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Causes, clinical manifestations, diagnosis, and evaluation of hyperkalemia in children

Causes, clinical manifestations, diagnosis, and evaluation of hyperkalemia in children
Literature review current through: Jan 2024.
This topic last updated: May 17, 2023.

INTRODUCTION — Hyperkalemia is defined as a serum or plasma potassium that is higher than the upper limit of normal potassium, which typically is considered to be 5.5 mEq/L (mmol/L) (table 1). Although children are less likely to develop hyperkalemia than adults, pediatric hyperkalemia is not an uncommon occurrence. Severe hyperkalemia (potassium level greater than 7 mEq/L [mmol/L]) is a serious medical problem that needs immediate attention.

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

NORMAL POTASSIUM BALANCE AND LEVELS — Homeostatic mechanisms regulate potassium balance to maintain high intracellular levels required for cellular functions (eg, metabolism and growth) and low extracellular concentration to preserve the steep concentration gradient across the cell membrane needed for nerve excitation and muscle contraction. After a bolus of potassium intake, these normal physiologic processes preserve the intra- and extracellular balance via transcellular potassium movement regulated by cell membrane Na-K-ATPase (mediated by insulin and alpha and beta-2 adrenergic agonists) and urinary potassium excretion (mostly mediated by aldosterone). In children, positive potassium balance is needed for growth, whereas in adults, homeostasis is directed towards a zero potassium balance.

Normal serum and plasma potassium concentrations in children and adolescents are similar to levels in adults. However, infants have a higher normal range of potassium because of their reduced urinary potassium excretion, caused by their relatively increased aldosterone insensitivity and decreased glomerular filtration rate (GFR) (table 1). (See "Causes and evaluation of hyperkalemia in adults", section on 'Brief review of potassium physiology'.)

PATHOPHYSIOLOGY — Hyperkalemia in children is caused by derangements of the homeostatic mechanisms that normally regulate potassium balance, which are the same as those that occur in adults. Understanding the underlying physiology is helpful in the diagnostic evaluation and treatment of children with hyperkalemia. (See "Causes and evaluation of hyperkalemia in adults", section on 'Brief review of potassium physiology'.)

Pediatric hyperkalemia is due to one or a combination of the following mechanisms:

Excessive increase in potassium intake

Transcellular movement of intracellular potassium into the extracellular space

Decreased renal excretion of potassium

Persistent hyperkalemia generally requires impaired urinary potassium excretion.

CAUSES — In the following sections, the causes of pediatric hyperkalemia are classified based on the underlying physiologic process (table 2).

Increased potassium intake — In normal children, large increases in usual dietary sources of potassium are unlikely to lead to sustained hyperkalemia as normally intact homeostatic mechanisms protect against elevated extracellular potassium. (See 'Normal potassium balance and levels' above.)

Rarely, normal homeostatic mechanisms can be overwhelmed by excessively large loads of potassium that may be delivered in intravenous (IV) fluids, parenteral nutrition, IV medications with a high potassium content (eg, potassium penicillin), or massive transfusions of blood [1]. However, this is unlikely to occur with correct prescription and administration of these substances in a child with normal cardiovascular and kidney function. Infants and small children are more likely to develop clinically significant hyperkalemia because, for a given intake, the rise in potassium concentration is greater as these patients have a smaller volume of distribution. (See "Red blood cell transfusion in infants and children: Administration and complications", section on 'Metabolic toxicity'.)

Transcellular movement of potassium

Cellular injury — Breakdown of normal tissue or rapid cell lysis can result in the release of large amounts of intracellular potassium along with other intracellular electrolytes into the extracellular space. This most often occurs in children in the following settings:

Rhabdomyolysis from crush injury sustained in accidents or natural disasters (see "Crush-related acute kidney injury", section on 'Biochemical abnormalities')

Extreme exercise resulting in significant muscle injury (see "Exertional heat illness in adolescents and adults: Management and prevention")

Tumor lysis syndrome in children with large tumor burden (eg, leukemia or lymphoma) while undergoing chemotherapy (see "Tumor lysis syndrome: Pathogenesis, clinical manifestations, definition, etiology and risk factors", section on 'Clinical manifestations')

Severe hemolytic processes (see "Clinical features and diagnosis of heme pigment-induced acute kidney injury", section on 'Potassium')

Acute kidney injury may also be present in patients with the above conditions, which exacerbates hyperkalemia due to impaired urinary potassium excretion.

