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Management of hyperkalemia in children

Management of hyperkalemia in children
Literature review current through: Jan 2024.
This topic last updated: Jan 10, 2024.

INTRODUCTION — Hyperkalemia is typically defined as a serum or plasma potassium greater than 5.5 mEq/L (mmol/L). However, the upper limit of normal in preterm infants and young infants may be as high as 6.5 mEq/L (mmol/L). Although children are less likely to develop hyperkalemia compared with adults, pediatric hyperkalemia is not an uncommon occurrence. Severe hyperkalemia (potassium level ≥7 mEq/L [mmol/L]) is a serious medical problem that requires immediate attention.

The management of hyperkalemia in children is reviewed here. The etiology, clinical findings, diagnosis, and evaluation of pediatric hyperkalemia are presented separately. (See "Causes, clinical manifestations, diagnosis, and evaluation of hyperkalemia in children".)

URGENCY OF THERAPY — The urgency of treatment of hyperkalemia varies with the level of extracellular (serum/plasma) potassium, rapidity of the increase in potassium, and presence of associated hyperkalemic symptoms (algorithm 1).

The urgency and type of therapy are similar to those used in adults and are based on the severity of hyperkalemia and its potential to be life-threatening. (See "Treatment and prevention of hyperkalemia in adults", section on 'Determining the urgency of therapy'.)

Initial emergent therapy is directed toward patients who are at risk for life-threatening cardiac conduction disturbances due to hyperkalemia (table 1 and figure 1). The onset of action of emergent interventions is immediate (see "Causes, clinical manifestations, diagnosis, and evaluation of hyperkalemia in children", section on 'Cardiac conduction abnormalities' and 'Rapid measures to counteract adverse cardiac effects' below):

Patients with clinical signs and symptoms of hyperkalemia – Children with electrocardiographic (ECG) changes, including widening of the QRS complex, loss of P waves, or arrhythmias (figure 1), and those with muscular weakness or paralysis. However, emergent therapy is not initiated for isolated peaked T waves, which is typically associated with levels between 5.5 to 6.5 mEq/L (mmol/L). (See "Causes, clinical manifestations, diagnosis, and evaluation of hyperkalemia in children", section on 'Symptomatic patients' and "Causes, clinical manifestations, diagnosis, and evaluation of hyperkalemia in children", section on 'Cardiac conduction abnormalities'.)

Asymptomatic children with potassium levels ≥7 mEq/L (mmol/L).

Patients with potassium levels between 6 and 7 mEq/L (mmol/L) who are at risk for continued rapid rise in extracellular potassium due to ongoing intracellular potassium release (eg, tumor lysis syndrome or rhabdomyolysis from a major crush injury).

Nonemergent treatment of hyperkalemia is provided as:

Prompt but not emergent intervention for asymptomatic children with acute hyperkalemia with potassium levels below 7 mEq/L (mmol/L) and who are not at risk for rapid increase in potassium. Treatment is focused on lowering potassium levels over 6 to 12 hours.

Adjunctive interventions for patients who are receiving initial emergent therapeutic interventions.

Chronic hyperkalemia – Asymptomatic patients with chronic hyperkalemia with levels less than 7 mEq/L (mmol/L). These patients generally do not need urgent lowering of the potassium level.

OVERVIEW OF TREATMENT — The following are therapeutic interventions for pediatric hyperkalemia (table 1). The choice of therapy depends on the urgency of therapy, based on the severity of hyperkalemia and its potential to be life-threatening (algorithm 1). As therapy is initiated, it is important to confirm that the child is hyperkalemic, especially if the clinical setting makes the diagnosis of hyperkalemia unlikely. An electrocardiogram (ECG) should be obtained in children with potassium >6 mEq/L (mmol/L) who are otherwise healthy or in whom there is a suspected rapid rise in potassium. If there are signs indicative of conduction abnormalities, the patient should be placed on a cardiac monitor or serial ECGs should be obtained. (See "Causes, clinical manifestations, diagnosis, and evaluation of hyperkalemia in children", section on 'Cardiac conduction abnormalities'.)

Emergent management counteracts the adverse cardiac effects of severe hyperkalemia. It includes intravenous (IV) calcium infusion to stabilize the cardiac membrane and measures to shift extracellular potassium into the cells (eg, insulin therapy and inhaled beta-adrenergic agents). (See 'Initial emergent therapy' below and "Causes, clinical manifestations, diagnosis, and evaluation of hyperkalemia in children", section on 'Cardiac conduction abnormalities'.)

Removal of potassium – The three interventions available for potassium removal in children are diuretics, cation exchange resin, and dialysis. (See 'Therapies removing potassium from the body' below.)

