Pediatric Hyperkalemia 

Updated: Dec 30, 2019
Author: Michael J Verive, MD, FAAP; Chief Editor: Timothy E Corden, MD 



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.

Teach patients to recognize the symptoms of hyperkalemia, such as palpitations, dizziness, and weakness.


Potassium is the primary intracellular cation; more than 95-98% of the total body potassium is found in the intracellular space, primarily in muscle.[2] 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.[3] 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.[4] 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[5, 6] or II[7] ), 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"),[8] 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.[9]

Pediatric hyperkalemia. Peaked T waves. Pediatric hyperkalemia. 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).

Pediatric hyperkalemia. Sinusoidal wave. Pediatric hyperkalemia. Sinusoidal wave.

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


Effect on Plasma K+




Increases sodium resorption, and increases K+ excretion



Stimulates K+ entry into cells by increasing sodium efflux (energy-dependent process)

Beta-adrenergic agents


Increases skeletal muscle uptake of K+

Alpha-adrenergic agents


Impairs cellular K+ uptake

Acidosis (decreased pH)


Impairs cellular K+ uptake

Alkalosis (increased pH)


Enhances cellular K+ uptake

Cell damage


Intracellular K+ release



Cell membrane depolarization



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[7]

  • 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 intensive care units), 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, angiotensin-converting enzyme [ACE] inhibitors, angiotensin II blockers, trimethoprim, nonsteroidal anti-inflammatory agents [NSAIDs]) may also lead to the development of hyperkalemia.

Rarely, a Mendelian syndrome known as familial hyperkalemic hypertension (FHHt) or pseudohypoaldosteronism II may manifest as hyperkalemia in children.[7] The involvement of relatively newly discovered genes KLHL3 and CUL3 appear to play a role in the pathophysiology of FHHt. Clinicians should actively search for abnormalities in blood pressure in the setting of pediatric hyperkalemia with a normal glomerular filtration rate.[7]



United States data

Hyperkalemia is a manifestation of a disease and is not a disease by itself. The incidence of hyperkalemia in the pediatric population is unknown, but is considered rare.[7] However, the prevalence of hyperkalemia in extremely low birth weight premature infants can exceed 50%.[17] Hyperkalemia in pediatric patients is most commonly associated with renal insufficiency, acidosis, and with diseases that involve defects in mineralocorticoid, aldosterone, and insulin function.[18]  In addition, hemolysis in blood specimens owing to difficulties in obtaining samples may also be a factor.[7]

Race-, sex-, and age-related demographics

No racial predilection nor 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.[19]

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).[18]


Patient prognosis depends on the etiology of the hyperkalemia.


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.

Separately, hyperkalemia appears to be an independent risk factor for death in children with diarrhea requiring mechanical ventilation.[20]


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.




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

Physical Examination

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.



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



Laboratory Studies

Laboratory studies depend on the etiology of hyperkalemia but may include the following:

  • Serum electrolyte tests

  • Serum BUN and creatinine tests

  • Urinalysis (UA)

Depending on the etiology or on clinical suspicion, other studies to consider include the following:

  • Arterial or free-flowing venous blood gas sampling (for acid-base disorders): Capillary blood gas sampling should not routinely be used to evaluate for hyperkalemia due to significant risks of factitious hyperkalemia.

  • Serum uric acid and phosphorous tests (for tumor lysis syndrome)

  • Serum creatinine phosphokinase (CPK) and calcium measurements (for rhabdomyolysis)

  • Urine myoglobin test (for crush injury or rhabdomyolysis; suspect if UA reveals blood in the urine but no RBCs are seen on urine microscopy)

  • Specific drug level tests for suspected toxicity (digoxin)

  • CBC count (for thrombocytosis, leukocytosis, or malignancy)

  • Urine electrolyte tests, including potassium and osmolality (osm) tests

  • Plasma osm test

When the etiology of hyperkalemia remains unclear, calculation of the transtubular potassium gradient (TTKG) using the following formula may be useful: TTKG = (K+ urine X Osm plasma)/(K+ plasma X Osm urine)

The normal TTKG varies from 5-15. In the setting of hyperkalemia with normal renal excretion of potassium, the TTKG should be greater than 10. A TTKG of less than 8 in the setting of hyperkalemia implies inadequate potassium excretion, which is usually secondary to aldosterone deficiency or unresponsiveness. Checking a serum aldosterone level may be helpful.


An ECG is essential in all children in whom hyperkalemia is suspected. ECG reveals the sequence of changes as follows:

  • Serum K+ 5.5-6.5 mEq/L - Tall, peaked T waves with narrow base, best seen in precordial leads (as is shown in the image below)

    Pediatric hyperkalemia. Peaked T waves. Pediatric hyperkalemia. Peaked T waves.
  • Serum K+ 6.5-8.0 mEq/L - Peaked T waves, prolonged PR interval, decreased or disappearing P wave, widening of QRS, amplified R wave

  • Serum K+ greater than 8.0 mEq/L - Absence of P wave; progressive QRS widening, intraventricular/fascicular/bundle branch blocks; progressive widening of QRS, eventually merging with the T wave just before cardiac arrest, forming the sine wave pattern (as is shown in the image below)

    Pediatric hyperkalemia. Sinusoidal wave. Pediatric hyperkalemia. Sinusoidal wave.