Metabolic acidosis — In children, metabolic acidosis is the most common cause of intracellular potassium movement to the extracellular space without cellular injury. In this setting, the intracellular movement of hydrogen ions causes the potassium to shift into the extracellular space to maintain electroneutrality. Metabolic acidosis is often caused by or is associated with a decreased effective arterial blood volume, which may impact urinary potassium excretion. The reestablishment of adequate perfusion generally results in the restoration of both normal acid-base status and urinary potassium excretion. (See 'Decreased effective arterial blood volume' below.)

A similar transcellular shift can be seen in children with insulin deficiency and diabetic ketoacidosis and is discussed in greater detail separately. (See "Potassium balance in acid-base disorders" and "Diabetic ketoacidosis in children: Clinical features and diagnosis", section on 'Serum potassium'.)

Hyperkalemic periodic paralysis — Children with hyperkalemic periodic paralysis can present with hyperkalemia caused by transcellular relocation of potassium. Hyperkalemic periodic paralysis is an autosomal dominant condition that encodes for a protein of the sodium channel of skeletal muscles. In these patients, the sodium channel closes too slowly, leading to intracellular potassium movement into the extracellular space, which results in hyperkalemia and muscle weakness. Hyperkalemic periodic paralysis can present in infancy and needs to be considered in any young child with hyperkalemia and concomitant muscle weakness. (See "Hyperkalemic periodic paralysis".)

Abnormalities in renal excretion

Acute and chronic kidney disease — In children with acute or chronic kidney disease, urinary potassium excretion may be reduced due to a decrease in glomerular filtration rate (GFR) and/or tubular dysfunction.

Glomerular filtration rate — Hyperkalemia is not commonly observed until the GFR falls below 30 mL/min per 1.73 m2. At this reduced level of GFR, urinary potassium excretion is impaired because the decreased distal delivery of sodium limits its exchange with potassium in the collecting tubule.

Tubular dysfunction — Impaired potassium excretion due to tubular dysfunction (eg, aldosterone insensitivity or deficiency) may occur in the following clinical settings:

Hypoaldosteronism (type 4 renal tubular acidosis) – Hyperkalemia may be caused by either aldosterone deficiency or resistance even when the GFR is well preserved. Aldosterone resistance is a common finding in children with obstructive uropathy or reflux nephropathy and is often referred to as type 4 renal tubular acidosis. (See "Etiology and clinical manifestations of renal tubular acidosis in infants and children", section on 'Aldosterone deficiency or resistance (type 4 renal tubular acidosis)'.)

Infants – Infants have a relatively lower rate of urinary potassium excretion because of a normally decreased response to aldosterone and lower GFR. As a result, infants generally have higher baseline serum/plasma potassium levels than older children (table 1). This is especially true for preterm infants who have lower GFR and more immature tubular function than term infants. (See "Neonatal acute kidney injury: Pathogenesis, etiology, clinical presentation, and diagnosis", section on 'Glomerular filtration rate' and "Neonatal acute kidney injury: Pathogenesis, etiology, clinical presentation, and diagnosis", section on 'Presentation due to other laboratory abnormalities'.)

Urinary tract infections – Infants with acute febrile urinary tract infection (ie, pyelonephritis) are at risk for hyperkalemia compared with patients who have other febrile illnesses [2]. It is thought that interstitial inflammation due to pyelonephritis exacerbates the decrease response to aldosterone that is normally seen in young infants, thus causing further distal tubular insensitivity to aldosterone. However, one small case series suggests that, in some infants, an underlying genetic variant of type 4 renal tubular acidosis may contribute to hyperkalemia [3].