Treatment of the underlying cause of hyperkalemia. (See 'Treatment of reversible causes' below.)

Elimination or reduction of potassium intake for patients, especially those with persistent hyperkalemia due to impairment of urinary potassium excretion. (See 'Chronic hyperkalemia' below.)

INITIAL EMERGENT THERAPY — Initial acute management of symptomatic and/or severe hyperkalemia (potassium level ≥7 mEq/L [mmol/L]) takes precedence over any diagnostic evaluation. Acute rapid transient measures include intravenous (IV) calcium infusion to stabilize the cardiac membrane and interventions that shift potassium from the extracellular space into the cells (table 1 and algorithm 1) [1].

However, these rapid measures are transient in nature and nonemergent measures to remove excess potassium from the body and treat any underlying reversible cause of hyperkalemia are administered concomitantly. (See 'Nonemergent therapy' below.)

Rapid measures to counteract adverse cardiac effects — Acute, rapid, transient measures include stabilizing the cardiac membrane and shifting potassium from the extracellular space into the cells (table 1) [1]. These interventions are administered to children with severe (potassium level ≥7 mEq/L [mmol/L]) and/or symptomatic hyperkalemia (electrocardiography [ECG] changes (figure 1) and muscular weakness or paralysis). Emergent therapy is also provided to children with potassium levels between 6 and 7 mEq/L (mmol/L) who are at risk for continued rapid rise in extracellular potassium due to intracellular potassium release (eg, tumor lysis syndrome or rhabdomyolysis from a major crush injury).

Calcium infusion — Calcium gluconate (10 percent solution) is given at a dose of 0.5 mL/kg (maximum dose 20 mL [2 g]) by IV infusion over five minutes. Time to onset of action is immediate.

In the clinical setting of a cardiac arrest or impending arrest, calcium chloride is typically used rather than calcium gluconate because it results in a more rapid increase in the serum ionized calcium. The dose of IV calcium chloride is 20 mg/kg (maximum dose 1000 mg) given over 5 to 10 minutes. (See "Primary drugs in pediatric resuscitation", section on 'Calcium'.)

Although the protective effect of infused calcium is rapid in onset, its duration may be short lived and a repeat dose may be needed for persistent ECG changes or arrhythmias. Concomitant therapies that promote the shift of potassium into the intracellular space should also be initiated as quickly as possible. (See 'Insulin and glucose therapy' below.)

Calcium directly antagonizes the hyperkalemia-induced depolarization of the resting cardiac membrane. Calcium therapy results in decreased membrane excitability and reduces the risk of developing cardiac conduction abnormalities and arrhythmias [2]. (See "Clinical manifestations of hyperkalemia in adults", section on 'Pathogenesis'.)

Insulin and glucose therapy — The combination of IV insulin and glucose is the preferred method to shift extracellular potassium into the cell. Insulin administration drives extracellular potassium into the cells by enhancing the activity of the Na-K ATPase pump in skeletal muscles. Glucose is given concomitantly to prevent hypoglycemia. The effect of insulin begins in 10 to 20 minutes and peaks at 30 to 60 minutes. The major adverse effect is hypoglycemia, and serum glucose level should be measured one hour after the administration of insulin even when glucose is administered. (See "Treatment and prevention of hyperkalemia in adults", section on 'Insulin with glucose' and "Approach to hypoglycemia in infants and children", section on 'Treatment'.)

In children, regular insulin (dose of 0.1 units per kg, maximum dose of 10 units) is given along with a dextrose (glucose) dose of 0.5 g/kg over 30 minutes. The administration of dextrose is based on the age of the patient, as follows:

Younger than five years of age – Give 10 percent dextrose (100 mg/mL) at a dose of 5 mL/kg

Five years of age and older – Give 25 percent dextrose (250 mg/mL) at a dose of 2 mL/kg (maximum dose 25 g)

Other measures to shift extracellular K+ — Other interventions that shift potassium from the extracellular spaces into the cells include inhaled beta-adrenergic agonists and IV sodium bicarbonate, which are rapid in onset but generally have limited duration of action. (See "Treatment and prevention of hyperkalemia in adults".)

Inhaled beta-adrenergic agonists — Inhaled beta-adrenergic agonists are alternatives to IV insulin and glucose infusion in children who do not have secure IV access. Several case reports and series have demonstrated a decrease of serum potassium of 1 to 1.5 mEq/L (mmol/L) within an hour of administration of inhaled beta-adrenergic agonists [3]. This intervention has also been shown to be effective and safe in mechanically ventilated preterm neonates [4].

