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Official reprint from UpToDate www.uptodate.com ©2016 UpToDate

Hypokalemia in children

Authors: Michael J Somers, MD, Avram Z Traum, MDSection Editor: Tej K Mattoo, MD, DCH, FRCPDeputy Editor: Melanie S Kim, MD

All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: Sep 2016. | This topic last updated: Aug 22, 2016.

INTRODUCTION — Hypokalemia is defined as a serum or plasma potassium that is less than the normal value.Most reference laboratories establish the lower pediatric limit of normal serum potassium between 3 and 3.5mEq/L. However, symptoms are unlikely to occur in most healthy children until serum potassium is below 3mEq/L.

The etiology, clinical findings, diagnosis, evaluation, and management of pediatric hypokalemia are reviewedhere. Hypokalemia in adults is discussed separately. (See "Clinical manifestations and treatment of hypokalemiain adults" and "Causes of hypokalemia in adults" and "Evaluation of the adult patient with hypokalemia".)

EPIDEMIOLOGY — Hypokalemia is relatively common among hospitalized pediatric patients, especially thosewho are critically ill [1­3]. In one study of 667 children cared for in a single­center pediatric intensive care unit inthe United States during the calendar year 2006, 40 percent of the patients had a serum potassium level below3.5 mEq/L [1]. This included patients with severe hypokalemia, defined as potassium level less than 2.5 mEq/L (4percent); moderate hypokalemia, defined as potassium level 2.5 to less than 3 mEq/L (12 percent); and mildhypokalemia, defined as potassium level from 3 to less than 3.5 mEq/L (24 percent). Hypokalemia wasassociated with diagnoses of cardiac disease, renal failure, or shock [1].

In developing countries, severe hypokalemia (potassium level <2.5 mEq/L) is often observed in children withdiarrhea and severe acute malnutrition, and is associated with an increased risk of mortality [4].

POTASSIUM BALANCE AND LEVELS

Definition — Potassium is primarily an intracellular cation with cells containing approximately 98 percent of totalbody potassium. Hypokalemia is defined as serum level below the normal value, which is usually defined as 3.5mEq/L.

Homeostatic mechanisms — Homeostatic mechanisms regulate potassium balance in order to maintain highintracellular levels required for cellular functions (metabolism and growth), and low extracellular concentration topreserve the steep concentration gradient across the cell membrane needed for nerve excitation and musclecontraction. In children, positive potassium balance is needed for growth, whereas in adults, homeostasis isdirected towards a zero potassium balance.

After a bolus of potassium intake, normal physiologic processes preserve the intra­ and extracellular balance viaintracellular potassium movement, which is regulated by cell membrane Na­K­ATPase (mediated by insulin, andalpha­ and beta­2 adrenergic agonists), and urinary potassium excretion (primarily mediated by aldosterone).Although normal serum and plasma potassium concentrations in children and adolescents are similar to levels inadults, infants have a higher normal range of potassium because of their reduced urinary potassium excretion,which is caused by their relatively increased aldosterone insensitivity and decreased glomerular filtration rate

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(GFR) (table 1). (See "Causes and evaluation of hyperkalemia in adults", section on 'Brief review of potassiumphysiology'.)

Pathogenesis of hypokalemia — Hypokalemia in children is caused by derangements of the hemostaticmechanisms 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 withhypokalemia.

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

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

Decreased intake — Decreased intake alone is unlikely to cause hypokalemia in healthy children. However,prolonged decreased intake (eg, malnutrition or anorexia) in combination with increased potassium losses via thekidney or gastrointestinal tract can lead to significant potassium depletion.

Increased intracellular uptake — As noted above, the normal distribution of potassium between cells and theextracellular fluid is primarily maintained by the Na­K­ATPase pump in the cell membrane. Increased activity ofthe Na­K­ATPase pump and/or alterations in other potassium transport pathways can result in transienthypokalemia due to increased potassium entry into cells from the extracellular space.

Alkalosis — Either respiratory or metabolic alkalosis can be associated with hypokalemia. In this setting,intracellular potassium movement is promoted to maintain electroneutrality as hydrogen ions exit the cell inresponse to the increase in extracellular pH. In general, serum potassium concentration falls by less than 0.4mEq/L for every 0.1 unit rise in pH.