Sickle cell disease – In children with sickle cell disease and renal tubular injury due to impaired medullary blood flow, impaired aldosterone sensitivity leads to reduced urinary potassium excretion and hyperkalemia. (See "Sickle cell disease effects on the kidney", section on 'Pathogenesis'.)

Decreased effective arterial blood volume — A common cause of pediatric hyperkalemia is decreased effective arterial blood volume that leads to poor tissue perfusion and metabolic acidosis (which results in transcellular potassium movement) and a reduction in urinary potassium excretion. In these patients, sodium and water reabsorption is increased in the proximal portion of the nephron, resulting in a reduction in sodium delivery to the collecting tubule. This leads to functional impairment of urinary potassium excretion as there is a limited amount of sodium available for potassium exchange in the collecting tubule. Although this phenomenon is often referred to as a functional renal tubular acidosis, or impaired aldosterone mediated urinary potassium and acid excretion, there is no abnormality in the ion channels or mineralocorticoid receptors of the distal nephron. Such patients are at risk for developing hyperkalemia with potassium administration in IV fluids or medications. (See 'Metabolic acidosis' above and "Overview and pathophysiology of renal tubular acidosis and the effect on potassium balance".)

Infants and young children are at risk of developing clinically significant dehydration and hemodynamic instability with acute illness as they have a higher surface area-to-volume ratio with proportionally greater insensible losses than older patients. In addition, they have an increased resistance to aldosterone. As a result, it is not uncommon to see hyperkalemia as an associated finding of impaired effective circulation in critically ill infants and young children [4]. (See "Clinical assessment of hypovolemia (dehydration) in children".)

In some children with chronic marginal hydration and a diet low in sodium content, high potassium levels may be seen as a result of reduced distal delivery of sodium. This is most often seen in infants who have ongoing feeding problems and a dietary intake of breast milk or infant formula, both of which have low sodium content.

Decreased activity of the renin-angiotensin-aldosterone system — Although rare, congenital or acquired endocrine anomalies that impair the renin-angiotensin-aldosterone system can result in hyperkalemia, particularly in infants or young children:

Congenital adrenal hyperplasia (CAH) results in significant underproduction of mineralocorticoids (eg, aldosterone) and ensuing early sodium wasting and severe hyperkalemia. (See "Causes of primary adrenal insufficiency in children", section on 'Congenital adrenal hyperplasia'.)

Other causes of primary adrenal insufficiency are rarer than CAH and may also present with hyperkalemia. In a case series of 20 consecutive patients with primary adrenal insufficiency that was not due to CAH, approximately one-half of the cohort presented with serum potassium levels >5 mEq/L, although almost all of the patients had hyponatremia and hypotension [5]. (See "Causes of primary adrenal insufficiency in children".)

Pseudohypoaldosteronism, which is even rarer than disorders of primary adrenal insufficiency, is caused by abnormal mineralocorticoid receptor activity resulting in salt wasting, hyperkalemia, metabolic acidosis, and high levels of serum aldosterone. In its autosomal dominant form, only the renal tubular function is affected and its clinical impact may wane as the child grows with further maturation of tubular sodium transport. In its autosomal recessive form (pseudohypoaldosteronism type 1), severe mutations in the epithelial sodium channel in the distal tubule have been described and affected patients generally present early in life, have salt wasting from aldosterone targeted organs (kidney, colon, and sweat glands), and require aggressive sodium supplementation to maintain electrolyte balance [6]. (See "Causes of primary adrenal insufficiency in children", section on 'End-organ unresponsiveness' and "Genetic disorders of the collecting tubule sodium channel: Liddle syndrome and pseudohypoaldosteronism type 1".)

Medications – Children being treated with potassium-sparing diuretics (eg, spironolactone or eplerenone) or one of the angiotensin-converting enzyme inhibitors or angiotensin receptor blockers may develop hyperkalemia because of decreased mineralocorticoid production or activity. Use of these medications in children is rare outside of children with intrinsic kidney or cardiac dysfunction, and these children may also be at risk of developing hyperkalemia due to other risk factors such as low GFR or decreased effective arterial volume.