Beta-adrenergic agonists should be avoided in children manifesting any preexisting cardiac arrhythmia, and children should be on a cardiac monitor during administration. Tachycardia and tremors are common side effects but are usually short lived.

Dosing of albuterol is based on the child's weight, as follows:

Neonates – 0.4 mg

Infants and small children <25 kg – 2.5 mg

Children between 25 and 50 kg – 5 mg

Older children and adolescents >50 kg – 10 mg (doses up to 20 mg have been used)

Albuterol can be given concomitantly with the combination of IV insulin and glucose, or sequentially for patients who may not respond adequately to insulin/glucose therapy.

Sodium bicarbonate — Increasing the extracellular pH with sodium bicarbonate leads to hydrogen ion movement from the cell into the extracellular space. As a result, extracellular potassium moves into the cell to maintain electroneutrality. However, it remains uncertain if bicarbonate therapy is beneficial and it should not be the only therapy used in the management of hyperkalemia. (See "Treatment and prevention of hyperkalemia in adults", section on 'Sodium bicarbonate'.)

In children, the dose of bicarbonate is 1 mEq/kg (maximum dose 50 mEq) administered IV over 10 to 15 minutes. It can be given as 1 mL/kg of an 8.4 percent solution or, for children less than six months of age, as 2 mL/kg of a 4.2 percent solution. Although dosing can be repeated, there is a risk of developing hypernatremia with repeated administration.

Monitoring response — Continuous cardiac monitoring and serial ECGs are used to monitor the response of patients with severe hyperkalemia who require rapidly acting therapies. The serum potassium should be measured at one to two hours after the initiation of treatment.

The timing of further measurements is determined by the serum potassium concentration and the response to therapy. Patients who receive insulin, with or without dextrose, should undergo hourly glucose measurements for up to six hours to monitor for hypoglycemia.

Emergent therapy can be readministered to patients who fail to respond (potassium remains above 7 mEq/L [mmol/L], ECG changes or muscular symptoms persist, or continued rise of potassium).

NONEMERGENT THERAPY — Nonemergent measures for pediatric hyperkalemia include treating any reversible disorder that contributes to hyperkalemia and interventions to remove excess potassium from the body.

Clinical setting — Nonemergent therapy for pediatric hyperkalemia is used in the following clinical settings:

As adjunctive therapy for patients with severe or life-threatening hyperkalemia who are receiving initial emergent interventions as these measures are only transient in nature. (See 'Initial emergent therapy' above.)

For asymptomatic children with acute hyperkalemia with potassium levels below 7 mEq/L (mmol/L) and who are not at risk for a rapid increase in potassium. Treatment is focused on lowering potassium levels over 6 to 12 hours.

Treatment of reversible causes — A variety of conditions can contribute to hyperkalemia. Many of these disorders are reversible, and management should focus on treating the underlying disease after ensuring initial emergent management of patients with potentially life-threatening hyperkalemia, as discussed above. (See "Causes, clinical manifestations, diagnosis, and evaluation of hyperkalemia in children", section on 'Causes'.)

Reversible causes of hyperkalemia include the following:

Hypovolemia, which impairs renal excretion of potassium, corrected with fluid repletion.

Congenital adrenal hyperplasia or adrenal insufficiency, which is corrected with hormonal therapy.

Medications (eg, spironolactone or angiotensin-converting enzyme inhibitors), which impair renal excretion of potassium, are discontinued.

Parenteral fluids or medications with excessively large loads of potassium are discontinued.

Metabolic acidosis, which promotes potassium movement from the cells into extracellular spaces, is corrected. (See "Approach to the child with metabolic acidosis".)

Therapies removing potassium from the body — The three available modalities for potassium removal in children are diuretics, cation exchange resin, and dialysis.

Diuretics — Loop and thiazide diuretics can improve urinary potassium excretion in children with adequate effective intravascular volume and renal function. This intervention may be useful in children with persistently elevated but nonurgent levels of hyperkalemia (potassium levels between 5.5 and 7 mEq/L [mmol/L]) and as an adjunctive therapy in those with more severe hyperkalemia.

In general, we use furosemide, a loop diuretic, at a dose of 1 mg/kg intravenously (IV). The maximum dose in children with normal renal function is 40 mg. However, in children with renal insufficiency, higher doses (up to 80 mg) may be required. Onset of effect on potassium typically occurs within one to two hours. If effective, furosemide may be given every six hours.

However, diuretic therapy has limited or no benefits in children with decreased effective circulating volume or moderate to severe renal dysfunction. In these patients, the use of cation exchange resins and/or dialysis may be needed.