In children with metabolic alkalosis, there is also an increased loss of urinary potassium. This is due to a rise inplasma bicarbonate concentration, resulting in a filtered bicarbonate load above its reabsorptive threshold, whichleads to increased distal delivery of sodium bicarbonate. At the distal tubule, sodium is exchanged for potassium,causing the increased loss in urinary potassium. (See 'Increased distal delivery of sodium and water' below.)

Increased insulin activity — Insulin promotes intracellular potassium movement by increasing the activity ofthe Na­K­ATPase pump, and is used therapeutically to treat severe hyperkalemia [5]. In particular, insulinadministration in children with diabetic ketoacidosis results in a fall in serum potassium due to the increasedinsulin­mediated intracellular movement of potassium. One small study also reported that insulin increased renalpotassium excretion [6]. (See "Treatment and complications of diabetic ketoacidosis in children", section on'Serum potassium'.)

Hypokalemia due to insulin­mediated potassium transcellular movement can also be seen in the refeedingsyndrome after prolonged starvation, or in children and adolescents with eating disorders [7]. (See "Anorexianervosa in adults and adolescents: The refeeding syndrome", section on 'Pathogenesis and clinical features' and"Failure to thrive (undernutrition) in children younger than two years: Management", section on 'Nutritionalrecovery syndrome (refeeding syndrome)'.)

Elevated beta­adrenergic activity — Nonselective (eg, isoproterenol and epinephrine) and selective (eg,albuterol and terbutaline) beta­adrenergic agents promote intracellular movement of potassium by increasing Na­K­ATPase pump activity. The use of these agents in children can decrease serum potassium levels, and in some

Decreased potassium intakeIncreased intracellular movement of potassiumExcessive loss of potassium via the gastrointestinal tract, kidney, or skin

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cases, result in hypokalemia [8,9]. (See "Acute asthma exacerbations in children: Inpatient management", sectionon 'Laboratory'.)

Hypokalemic periodic paralysis — Hypokalemic periodic paralysis is a rare neuromuscular condition thatpresents with sudden episodes of severe muscle weakness associated with hypokalemia. In these patients, thepotassium level can drop rapidly to below 2 mEq/L. Symptoms may be triggered by events associated withincreased adrenergic tone, such as exercise, stress, and high­carbohydrate meals.

Hypokalemic periodic paralysis is due to defects in muscle calcium and sodium channels. Most cases arehereditary and are primarily associated with a mutation in the gene that codes for the alpha­1 subunit of thedihydropyridine­sensitive calcium channel in skeletal muscle. These patients typically present in late childhood oradolescence. Acquired cases have been reported in patients with hyperthyroidism (referred to as thyrotoxicperiodic paralysis), and typically present in older patients between 20 and 30 years of age. (See "Hypokalemicperiodic paralysis" and "Thyrotoxic periodic paralysis".)

Other drugs (besides beta­adrenergic agonists)

Gastrointestinal losses — Gastrointestinal (GI) losses are the most common cause of hypokalemia in children.In particular, diarrheal potassium content (20 to 50 mEq/L) is relatively high compared with other body fluids [17].In developing countries, acute diarrhea with hypokalemia is associated with an increased risk of death [4,18].(See "Approach to the child with acute diarrhea in resource­limited countries", section on 'Fluid and electrolytes'.)

In contrast, upper GI losses (eg, vomiting, nasogastric drainage) are initially minimal as the potassium content isrelatively low (5 to 10 mEq/L). However, the loss of gastric secretions results in metabolic alkalosis that leads toincreased urinary potassium losses. As noted above, metabolic alkalosis leads to increased distal delivery ofsodium bicarbonate, which in combination with hypovolemia­induced hyperaldosteronism results in enhancedpotassium excretion as potassium is exchanged for sodium. (See 'Increased distal delivery of sodium and water'below.)

Increased urinary losses — Urinary potassium excretion is primarily due to secretion of potassium in the distalnephron by the principal cells in the connecting tubule and cortical collecting tubule. In the distal tubule, sodium isreabsorbed under the influence of mineralocorticoids (primarily aldosterone) and potassium is exchanged topreserve electroneutrality. Increased urinary potassium loss contributing to hypokalemia is typically due to one orboth of the following mechanisms:

Heavy metals: Barium toxicity is a rare cause of hypokalemia, caused by blockade of potassium channelslimiting their efflux from cells. Barium salts are found in fireworks and rodent toxins [10,11]. Barium sulfate isthe formulation used in radiographic procedures and is not absorbed from the gut. Cesium has beenreported as a rare cause of hypokalemia in adults due to its use as an alternative therapy for cancer, but hasnot been reported in children [12].

