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Pediatric Hyperkalemia Differential Diagnoses

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

Diagnostic Considerations

Important considerations

Clinicians should ensure they obtain historical data that may lead to the diagnosis of hyperkalemia, as in the case of a previously healthy toddler who presents with hyperkalemia and arrhythmias after ingesting potassium tablets. Failure to suspect hyperkalemia may prevent the physician from eliciting historical information about medications at home. If the practitioner does not suspect hyperkalemia, no appropriate treatment can be administered.

With congenital adrenal hyperplasia, hyperkalemia is frequently observed with hyponatremia in an infant who presents with circulatory collapse. Failure to recognize this disease entity prevents the physician from administering corticosteroids, which are essential to appropriate treatment of these children.

Failure to recognize ECG patterns of hyperkalemia (eg, tall, peaked T waves; tall, peaked sine waves) also leads to inappropriate treatment. For example, a child with chronic renal failure or congenital adrenal hyperplasia may present with nonspecific symptoms of nausea and vomiting yet have an elevated serum potassium level. Failure to obtain an ECG or the inability to recognize the classic ECG signs of hyperkalemia prevents the physician from obtaining appropriate serum electrolyte measurements and, more importantly, prevents the physician from instituting appropriate life-saving measures.

Special concerns

Patients with burns, crush injuries, and myopathies are at high risk of developing hyperkalemia, which is aggravated by the administration of succinylcholine. This drug should be avoided in such patients.

Differential Diagnoses

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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