Enteral cation exchange resins — Polystyrene sulfonates are cation exchange resins, which exchange sodium for potassium across the large intestine [5].

In children, sodium polystyrene sulfonate, the most commonly used cation exchanger, is administered at a dose of 1 g/kg every four hours (maximum dose 30 g). It is dissolved in water and is given enterally (oral or through a nasogastric tube) or as a retention enema. Each gram of resin may bind as much as 1 mEq of potassium, while releasing a comparable amount of sodium into the patient as the counterion. The onset of ion exchange is approximately one to two hours. The ensuing indigestible potassium polystyrene sulfonate complex is then excreted in the feces, thereby removing potassium from the body. The US Food and Drug Administration (FDA) is requiring the manufacturer to conduct studies to see whether sodium polystyrene sulfonate affects absorption of other drugs. Until these data are available, the FDA suggests that the administration of sodium polystyrene sulfonate be separated from other oral drugs by at least six hours.

In the past, sodium polystyrene sulfonate had been mixed with sorbitol to prevent intestinal obstruction caused by fecal impaction and constipation due to the concretion of the potassium polystyrene sulfonate complex. However, colonic necrosis and perforation have been reported in patients receiving this mixture, especially in the setting of post-gastrointestinal surgery or decreased colonic motility [6]. In 2009, the FDA recommended that sodium polystyrene sulfonate should not be administered with sorbitol. As an alternative, patients can be given a laxative (lactulose or polyethylene glycol 3350 (table 2)) to reduce the constipating effects of polystyrene sulfonates.

If sodium polystyrene sulfonate without sorbitol is not available, clinicians must consider whether treatment with sodium polystyrene sulfonate in sorbitol is necessary.

Cation exchangers are not beneficial in the emergent setting, as they have limited or no short-term benefit [7]. Nevertheless, it is a reasonable to initiate cation exchange resin therapy as soon as possible, especially in cases with (or suspected to have) persistent hyperkalemia, as it is the only therapy short of dialysis that can remove potassium from the body in most hyperkalemic children. Cation exchange therapy is used in patients with persistently moderately elevated potassium (5.5 to 6.5 mEq/L [mmol/L]) and as an adjunct for those with more severe hyperkalemia.

Sodium polystyrene sulfonate should not be given to the following patients (see "Treatment and prevention of hyperkalemia in adults", section on 'Do not use sodium polystyrene sulfonate (SPS) or other resins'):

Postoperative patients.

Patients with an ileus or who are receiving opiates.

Patients with a large or small bowel obstruction.

Preterm infants.

The use of oral sodium polystyrene should be avoided in all term neonates. Rectal administration should also not be considered in term infants who are at risk for intestinal hypomobility and/or necrotizing enterocolitis.

In adults, patiromer is the preferred cation exchanger. It exchanges calcium ions for potassium and is approximately 10 times more potent than sodium polystyrene sulfonate in potassium removal. In a small open-label trial in 14 adolescents with chronic kidney disease and hyperkalemia, treatment with patiromer for two weeks reduced serum potassium to <5 mEq/L in one-half of the participants [8]. This study was the basis for approval by the FDA for treatment of hyperkalemia in children ≥12 years. Sodium zirconium cyclosilicate, or ZS-9, is another cation exchange resin that is under consideration for FDA approval. (See "Treatment and prevention of hyperkalemia in adults", section on 'Patiromer or sodium zirconium cyclosilicate (SZC)'.)

Dialysis — In children unresponsive to diuretic or cation exchange resin therapy, or with severe renal dysfunction, dialysis may be necessary to remove excess potassium from the body in children with potassium levels >6.5 mEq/L (mmol/L) (see "Prevention and management of acute kidney injury (acute renal failure) in children", section on 'Kidney replacement therapy'). Generally, hemodialysis is the preferred modality to reduce potassium levels as it is the quickest and most controlled renal replacement treatment. Although peritoneal dialysis can be used, potassium removal is less efficient and less well controlled. In some centers, continuous renal replacement therapy may be a better option than hemodialysis because of availability, resources, and staffing. (See "Pediatric acute kidney injury: Indications, timing, and choice of modality for kidney replacement therapy", section on 'Modality'.)

CHRONIC HYPERKALEMIA — Persistent pediatric hyperkalemia is most commonly seen in children with chronic kidney disease. In these patients, medical therapy consists of a low-potassium diet, use of loop diuretic therapy, correction of metabolic acidosis with carbonate therapy, and avoidance of drugs that increase potassium levels such as spironolactone or one of the angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. (See "Causes, clinical manifestations, diagnosis, and evaluation of hyperkalemia in children", section on 'Decreased activity of the renin-angiotensin-aldosterone system'.)