Antipsychotic drugs: Hypokalemia has been reported in association with the use of risperidone andquetiapine in adults. Given the increasing use of this medication in children and adolescents, a high index ofsuspicion should be present in children with hypokalemia or cardiac arrhythmias who are prescribed thesemedications. (See "Causes of hypokalemia in adults", section on 'Antipsychotic drugs'.)

Chloroquine intoxication due to intracellular movement of potassium is an uncommon cause of severehypokalemia in children [13­16].

Increased delivery of sodium and water to the distal nephronIncreased mineralocorticoid activity

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Increased distal delivery of sodium and water — In children, the following conditions are associated withurinary potassium losses leading to lower serum potassium as a result of increased distal delivery of sodium.

Diuretics — Diuretic therapy (loop and thiazide diuretics) impairs sodium reabsorption in more proximalnephron segments leading to distal delivery of sodium. In addition, volume depletion leads to increasedaldosterone activity.

Nonreabsorbable ions — Nonreabsorbable anions are accompanied by sodium, resulting in distaldelivery of sodium, which is exchanged with potassium. Pediatric settings, in which the presence ofnonreabsorbable anions results in increased distal delivery of sodium, include excess filtered bicarbonate inpatients with excessive vomiting or with proximal (type 2) renal tubular acidosis (RTA), beta­hydroxybutyrate inpatients with diabetic ketoacidosis, and hippurate following toluene abuse (glue­sniffing). (See 'Gastrointestinallosses' above and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features,evaluation, and diagnosis", section on 'Serum potassium' and "Inhalant abuse in children and adolescents",section on 'Hypokalemia'.)

Osmotic diuresis — Osmotic diuresis can also result in increased distal delivery of sodium, resulting inhypokalemia. This is most commonly seen in children with diabetic ketoacidosis who have glucose osmoticdiuresis due to glycosuria, because the filtered glucose load exceeds the proximal tubular reabsorptive capacity.Administration of mannitol is a less frequent cause of hypokalemia due to osmotic diuresis. Hypovolemia mayalso result from osmotic diuresis if there is inadequate fluid replacement, which leads to increased aldosteroneactivity and enhanced distal potassium secretion. (See 'Increased mineralocorticoid activity' below.)

Genetic tubular disorders — Bartter and Gitelman syndromes are autosomal recessive diseases that arecaused by mutations in genes encoding tubular transport proteins involved in sodium reabsorption. In thesepatients, sodium absorption is disrupted leading to increased distal delivery of sodium, resulting in metabolicalkalosis and hypokalemia, similarly to findings seen in patients who receive chronic diuretic therapy. In addition,the volume depletion leads to increased levels of renin and aldosterone, which further enhances urinarypotassium losses. (See "Bartter and Gitelman syndromes".)

Tubular injury — Tubular injury due to tubulointerstitial diseases or cisplatin results in decreased sodiumreabsorption in more proximal nephron segments, leading to distal delivery of sodium, where potassium isexchanged for sodium. In one small case series of pediatric patients, tubulopathy due to cisplatin, which resultedin reduced potassium, persisted for months to years following completion of chemotherapy [19]. (See "Cisplatinnephrotoxicity", section on 'Salt wasting'.)

Distal (type 1) renal tubular acidosis (RTA) — In distal (type 1) RTA, increased urinary potassium loss isdue to enhanced potassium secretion needed to maintain electroneutrality because of the impaired distalacidification (ie, defective secretion of protons) (table 3). In addition, tubular cellular membrane permeability isalso increased, leading to potassium loss into the lumen along with protons. In contrast with proximal (type 2)RTA, as noted above, urinary potassium loss is due to increased distal delivery of sodium bicarbonate due to the

Diuretic therapyNonreabsorbable anions (eg, mannitol or bicarbonate)Osmotic diuresisGenetic tubular disorders (ie, Bartter and Gitelman syndromes)Tubular injury due to interstitial nephritis or cisplatinProlonged administration (several days) or a large amount of intravenous (IV) fluid with no potassiumsupplementation

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reduced proximal tubule's absorptive capacity for bicarbonate. (See "Etiology and clinical manifestations of renaltubular acidosis in infants and children" and 'Increased distal delivery of sodium and water' above.)