Pseudohyperkalemia — In pseudohyperkalemia, the elevated potassium level measured in the laboratory sample is not representative of the child's true potassium. In children, it is most commonly caused by hemolyzed blood samples due to difficulties in obtaining or handling blood samples [7,8]. This is especially true in young children, in whom a hemolyzed specimen is more likely to occur because a small needle (20 to 24 gauge) and syringe are often needed to obtain blood samples as vacuum devices are difficult to use in these patients with small vessels. In some settings, an indwelling small-gauged IV catheter and syringe are used for blood sampling, which also requires significant suction to obtain sufficient sample volumes. Hemolysis is six times more likely to occur when a syringe is used compared with a vacuum device [7].

Children are also much more likely to resist phlebotomy attempts and to cry and struggle throughout the procedure. In a child whose arm is being restrained, repetitive limb movement and contraction can lead to release of muscle cell potassium that may significantly raise the potassium content of the blood sample.

In children with marked leukocytosis (white cell count >50,000/microL) or thrombocytosis (platelet counts >500,000/microL), there may also be potassium loss from these cells after clotting of the blood sample. However, this is unlikely to cause significant hyperkalemia, with the possible exception of patients with leukemia or myeloproliferative disorders. In these patients, a plasma potassium assay decreases the chances of a falsely elevated result.

CLINICAL MANIFESTATIONS

Asymptomatic patients — Most children are asymptomatic as they have mild (<6 mEq/L [6 mmol/L]) or moderate elevations of potassium (between 6 to 7 mEq/L [6 to 7 mmol/L]). In these patients, hyperkalemia is typically detected when plasma or serum electrolytes are obtained for monitoring or because electrolyte abnormalities are suspected. This usually occurs in children with signs or symptoms of kidney disease (eg, hypertension, urinary abnormalities [hematuria and proteinuria], edema, and oliguria/anuria), significantly decreased effective arterial blood flow (eg, shock, severe gastroenteritis, or heart failure), and considerable cellular injury (eg, trauma or tumor lysis syndrome). (See 'Causes' above.)

Asymptomatic children with mild to moderate hyperkalemia may have electrocardiographic (ECG) changes as a result of hyperkalemic-associated cardiac conduction disturbances. (See 'Cardiac conduction abnormalities' below.)

Symptomatic patients — Children with severe hyperkalemia (potassium level >7 mEq/L [7 mmol/L]) may have the following clinical manifestations [9], which are similar to those seen in adult patients (see "Clinical manifestations of hyperkalemia in adults", section on 'Clinical manifestations'):

Muscle weakness or paralysis – Muscle weakness is usually ascending, beginning in the legs and progressing to the trunk and arms, which can progress to flaccid paralysis. These findings may mimic those seen in patients with Guillain-Barré syndrome. (See "Guillain-Barré syndrome in children: Epidemiology, clinical features, and diagnosis".)

Symptoms of cardiac conduction abnormalities – Patients with hyperkalemia may present with palpitations, syncope, or asystole depending on the severity of cardiac conduction disturbances.

Cardiac conduction abnormalities — Hyperkalemia is associated with significant and potentially life-threatening disturbances in cardiac conduction. ECG changes reflect the impact of increasing levels of serum and plasma potassium on the electrical activity of the heart, including aberrant atrial (P wave) and ventricular (QRS complex) depolarization and abnormal repolarization (T wave). These findings are based not only on the level of extracellular potassium but also on how quickly the change in potassium level has occurred over time. ECG changes that generally occur at a concentration >7 mEq/L (7 mmol/L) in children with chronic hyperkalemia may be seen at lower levels in children with an acute rapid rise in potassium, resulting in a swift decrease in the transmembrane potassium gradient. This may be seen in patients with tumor lysis or significant crush injury. In infants, ECG changes are usually seen at greater levels of potassium as the normal range is higher in this group of patients (table 1).

