eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Critical Care
Hyperkalemia
Updated: Feb 13, 2008
Introduction
Background
Hyperkalemia is defined as a higher than normal concentration of potassium (K+) ions in the circulating blood (serum potassium >5.5 mEq/L). Because hyperkalemia can cause lethal cardiac arrhythmia, it is one of the most serious electrolyte disturbances.
Pathophysiology
Potassium is the primary intracellular cation; more than 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 (3.5-5.0 mEq/L). 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.
Ninety percent of potassium excretion occurs in the urine; less than 10% of potassium excretion occurs through sweat or stool. Within the kidneys, potassium excretion occurs mostly in the principal cells of the cortical collecting duct (CCD). Potassium excretion depends on adequate luminal sodium delivery to the distal convoluted tubule (DCT) and CCD.
Laboratory hyperkalemia (fictitious or pseudohyperkalemia) can easily occur because of hemolysis during phlebotomy, especially with heel-poke and finger-stick phlebotomy, which are commonly performed in children. Hemolysis can also be caused by fist clenching during phlebotomy or during prolonged tourniquet application. 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 3 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.1
- Transcellular K+ 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 electro-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 toxins (digitalis intoxication or fluoride intoxication), succinylcholine, beta-adrenergic blockade, exercise, insulin deficiency, malignant hyperkalemia, and hyperkalemic periodic paralysis.
- Decreased K+ excretion: The most common cause of decreased potassium excretion leading to hyperkalemia is renal failure. Other causes include primary adrenal disease (eg, Addison disease, 21-hydroxylase deficiency), hyporeninemic hypoaldosteronism, renal tubular disease (pseudohypoaldosteronism I or II), or medications (eg, ACE inhibitors, angiotensin II blockers, spironolactone or other potassium-sparing diuretics).
Plasma potassium levels are generally maintained at 3.5-5 mEq/L. Levels greater than 7 mEq/L can lead to significant hemodynamic and neurologic consequences. 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. ECG findings are classic and begin with tenting of the T wave (see Media file 1), followed by lengthening and eventual disappearance of the P wave and widening of the QRS complex.2 Just before the heart stops, the QRS and T wave merge to form a sine wave (see Media file 2).
Select Factors Affecting Plasma Potassium
Open table in new window
Table
| Factor | Effect on Plasma K+ | Mechanism |
| Aldosterone | Decrease | Increases sodium resorption, which increases filtrate load to kidneys, leading to increased 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 |
| Factor | Effect on Plasma K+ | Mechanism |
| Aldosterone | Decrease | Increases sodium resorption, which increases filtrate load to kidneys, leading to increased 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 |
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. Hyperkalemia is most commonly associated with renal insufficiency and with diseases that involve defects in mineralocorticoid, aldosterone, and insulin function and causes of acidosis.
Mortality/Morbidity
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.
Race
No racial predilection is observed.
Sex
No sex-related predilection is observed.
Age
No age-related predilection is observed.
Clinical
History
- 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 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
- History of vomiting or diarrhea (which may indicate acute gastroenteritis)
- Cola-colored urine (which may indicate acute glomerulonephritis)
- Bloody stool (which may indicate indicating hemolytic-uremic syndrome [HUS])
- Recent enema use
- Presence of drugs in the household, 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)
- Neuromuscular disorder
- Malignant hyperthermia
Physical
High serum 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.