Increased mineralocorticoid activity — Increased mineralocorticoid activity enhances potassium urinaryexcretion.

Hypovolemia — In children, the most common cause of increased mineralocorticoid activity is due tosecretion of aldosterone (hyperaldosteronism) due to volume depletion.

Other etiologies — Other pediatric causes of increased mineralocorticoid activity are rare and include:

Other causes of urinary loss

Amphotericin B nephrotoxicity — Amphotericin B causes hypokalemia by disrupting cellular membranesand increasing membrane permeability. Potassium flows down its concentration gradient out of tubular epithelialcells into the lumen. A large study in adults comparing conventional amphotericin with the liposomal form found asignificant reduction in hypokalemia from 11.6 to 6.7 percent [20]. A review of children outside of the neonatalperiod receiving amphotericin found hypokalemia to be present in 47 percent of those measured, but none ofthose receiving liposomal amphotericin [21]. (See "Amphotericin B nephrotoxicity".)

Liddle syndrome — Liddle syndrome is caused by an autosomal dominant, gain­of­function mutation insubunits of the epithelial sodium channel (ENaC) that presents in childhood as hereditary hypokalemic metabolicalkalosis and hypertension. This genetic disorder has similar findings to apparent mineralocorticoid excess. (See"Genetic disorders of the collecting tubule sodium channel: Liddle's syndrome and pseudohypoaldosteronismtype 1".)

Aldosterone­secreting adenomas. (See "Clinical presentation and evaluation of adrenocortical tumors",section on 'Adrenocortical adenomas'.)

Glucocorticoid remediable aldosteronism (GRA) is an autosomal dominant disorder due to a fusion of thepromoter of the gene encoding aldosterone synthase in the adrenal zona fasciculata (involved in cortisolsynthesis) with the coding region of the related gene in the zona glomerulosa (involved in aldosteronesynthesis). This mutation increases the production of aldosterone, which can be suppressed byglucocorticoid administration. GRA typically presents with hypertension before 21 years of age. Thepotassium level is normal in the majority of patients, and if hypokalemia is present, it is usually mild. (See"Familial hyperaldosteronism", section on 'Familial hyperaldosteronism type I (FH type I) or glucocorticoid­remediable aldosteronism (GRA)'.)

Apparent mineralocorticoid excess (AME) is an autosomal recessive disorder due to mutations of the genethat encodes 11­beta­hydroxysteroid dehydrogenase type 2 isoform, which normally breaks down cortisol tocortisone. This genetic defect results in increased levels of renal cortisol, which binds to the mineralocorticoidreceptor. AME typically presents in infancy or early childhood with severe hypertension, failure to thrive, andmuscle weakness due to hypokalemia. Chronic ingestion of licorice containing glycyrrhetinic acid has asimilar effect. (See "Apparent mineralocorticoid excess syndromes (including chronic licorice ingestion)".)

Although the most common form of congenital adrenal hyperplasia (21­hydroxylase deficiency) leads todecreased aldosterone synthesis and hyperkalemia, other rarer forms of congenital adrenal hyperplasia areassociated with increased mineralocorticoid synthesis and hypokalemia. These include 17­alpha­hydroxylasedeficiency, which presents with hypertension, hypokalemia, and hypogonadism at puberty, and 11­beta­hydroxylase deficiency, which presents in neonates with virilization, hypertension, and hypokalemia. (See"Uncommon congenital adrenal hyperplasias", section on 'CYP17A1 deficiencies' and "Uncommoncongenital adrenal hyperplasias", section on '11­beta­hydroxylase deficiency'.)

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Cystic fibrosis and skin losses — Electrolyte abnormalities including hypokalemia have been reported inpatients with cystic fibrosis [22]. These findings typically occur in young children less than 2.5 years of age withvolume depletion, and often prior to making the diagnosis of cystic fibrosis.

CLINICAL MANIFESTATIONS — Clinical manifestations vary depending on the severity and acuity ofhypokalemia. Symptoms generally do not become manifest until the serum potassium is below 3 mEq/L unlessthere is a rapid significant fall in serum potassium.