Imaging Studies

Imaging studies are not generally indicated, except to assess the primary disease state (eg, excluding obstructive uropathy as a cause for acute renal failure).



Approach Considerations

Hyperkalemia, by itself, is not a disease and is generally the result of underlying causes,[21] such as congenital adrenal hyperplasia, acute renal failure, rhabdomyolysis, or tumor lysis syndrome.

Hyperkalemia is a true medical emergency, with three primary goals of immediate management (in addition to prompt discontinuation of potassium-containing fluids and medications that lead to hyperkalemia), as summarized under Medical Care.[22, 23]

Close electrocardiographic monitoring is warranted.

Surgical intervention

Tumor debulking may be considered to decrease the risk of hyperkalemia from tumor lysis syndrome for solid tumors.[24]

Outpatient monitoring

Continuing care relates to the basic disease process that led to the hyperkalemia.

In patients with salt-wasting congenital adrenal hyperplasia, corticosteroid and mineralocorticoid supplementation are necessary.

Continued renal replacement therapy may be needed for patients with acute renal failure.

Patients with chronic mineralocorticoid deficiency require mineralocorticoid supplementation (eg, fludrocortisone).

Medical Care

Goals of management

Stabilization of myocardial cell membrane

Stabilize the myocardial cell membrane to prevent lethal cardiac arrhythmia (and to gain time to shift potassium intracellularly and enhance potassium elimination: Intravenous (IV) calcium chloride or gluconate

Enhancement of cellular uptake of potassium

This achieved with the following:

  • Sodium bicarbonate IV

  • Regular insulin and glucose IV

  • Beta-adrenergic agents, such as albuterol (used to manage hyperkalemia with variable results), terbutaline, dobutamine

Enhancement of total body potassium elimination

This achieved with the following:

  • Sodium polystyrene sulfonate (Kayexalate) orally (PO)/rectally (PR) (Note: Sodium polystyrene sulfonate may not be an appropriate first-line agent in children with severe acute hyperkalemia who require a >25% reduction in serum potassium levels or those at high risk for cardiac arrhythmias.[25] )

  • Furosemide (only if renal function is maintained)

  • Emergent hemodialysis

Clinical management

Arrhythmias due to hyperkalemia are very difficult to treat with defibrillation, epinephrine, or antiarrhythmic drugs without emergently lowering the serum potassium level.

After initial stabilization, further workup should be performed to diagnose the etiology of the hyperkalemia. Children with acquired Addison disease or other primary adrenal disease require stress-dose steroid supplementation and children with hypoaldosteronism require mineralocorticoid supplementation.

Emergent hemodialysis is sometimes necessary to treat severe symptomatic hyperkalemia that is resistant to drug therapy, particularly in patients without adequate renal function.

Even in patients with severe hyperkalemia and a high gradient, peritoneal dialysis (PD) is not as efficient as hemodialysis in the removal of potassium. Rates of removal with PD are almost equal to the removal rate using sodium polystyrene sulfonate (Kayexalate).

Continuous arteriovenous hemofiltration with dialysis (CAVHD) or continuous veno-venous hemofiltration with dialysis (CVVHD) have also been used to remove potassium. However, potassium removal with these methods is similar to that of PD and sodium polystyrene sulfonate (Kayexalate). CVVHD or CAVHD may be used for long-term removal of potassium, but in acute, severe, life-threatening hyperkalemia unresponsive to medical therapy, hemodialysis remains the procedure of choice.

Following emergent management and stabilization of hyperkalemia, the patient should be hospitalized, and further workup should be initiated to determine the inciting cause and to prevent recurrence.


Patients with acute life-threatening hyperkalemia should receive care in a pediatric or neonatal intensive care unit capable of providing emergent hemodialysis.

Any child who develops hyperkalemia as a result of renal failure should be referred to a pediatric nephrologist for continuing care.


Potassium intake must be closely monitored (and possibly restricted) in patients with renal failure.


Consultations with the following specialists may be necessary in cases of hyperkalemia that result from certain conditions or disease states:

  • Pediatric intensivist or neonatologist: Management of life-threatening hyperkalemia (hyperkalemia with ECG changes)

  • Nephrologist: Hyperkalemia associated with renal failure

  • Hematologist/oncologist: Hyperkalemia resulting from tumor lysis syndrome

  • Social services specialist: Children who develop hyperkalemia following unintentional ingestions or poisonings

  • Nutritional support specialist: Particularly for patients whose hyperkalemia is caused by renal failure, which requires close regulation of potassium and sodium intake

  • Endocrinologist: Patients with suspected mineralocorticoid abnormalities such as congenital adrenal hyperplasia



Medication Summary

Treatment for severe hyperkalemia consists of 3 steps: (1) immediate stabilization of the myocardial cell membrane, (2) rapidly shifting potassium intracellularly, and (3) enhancing total body potassium elimination (see Medical Care).

