • Methotrexate [15]
  • Propofol infusion syndrome
  • Tumor lysis syndrome
  • Succinylcholine use in a child with neuromuscular disease, prolonged bed rest (including patients in ICUs), or more than 24 hours after crush or burn injury [16]

Hyperkalemia due to decreased K+ excretion may result from the following:

  • Acute renal failure
  • Primary adrenal disease (Addison disease, salt-wasting congenital adrenal hyperplasia)
  • Hyporeninemic hypoaldosteronism
  • Renal tubular disease

Certain types of medications (eg, potassium sparing diuretics, ACE inhibitors, angiotensin II blockers, trimethoprim, nonsteroidal anti-inflammatory agents [NSAIDs]) may also lead to the development of hyperkalemia.

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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Peaked T waves.
Sinusoidal wave.
Hyperkalemia diagnosis and treatment flow chart.
Table. Select Factors Affecting Plasma Potassium
Factor Effect on Plasma K+ Mechanism
Aldosterone Decrease Increases sodium resorption, and increases K+ excretion
Insulin Decrease Stimulates K+ entry into cells by increasing sodium efflux (energy-dependent process)
Beta-adrenergic agents Decrease Increases skeletal muscle uptake of K+
Alpha-adrenergic agents Increase Impairs cellular K+ uptake
Acidosis (decreased pH) Increase Impairs cellular K+ uptake
Alkalosis (increased pH) Decrease Enhances cellular K+ uptake
Cell damage Increase Intracellular K+ release
Succinylcholine Increase Cell membrane depolarization
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