Clinical findings include:

Neuromuscular and cardiac symptoms induced by hypokalemia are related to alterations in the generation of theaction potential, which is dependent on the transcellular potassium gradient. (See "Clinical manifestations andtreatment of hypokalemia in adults", section on 'Pathogenesis of symptoms'.)

Muscular weakness — Hypokalemia can induce skeletal muscle weakness and, in some severe cases,paralysis. Patients are generally asymptomatic until the potassium drops below 2.5 mEq/L or at higher levels ifthere is a sudden precipitous drop in potassium. Muscle weakness typically starts in the proximal muscles of thelower extremities and progresses upwards to the trunk and upper extremities. As the potassium drops below 2mEq/L, severe weakness progresses, involving respiratory muscles, which may result in respiratory failure anddeath.

Hypokalemia can also induce smooth muscle weakness, which is manifested as ileus [23]. Affected patients maycomplain of abdominal distension, anorexia, nausea, vomiting, and/or constipation.

In addition to causing muscle weakness, severe potassium depletion (serum potassium less than 2.5 mEq/L) canlead to muscle cramps and/or fasciculations, rhabdomyolysis, and myoglobinuria. A potential diagnostic problemis that the release of potassium from the cells with rhabdomyolysis can mask the severity of the underlyinghypokalemia with misleading values of normal or high serum/plasma values. (See "Causes of rhabdomyolysis"and "Causes of rhabdomyolysis", section on 'Electrolyte disorders'.)

Cardiac findings — Hypokalemia may adversely affect the cardiac conduction, resulting in arrhythmias includingpremature atrial and ventricular beats, sinus bradycardia, paroxysmal atrial or junctional tachycardia,atrioventricular block, and ventricular tachycardia or fibrillation. Hypokalemia is also associated with characteristicECG changes including PR prolongation, flattening of T waves, and ST depression. With more profoundhypokalemia, U waves can emerge after the T waves, as best seen in the precordial leads [23,24]. (See "Clinicalmanifestations and treatment of hypokalemia in adults", section on 'Cardiac arrhythmias and ECG abnormalities'.)

Renal manifestations — Prolonged hypokalemia can cause renal dysfunction, particularly impairedconcentrating ability that presents as polyuria and/or polydipsia. (See "Hypokalemia­induced renal dysfunction".)

DIAGNOSIS — The diagnosis of hypokalemia is made by the detection of a plasma or serum potassium level thatis below the normal range, usually 3.5 mEq/L. In infants, the normal range of potassium is greater than in olderchildren and adults because of their reduced urinary potassium excretion (table 1). In many instances, thediagnosis is made incidentally when plasma or serum electrolytes are obtained during an evaluation for anothercondition, especially in children with levels between 3 and 3.5 mEq/L, whereas levels below 3 mEq/L are moreoften associated with clinical signs and symptoms.

Muscle weakness and paralysisCardiac arrhythmias and electrocardiogram (ECG) changesImpaired urinary concentrating ability and other renal abnormalities

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It is important to note that potassium levels may vary by measurement technique. Normal values are typicallybased on measurements from the central hospital automated blood biochemistry autoanalyzers. In one study inchildren, potassium levels were lower by a mean difference of 0.4 mEq/L when measured by blood gas analyzerscompared with values obtained from the central laboratory [25]. However, in another study that evaluatedsamples from adult patients, there was no difference in levels between the two techniques [26]. These differingresults may be due to the use of different blood gas analyzers. Clinicians should be aware of these differences intheir own institutions before interpreting potassium measurements based on blood gas results.

Of note, serum or plasma potassium is not reflective of total potassium stores, as 98 percent of potassium isintracellular. Settings in which there is a transcellular movement of potassium into the cell can lead to the falseassumption of total body potassium depletion. This may lead to unnecessary potassium repletion rather thancorrecting the underlying cause of increased intracellular potassium uptake (eg, alkalosis or administration ofinsulin). Conversely, a normal or elevated potassium level in a setting of potassium movement out of the cell (eg,diabetic ketoacidosis) may mask true total body potassium depletion.

DIFFERENTIAL DIAGNOSIS — In symptomatic patients, diseases associated with muscle weakness andparalysis are differentiated from hypokalemia by the finding of an abnormally low potassium level. These includemyositis due to either bacterial or viral infection, conversion disorder, and Guillain­Barré syndrome. (See"Etiology and evaluation of the child with weakness".)