Causes
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
- Hemolysis or tissue ischemia during phlebotomy
- Thrombocytosis or leukocytosis (affects serum K+ but not plasma K+)
- Hyperkalemia due to increased K+ intake
- Blood transfusion (increasing risk with duration of cell storage)
- Intravenous (IV) or oral potassium
- Maintenance K+ in IVF or oral solutions combined with decreased renal function
- Hyperkalemia due to transcellular K+ shift
- Metabolic acidosis
- Acute tubular necrosis
- Electrical burns
- Thermal burns
- Cell depolarization
- Congenital adrenal hyperplasia
- Head trauma
- Rhabdomyolysis
- Digitalis toxicity
- Tumor lysis syndrome
- Succinylcholine use in a child with neuromuscular disease, prolonged bedrest (including patients in ICUs), or more than 24 hours after crush or burn injury3
- Hyperkalemia due to decreased K+ excretion
- Acute renal failure
- Primary adrenal disease
- Hyporeninemic hypoaldosteronism
- Renal tubular disease
- Medications (eg, potassium sparing diuretics, ACE inhibitors, angiotensin II blockers)
More on Hyperkalemia |
 Overview: Hyperkalemia |
| Differential Diagnoses & Workup: Hyperkalemia |
| Treatment & Medication: Hyperkalemia |
| Follow-up: Hyperkalemia |
| Multimedia: Hyperkalemia |
| References |
| Next Page » |
References
Bhananker SM, Ramamoorthy C, Geiduschek JM, Posner KL, Domino KB, Haberkern CM, et al. Anesthesia-related cardiac arrest in children: update from the Pediatric Perioperative Cardiac Arrest Registry. Anesth Analg. Aug 2007;105(2):344-50. [Medline].
Mattu A, Brady WJ, Robinson DA. Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med. Oct 2000;18(6):721-9. [Medline].
Piotrowski AJ, Fendler WM. Hyperkalemia and cardiac arrest following succinylcholine administration in a 16-year-old boy with acute nonlymphoblastic leukemia and sepsis. Pediatr Crit Care Med. Mar 2007;8(2):183-5. [Medline].
Behrman R, Kliegman R, Jenson H. Nelson Textbook of Pediatrics. 17th Ed. Philadelphia, PA: WB Saunders; 2004.
Brenner B. Brenner & Rector's The Kidney. 7th ed. St Louis, MO: WB Saunders; 2004.
Finberg L, Kravath R, Hellerstein S. Potassium. In: Water and Electrolytes in Pediatrics: Physiology, Pathophysiology, and Treatment. Philadelphia, PA: WB Saunders; 1993:70-1.
Goldfrank LR, ed. Goldfrank's Toxicologic Emergencies. 6th ed. Stanford, CT: Appleton & Lange; 1998.
Kokko, JP, Tannen RL. Potassium disorders. In: Fluids and Electrolytes. Philadelphia, PA: WB Saunders; 1990:195-300.
Lieh-Lai, M, Asi-Bautista, M, Ling-McGeorge, K. Hyperkalemia. In: Pediatric Acute Care Handbook. Philadelphia, PA: Lippincott, Williams, & Wilkins; 1995.
Maxwell MH, Kleeman CR. Maxwell and Kleeman's Clinical Disorders of Fluid and Electrolyte Metabolism. 5th Ed. New York, NY: McGraw-Hill; 1994.
Odegard KC, DiNardo JA, Kussman BD, Shukla A, Harrington J, Casta A, et al. The frequency of anesthesia-related cardiac arrests in patients with congenital heart disease undergoing cardiac surgery. Anesth Analg. Aug 2007;105(2):335-43. [Medline].
Further Reading
Keywords
hyperkaliemia, hyperpotassemia, potassium, potassium level, serum potassium level, K+, potassium excretion, potassium intake, hemolysis, phlebotomy, fictitious hyperkalemia, pseudohyperkalemia, true hyperkalemia, renal insufficiency, transcellular potassium shift, thrombocytosis, aldosterone, acute hyperkalemia, severe hyperkalemia, hemodialysis, total body potassium, laboratory hyperkalemia, acidosis, tumor lysis syndrome, rhabdomyolysis, insulin deficiency, malignant hyperkalemia, hyperkalemic periodic paralysis, primary adrenal disease, Addison disease, 21-hydroxylase deficiency, hyporeninemic hypoaldosteronism, renal tubular disease, gastroenteritis, acute glomerulonephritis, hemolytic-uremic syndrome, HUS, hypertension, diabetes, respiratory failure, metabolic acidosis, congenital adrenal hyperplasia, head trauma, thermal burns, electrical burns