If medical therapy fails to control hyperkalemia, renal replacement therapy must be considered. (See "Chronic kidney disease in children: Complications", section on 'Hyperkalemia'.)

SUMMARY AND RECOMMENDATIONS

Definition – Hyperkalemia is typically defined as a serum or plasma potassium greater than 5.5 mEq/L (mmol/L). However, the upper limit of normal in infants may be as high as 6.5 mEq/L (mmol/L). Although children are less likely to develop hyperkalemia compared with adults, pediatric hyperkalemia is not an uncommon occurrence and severe hyperkalemia (potassium level ≥7 mEq/L [mmol/L]) is a serious medical problem and potentially life-threatening condition that requires immediate attention. (See "Causes, clinical manifestations, diagnosis, and evaluation of hyperkalemia in children", section on 'Cardiac conduction abnormalities'.)

Urgency of therapy – The urgency and type of intervention are based on the degree and rapidity of potassium elevation, presence or absence of symptoms, and electrocardiographic (ECG) findings (algorithm 1). The most serious manifestations of hyperkalemia are cardiac conduction abnormalities and arrhythmias, which generally occur when potassium concentration is ≥7 mEq/L (mmol/L) (figure 1). (See 'Urgency of therapy' above and 'Overview of treatment' above.)

Emergency management before diagnostic evaluation – Initial emergency management of severe or symptomatic hyperkalemia takes precedence over any diagnostic evaluation because hyperkalemia is a potentially life-threatening condition. As therapy is initiated, it is important to confirm that the child is hyperkalemic, especially if the clinical setting makes the diagnosis of hyperkalemia unlikely, and to obtain an ECG in children with potassium >6 mEq/L (mmol/L) who are otherwise healthy or in whom there is a suspected rapid rise in potassium (table 1). (See 'Overview of treatment' above.)

Emergency management – For patients with severe hyperkalemia (potassium level >7 mEq/L [mmol/L]), those with signs or symptoms of hyperkalemia (ECG changes (figure 1) or muscular weakness or paralysis), or patients with potassium levels between 6 to 7 mEq/L (mmol/L) who are at risk for further increases in potassium, we recommend administering initial emergent therapeutic interventions directed toward counteracting the adverse cardiac effects (Grade 1A). These measures, which are transient in effect, include the following:

Calcium – Intravenous (IV) infusion of calcium gluconate 10 percent solution at a dose of 0.5 mL/kg (maximum dose 20 mL [2 g]) over five minutes. (See 'Calcium infusion' above.)

Insulin and glucose – Therapy to shift extracellular potassium into cells including: (1) IV administration of regular insulin and glucose, and/or (2) inhaled beta-adrenergic agonists, such as albuterol (salbutamol). (See 'Insulin and glucose therapy' above and 'Inhaled beta-adrenergic agonists' above.)

Do not use sodium bicarbonate as the sole agent – Sodium bicarbonate also causes transcellular potassium movement, but its beneficial effect is uncertain. As a result, we do not recommend the use of sodium bicarbonate as the sole intervention to shift potassium intracellularly (Grade 1B). (See 'Sodium bicarbonate' above.)

Nonemergency management – After initial emergent management of the child with potentially life-threatening hyperkalemia or asymptomatic patients who present with more modest hyperkalemia (potassium levels <7 mEq/L [mmol/L]), further management consists of identification and treatment of reversible causes of hyperkalemia and removal of excess potassium from the body. Therapy to remove body potassium includes the following (see 'Nonemergent therapy' above):

Diuretics and cation exchange resin – Diuretics and cation exchange resin are used in patients with persistent, moderately elevated potassium (5.5 to 6.5 mEq/L [mmol/L]) and as adjuncts for those with more severe hyperkalemia. (See 'Diuretics' above and 'Enteral cation exchange resins' above.)

Dialysis – Dialysis therapy is reserved for patients with persistent hyperkalemia who are unresponsive to diuretic or cation exchange therapy. In general, hemodialysis is the preferred modality to reduce potassium levels as it is the quickest and most controlled renal replacement treatment. (See 'Dialysis' above.)

Chronic hyperkalemia – Persistent chronic pediatric hyperkalemia is most commonly seen in children with chronic kidney disease. In these patients, medical therapy consists of a low-potassium diet, use of loop diuretic therapy, correction of metabolic acidosis with carbonate therapy, and avoidance of drugs that increase potassium. If medical therapy fails to control hyperkalemia, renal replacement therapy must be considered. (See 'Chronic hyperkalemia' above and "Chronic kidney disease in children: Complications", section on 'Hyperkalemia'.)

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