In addition, all sources of exogenous potassium should be immediately discontinued; including intravenous (IV) and oral (PO) potassium supplementation, total parenteral nutrition, and any blood product transfusion. Drugs associated with hyperkalemia should also be discontinued.

Albuterol and other beta-adrenergic agents induce the intracellular movement of potassium via the stimulation of the sodium/potassium–adenosine triphosphate (Na+/K+ -ATP) pump. Studies have shown that IV salbutamol (not available in the United States) is highly effective in lowering serum potassium levels. Some studies in adults and children using nebulized albuterol indicate that this method of therapy is effective in lowering serum potassium levels. However, peak response is unclear; therefore, it has not been established as the first line of therapy in severe hyperkalemia.

Myocardium stabilizers

Class Summary

Calcium does not lower serum potassium levels. It is primarily used to protect the myocardium from the deleterious effects of hyperkalemia (ie, arrhythmias) by antagonizing the membrane actions of potassium.

Calcium chloride

IV calcium is indicated in all cases of severe hyperkalemia (ie, >7 mEq/L), especially when accompanied by ECG changes. Calcium chloride contains about 3 times more elemental calcium than an equal volume of calcium gluconate. Therefore, when hyperkalemia is accompanied by hemodynamic compromise, calcium chloride is preferred over calcium gluconate.

Administration of calcium should be accompanied by the use of other therapies that actually help lower the K+ serum levels.

Other calcium salts (eg, glubionate, gluceptate) have even less elemental calcium than calcium gluconate and are generally not recommended for therapy of hyperkalemia. Calcium chloride 1 g = 270 mg (13.5 mEq) of elemental calcium.

Calcium gluconate 1 g = 90 mg (4.5 mEq) of elemental calcium.

Intracellular transporters

Class Summary

Regular insulin and glucose cause a transcellular shift of potassium into muscle cells, thereby temporarily lowering K+ serum levels.

Insulin and dextrose, IV

Regular insulin presence results in intracellular movement of glucose, followed by K+ entry into muscle cells. Although effect is almost immediate, it is temporary, and, therefore, should be followed by therapy that actually enhances potassium clearance (eg, sodium polystyrene sulfonate).

Alkalinizing agents

Class Summary

Sodium bicarbonate IV is used as a buffer that breaks down to water and carbon dioxide after binding free hydrogen ions.

Sodium bicarbonate

IV infusion helps shift K+ into cells, further lowering serum K+ levels. Can be considered in treatment of hyperkalemia even in absence of metabolic acidosis. Also increases sodium delivery to the kidney, which assists in potassium excretion.

Exchange resins

Class Summary

Sodium polystyrene sulfonate is an exchange resin that can be used to treat mild-to-moderate hyperkalemia. Each mEq of potassium is exchanged for 1 mEq of sodium.

Sodium polystyrene sulfonate (Kayexalate)

Exchanges sodium for potassium and binds it in the gut, primarily in large intestine, and decreases total body potassium. Onset of action after PO administration ranges from 2-12 hours and is longer when administered PR.

Do not use as a first-line therapy for severe life-threatening hyperkalemia. Use in second stage of therapy to reduce total body potassium.


Questions & Answers


What is hyperkalemia?

What is the pathophysiology of hyperkalemia?

What is the prevalence of pediatric hyperkalemia?

What determines the prognosis of hyperkalemia?

What is the morbidity and mortality associated with hyperkalemia?

What are the possible complications of hyperkalemia?


What is the focus of clinical history for the evaluation of pediatric hyperkalemia?

Which physical findings are characteristic of pediatric hyperkalemia?

What causes pediatric hyperkalemia?


When should pediatric hyperkalemia be suspected?

What are the signs and symptoms of congenital adrenal hyperplasia-caused pediatric hyperkalemia?

Which findings on ECG are characteristic of pediatric hyperkalemia?

Which patients are at high risk for developing hyperkalemia aggravated by succinylcholine?

What are the differential diagnoses for Pediatric Hyperkalemia?


What is the role of lab tests in the workup of pediatric hyperkalemia?

What is the role of ECG in the workup of pediatric hyperkalemia?

What is the role of imaging studies in the workup of pediatric hyperkalemia?


How is pediatric hyperkalemia treated?

How is the myocardial cell membrane stabilized during the treatment of pediatric hyperkalemia?

How is the cellular uptake of potassium enhanced during the treatment of pediatric hyperkalemia?

How is total body potassium elimination enhanced during the treatment of pediatric hyperkalemia?

What is included in the clinical management of pediatric hyperkalemia?

When is patient transfer indicated for the treatment of pediatric hyperkalemia?

Which dietary modifications are used in the treatment of pediatric hyperkalemia?

Which specialist consultations are beneficial to patients with pediatric hyperkalemia?


What is the role of medications in the treatment of pediatric hyperkalemia?

Which medications in the drug class Exchange resins are used in the treatment of Pediatric Hyperkalemia?

Which medications in the drug class Alkalinizing agents are used in the treatment of Pediatric Hyperkalemia?

Which medications in the drug class Intracellular transporters are used in the treatment of Pediatric Hyperkalemia?

Which medications in the drug class Myocardium stabilizers are used in the treatment of Pediatric Hyperkalemia?