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Pediatric Hyperkalemia

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

Background

Hyperkalemia is defined as a serum potassium concentration greater than the upper limit of the normal range; the range in children and infants is age-dependent, whereas the range for adults is approximately 3.5-5.5 mEq/L. The upper limit may be considerably high in young or premature infants, as high as 6.5 mEq/L.[1] Because hyperkalemia can cause lethal cardiac arrhythmia, it is one of the most serious electrolyte disturbances.

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Pathophysiology

Potassium is the primary intracellular cation; more than 95-98% of the total body potassium is found in the intracellular space, primarily in muscle. Normal homeostatic mechanisms serve to precisely maintain the serum potassium level within a narrow range. The primary mechanisms for maintaining this balance are the buffering of extracellular potassium against a large intracellular potassium pool (via the sodium-potassium pump) and urinary excretion of potassium.

Under normal, nonpathologic conditions, approximately 90% of potassium excretion occurs in the urine, with less than 10% of potassium excreted through sweat or stool. Within the kidneys, potassium excretion occurs mostly in the principal cells of the cortical collecting duct (CCD). Urinary potassium excretion depends on adequate luminal sodium delivery to the distal convoluted tubule (DCT) and CCD, as well as the effect of aldosterone and other adrenal corticosteroids with mineralocorticoid activity.

Laboratory hyperkalemia (fictitious or pseudohyperkalemia) can easily occur because of hemolysis, tissue lysis, and "milking" of extremities (which can introduce a significant amount of interstitial fluid into the blood sample) during phlebotomy, especially with heel-poke and finger-stick phlebotomy, which are commonly performed in infants and small children. Hemolysis can also be caused by fist clenching during phlebotomy or during prolonged tourniquet application, which can also lead to an acidotic sample with resultant hyperkalemia). Blood sampled "upstream" of an intravenous line with potassium-containing fluid (or from a multiple lumen central venous catheter where the sampling lumen is near the lumen containing potassium-rich infusate) can have falsely elevated levels of potassium that do not reflect circulating levels.

Similarly, serum potassium levels may be falsely lowered by sampling upstream of a catheter delivering fluid deficient in potassium or when a small blood sample is obtained and placed in testing media low in potassium, which may be the case with specific point-of-care analyzers.[2] When in doubt, blood samples should be obtained and tested using standard methods.

Thrombocytosis can also lead to false elevations of serum potassium levels. The normal serum potassium level is 0.4 mEq/L higher than the plasma level because of potassium release during clot formation. For every 100,000/mL elevation in the platelet count, the serum potassium increases by approximately 0.15 mEq/L. This can easily be corrected based on a measurement of whole blood potassium level. A similar effect on serum but not plasma potassium can also be seen with leukocytosis.

True hyperkalemia is caused by one of the following three basic mechanisms, although the root cause for any individual patient is often multifactorial:

  • Increased K + intake: Increased K + intake is most commonly caused by intravenous or oral potassium supplementation. Packed RBCs (PRBCs) also carry potentially high concentrations of potassium that can lead to hyperkalemia during PRBC transfusion. [3] Since serum potassium levels represent only a small percentage (usually < 2-5%) of total body potassium stores, long-term increases in potassium intake are only rarely associated with significant serum hyperkalemia, unless excretion is inadequate.
  • Decreased potassium excretion: The most common cause of decreased potassium excretion leading to hyperkalemia is oliguric renal failure. Other causes include primary adrenal disease (eg, Addison disease, salt-wasting forms of congenital adrenal hyperplasia), hyporeninemic hypoaldosteronism, renal tubular disease (pseudohypoaldosteronism I [4] or II), or medications (eg, ACE inhibitors, angiotensin II blockers, spironolactone or other potassium-sparing diuretics).
  • Transcellular potassium shifts: In a transcellular potassium shift, a hydrogen ion enters a cell and leads to decreased K + uptake by the cell in order to maintain electrical neutrality. Acidosis is the most common cause of hyperkalemia due to transcellular potassium shift, but any process that leads to cellular injury or death (eg, tumor lysis syndrome, rhabdomyolysis, crush injury, massive hemolysis) can cause hyperkalemia, as intracellular potassium is released by disruption of the cell membrane. Other causes of hyperkalemia due to transcellular shift of potassium include propofol ("propofol infusion syndrome"), [5] toxins (digitalis intoxication or fluoride intoxication), succinylcholine, beta-adrenergic blockade, strenuous or prolonged exercise, insulin deficiency, malignant hyperthermia, and hyperkalemic periodic paralysis.

Plasma potassium levels are generally maintained at 3.5-5 mEq/L in adults, with higher levels in neonates and small infants. levels greater than 7 mEq/L can lead to significant hemodynamic and neurologic consequences, while levels exceeding 8.5 mEq/L can cause respiratory paralysis or cardiac arrest and can quickly be fatal. High levels of potassium cause abnormal heart and skeletal muscle function by lowering cell-resting action potential and preventing repolarization, leading to muscle paralysis. Classic ECG findings begin with tenting of the T wave (as is shown in the image below), followed by lengthening and eventual disappearance of the P wave and widening of the QRS complex.[6]

Peaked T waves. Peaked T waves.

Prior to asystole, the QRS and T wave may merge to form a sinusoidal wave (as is shown in the image below).

Sinusoidal wave. Sinusoidal wave.

Table. Select Factors Affecting Plasma Potassium (Open Table in a new window)

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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Prognosis

Patient prognosis depends on the etiology of the hyperkalemia.

Morbidity/mortality

Sudden and rapid onset of hyperkalemia can be fatal. With slow or chronic increase in potassium levels, adaptation occurs via renal excretion, with fractional potassium excretion increasing by as much as 5-10 times the reference range.

Complications

If untreated, severe hyperkalemia can result in cardiac arrhythmia or death.

Treatment of pseudohyperkalemia may result in hypokalemia; thus, treatment of non–life-threatening hyperkalemia should be deferred pending verification of hyperkalemia.

Failure to determine and treat the underlying disease process causing hyperkalemia can predispose patients to recurrent, life-threatening hyperkalemia.

Race

No racial predilection is observed.

Sex

No sex-related predilection is observed. However, neuromuscular disorders including myotonic and muscular dystrophies and related disorders that can predispose patients to hyperkalemia with succinylcholine administration are more prevalent in males.[7]

Age

Extremely low birth weight premature infants are particularly prone to hyperkalemia primarily due to immature renal function. Even otherwise full-term infants may have transient hyperkalemia and hyponatremia due to decreased responsiveness to aldosterone (pseudohypoaldosteronism I).[8]

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Epidemiology

Frequency

United States

Hyperkalemia is a manifestation of a disease and is not a disease by itself. The incidence of hyperkalemia in the pediatric population is unknown, although the prevalence of hyperkalemia in extremely low birth weight premature infants can exceed 50%.[9] Hyperkalemia in pediatric patients is most commonly associated with renal insufficiency, acidosis, and with diseases that involve defects in mineralocorticoid, aldosterone, and insulin function.[8]

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Contributor Information and Disclosures
Author

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.

References
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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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