The following is the general range of serum/plasma potassium levels expressed as mEq/L or mmol/L and the corresponding ECG changes.

Between 5.5 to 6.5 – Tall peaked T waves with a narrow base and shortening of the QT interval (waveform 1).

Between 6.5 to 8.0 – Peaked T waves, prolonged PR interval, decreased or disappearing P wave, widening QRS complex, and amplified R wave (waveform 2).

Greater than 8.0 – Absent P wave, bundle branch block, progressive widening of QRS complex that eventually merges with the T wave to form a sinusoidal pattern. This is followed by ventricular fibrillation or asystole.

Not all children with hyperkalemia will manifest ECG changes, and the absence of ECG change does not preclude the need for potential therapy for significant potassium elevation. (See "Management of hyperkalemia in children".)

DIAGNOSIS — The diagnosis of hyperkalemia is made by the detection of an elevated plasma or serum potassium level. In infants, the normal range of potassium is greater than in older children and adults because of their reduced urinary potassium excretion (table 1).

It is important to note that potassium levels may vary by measurement technique. Normal values are typically based on measurements from the central hospital automated blood biochemistry autoanalyzers. In intensive care unit and emergency department settings, there is increasing utilization of point-of-care-testing blood chemistry analyzers that allow rapid and accurate assessment of potassium levels from whole blood samples, with results that are similar to those found with blood gas analyzers. However, one study in children reported that potassium levels were lower by a mean difference of 0.4 mEq/L when measured by blood gas analyzers compared with values obtained from the central laboratory [10]. As a result, clinicians should be aware of any differences in potassium measurements in their own institutions between the central laboratory and point-of-care analyzers while interpreting potassium levels.

Because a common cause of high serum potassium values is due to hemolyzed specimens, which are due to difficulties in obtaining blood samples in children (ie, pseudohyperkalemia), an elevated potassium level should be confirmed in any child in whom the clinical setting makes hyperkalemia unlikely [7]. Repeat testing should be done with a nonhemolyzed specimen (free-flowing venous blood sample). If it is not possible to obtain a free-flowing venous blood sample, an arterial blood sample should be acquired prior to instituting any diagnostic evaluation or potassium lowering therapies in an asymptomatic child with a low clinical suspicion of true hyperkalemia. (See 'Pseudohyperkalemia' above.)

DIFFERENTIAL DIAGNOSIS — In asymptomatic patients, the primary differential diagnosis is pseudohyperkalemia, which is differentiated from true hyperkalemia by a normal repeat potassium level, as discussed above. (See 'Pseudohyperkalemia' above and 'Diagnosis' above.)

In symptomatic patients, diseases associated with specific symptoms are differentiated from hyperkalemia by the finding of an elevated potassium level.

Acute muscle weakness and paralysis – Conditions that present with muscle weakness include infections (eg, polio and West Nile virus infection), toxins (eg, botulism), hypocalcemia and hypermagnesemia, and Guillain-Barré syndrome. (See "Etiology and evaluation of the child with weakness".)

Palpitation and syncope – Hyperkalemia is differentiated from the large number of other causes of palpation and syncope (table 3 and table 4) by an elevated potassium level and characteristic echocardiographic findings. In children with palpitations and syncope, rapid assessment is imperative as these symptoms may be associated with a life-threatening condition such as cardiac conduction abnormalities. Initial evaluation is focused on determining whether the patient appears ill or not, if there is an underlying life-threatening cause, and if there is a risk of imminent shock (algorithm 1 and algorithm 2). The evaluations for palpitations and syncope are discussed elsewhere. (See "Approach to the child with palpitations" and "Emergency evaluation of syncope in children and adolescents".)

EVALUATION TO DETERMINE UNDERLYING ETIOLOGY

Initial management — Because hyperkalemia is a potentially life-threatening condition, initial management of elevated potassium takes precedence over any diagnostic evaluation. The urgency and type of intervention are based on the degree of potassium elevation, presence or absence of symptoms, and electrocardiographic (ECG) findings. These measures include stabilizing the cardiac membrane, decreasing extracellular potassium level, and reducing bodily potassium stores [9]. (See "Management of hyperkalemia in children".)

After the initial management, further evaluation focuses on determining the etiology as subsequent care is based on the underlying cause of hyperkalemia. The assessment includes a focused history and physical examination and, if needed, laboratory testing. (See 'Causes' above.)

History and physical examination — The history and physical examination often clearly point to the underlying etiology, and there is little need for further extensive diagnostic evaluation.

Historical clues — Historical clues may be indicative of a specific etiology:

History of chemotherapy in a child with a large tumor load is indicative of tumor lysis syndrome

History of an unusually large intake of potassium due to intravenous (IV) fluids, parenteral nutrition, medications (eg, potassium penicillin), or massive transfusion

Known kidney disease

Decreased urine output may be suggestive of kidney disease or reduced effective arterial perfusion

History of massive trauma, excessive exercise, and/or muscular cramp (which also can be a finding of hyperkalemia) is suggestive of rhabdomyolysis

History of significant hemolysis

Physical findings — The following physical findings are suggestive of an underlying etiology for hyperkalemia:

Hypertension and edema may be indicative of kidney disease

Decreased peripheral pulses, low blood pressure, tachycardia, and delayed capillary refill are often signs of significant reduced effective arterial perfusion

Muscular tenderness may be seen in patients with rhabdomyolysis

Further laboratory testing — As noted above, an elevated potassium value should be confirmed prior to any further extensive testing in asymptomatic patients in whom there is a high index of suspicion for pseudohyperkalemia. (See 'Pseudohyperkalemia' above.)

In some children, the cause of a persistently high potassium level is not evident and further laboratory testing is performed as follows (table 5):

Serum blood urea nitrogen and creatinine to assess kidney function.

Urinalysis to detect kidney disease.

Complete blood count, platelets, and serum lactic dehydrogenase to assess for blood dyscrasia or hemolysis.

If rhabdomyolysis is suspected, serum creatine kinase to detect muscle injury and, if present, its severity.

Blood electrolytes to detect other electrolyte abnormalities such as metabolic acidosis.

Serum aldosterone and plasma renin activity in patients in whom there is clinical suspicion for underlying endocrinopathy (eg, adrenal hyperplasia). (See "Causes of primary adrenal insufficiency in children", section on 'Congenital adrenal hyperplasia'.)

Urine chemistries should be obtained in patients at the same time or shortly after the measurement of blood studies to assess renal tubular function regarding sodium reabsorption and urinary potassium excretion.

Urine potassium levels – In most children, hyperkalemia should result in a random urinary potassium level that exceeds 20 mEq/L and often exceeds 40 mEq/L. Very high random urinary potassium values (>80 to 100 mEq/L) are very suggestive that hyperkalemia is due to excessive potassium intake or cellular release and not due to an abnormality in urinary potassium excretion.

Urine sodium levels – Low random urinary sodium values (<20 mEq/L) demonstrate that there is avid renal sodium absorption, which may limit the amount of sodium available for potassium exchange at the distal renal tubule. Optimizing the effective volume and providing more sodium to the child will increase distal tubular sodium delivery thereby improving potassium excretion.

Transtubular potassium gradient (TTKG) – Although the TTKG had been used to distinguish hypoaldosteronism from other causes of hyperkalemia, on further evaluation, the assumptions underlying the use of this tool were found not to be valid. As a result, TTKG should not be used to evaluate patients with hyperkalemia. (See "Causes and evaluation of hyperkalemia in adults", section on 'Transtubular potassium gradient'.)

SUMMARY AND RECOMMENDATIONS

Pathophysiology and causes – Pediatric hyperkalemia is caused by derangements of the normal homeostatic mechanisms that regulate potassium balance, which are the same as those that occur in adults (table 2). (See 'Pathophysiology' above.)

Large increase in potassium intake is an uncommon cause of sustained hyperkalemia in healthy children. This may occur infrequently due to a large infusion of potassium through intravenous (IV) solutions (including parenteral nutrition), potassium-containing medications, or massive transfusion. (See 'Increased potassium intake' above.)

Transcellular movement of intracellular potassium into the extracellular space can cause pediatric hyperkalemia due to either cellular injury (eg, rhabdomyolysis, tumor lysis syndrome, or severe hemolysis) or significant shift of potassium seen in patients with metabolic acidosis, diabetic ketoacidosis, or hyperkalemic periodic paralysis. (See 'Transcellular movement of potassium' above.)

Decreased renal excretion of potassium is the most common cause of persistent hyperkalemia. Etiologies include kidney disease, decreased effective arterial circulation, or decreased activity or sensitivity to the renin-aldosterone system. (See 'Abnormalities in renal excretion' above.)

Pseudohyperkalemia is common in children because hemolyzed specimens are often observed due to difficulties in obtaining blood samples, especially in infants and small children. As a result, an elevated potassium level should be confirmed in any child in whom the clinical setting makes hyperkalemia unlikely. (See 'Pseudohyperkalemia' above and 'Diagnosis' above.)

Clinical manifestations

Most children with hyperkalemia are asymptomatic as they have mild (serum or plasma potassium <6 mEq/L [6 mmol/L]) or moderate elevations of serum or plasma potassium (potassium between 6 to 7 mEq/L [6 to 7 mmol/L]). In these patients, hyperkalemia is typically detected when plasma or serum electrolytes are obtained because electrolyte abnormalities are suspected (eg, kidney disease).

Clinical manifestations in children with severe hyperkalemia (potassium level >7 mEq/L [7 mmol/L]) include muscle weakness or paralysis, as well as palpitations and syncope due to cardiac conduction abnormalities. (See 'Clinical manifestations' above.)

Hyperkalemia is associated with significant and potentially life-threatening disturbances in cardiac conduction. Electrocardiographic changes (ECG) reflect the impact of increasing levels of serum and plasma potassium on the electrical activity of the heart including aberrant atrial (P wave) and ventricular (QRS complex) depolarization and abnormal repolarization (T wave) (waveform 1 and waveform 2). (See 'Cardiac conduction abnormalities' above.)

Diagnosis – The diagnosis of hyperkalemia is made by the detection of an elevated plasma or serum potassium level. In infants, the normal range of potassium is greater than that of older children and adults because of their relatively lower urinary potassium excretion (table 1). (See 'Diagnosis' above.)

Differential diagnosis

In asymptomatic patients, the primary differential diagnosis is pseudohyperkalemia, which is differentiated from true hyperkalemia by a normal repeat potassium level that should be obtained from a free-flowing venous blood sample to reduce the risk of hemolysis. (See 'Diagnosis' above and 'Differential diagnosis' above.)

In symptomatic patients, an elevated potassium level and potassium-associated ECG changes differentiate hyperkalemia from conditions that may also present with muscle weakness and paralysis, or syncope and palpitations (table 3 and table 4). For patients with syncope or palpitations, rapid assessment is imperative as these symptoms may be due to a life-threatening disorder (including severe hyperkalemia) (algorithm 1 and algorithm 2). (See 'Differential diagnosis' above and "Approach to the child with palpitations" and "Emergency evaluation of syncope in children and adolescents".)

Evaluation for cause – After acute management of potentially life-threatening or serious hyperkalemia, further evaluation focuses on determining the etiology as subsequent care is based on the underlying cause of hyperkalemia. The assessment includes a focused history and physical examination and, if needed, laboratory testing (table 5). (See 'Evaluation to determine underlying etiology' above and "Management of hyperkalemia in children".)

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  3. Tseng MH, Huang JL, Huang SM, et al. Clinical features, genetic background, and outcome in infants with urinary tract infection and type IV renal tubular acidosis. Pediatr Res 2020; 87:1251.
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  9. Masilamani K, van der Voort J. The management of acute hyperkalaemia in neonates and children. Arch Dis Child 2012; 97:376.
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