EVALUATION TO DETERMINE UNDERLYING ETIOLOGY — Because severe hypokalemia is a potentially life­threatening condition, initial management takes precedence over any diagnostic evaluation. The urgency andtype of intervention are based on the magnitude of the potassium deficit and presence of symptoms.

History — The history often clearly points to the underlying etiology, and there is little need for further extensivediagnostic evaluation.

Historical clues include the following:

Physical examination — Once hypokalemia has been discerned, the initial physical assessment should includethe following:

Acute gastrointestinal (GI) illness with diarrhea or vomiting is the most common cause of hypokalemia inotherwise healthy children.

Decreased dietary potassium intake is typically not the main cause of hypokalemia, but may be anexacerbating factor, particularly in children with acute GI illness and potassium loss. (See 'Decreased intake'above.)

The use of medications that may promote intracellular potassium uptake (adrenergic agents [albuterol] orexogenous insulin), or increase renal potassium excretion (eg, diuretics). (See 'Causes' above.)

A positive family history of periodic paralysis or muscle weakness is suggestive of a genetic form of periodicparalysis. (See "Hypokalemic periodic paralysis".)

A diagnosis of thyrotoxic periodic paralysis should be considered in any patient with concomitant orpreceding symptoms of hyperthyroidism (weight loss, heat intolerance, tremor, palpitations, anxiety,increased frequency of bowel movements, and shortness of breath). (See "Thyrotoxic periodic paralysis".)

History of recurrent hypokalemia is suggestive of an underlying chronic pathologic condition, which warrantsfurther evaluation.

Cardiac rate and rhythm by auscultation to screen for arrhythmias.

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Laboratory studies — In symptomatic cases or if there is any concern for a cardiac arrhythmia, anelectrocardiogram (ECG) should be performed, and treatment should be immediately started to address anyclinically significant findings.

In the child with relatively mild hypokalemia with a history of present illness that suggests a clear etiology such asviral GI illness or diuretic therapy, there is little utility to an extensive laboratory evaluation.

In the case of a less clear­cut origin of hypokalemia, laboratory evaluation initially focuses on assessing whetheror not there is excessive renal potassium loss (table 4 and algorithm 1).

Urinary potassium excretion — The most common pediatric cause of increased urinary potassium excretionis hypovolemia, which results in increased mineralocorticoid activity due to secretion of aldosterone(hyperaldosteronism). In these children, hypokalemia and increased urinary potassium renal excretion resolvewith fluid and potassium repletion. (See "Treatment of hypovolemia (dehydration) in children".)

Other causes of excessive renal potassium losses are less common and are also less likely to have rapidimprovement to a normal potassium level with replacement therapy. In addition, unless the underlying etiology isaddressed (eg, chronic diuretic therapy or renal tubular acidosis [RTA]), potassium levels will usually fall again,once supplementation is withdrawn. (See 'Increased urinary losses' above and "Clinical manifestations andtreatment of hypokalemia in adults", section on 'Ongoing losses and the steady state'.)

Urinary potassium excretion is assessed using spot urine samples obtained concomitantly with serum chemistries(table 4). Although 24­hour urine collections will give the most accurate picture of renal potassium handling, theseare difficult to perform in many children and delay establishment of a diagnosis.

Further evaluation — For those children with hypokalemia and excessive urinary potassium excretion withoutan apparent etiology, further evaluation is warranted and is based on the presence or absence of an elevatedblood pressure (algorithm 1).

Muscle strength and tone.

Reflexes.

Evaluation of the effective circulating volume and respiratory status. These factors influence initialmanagement strategies and can prove useful in clarifying acid­base and volume balance in children withunclear origin of their hypokalemia.

Random urinary potassium levels <15 to 20 mmol/L should be seen in the setting of serum potassium levels<3 mmol/L. Substantially higher levels suggest excessive renal potassium losses.

Random levels are on occasion misleading, since spot values are influenced by water excretion at that time.In states of polyuria, spot urinary potassium levels may be lower than if urine output were normal. In states ofdecreased urine flow, random levels may appear >20 mmol/L even though overall daily potassium excretionis being appropriately conserved.

Spot potassium­to­creatinine ratios correct for any variations in urine volume in patients with stableglomerular filtration rate. A urine potassium­to­creatinine ratio should be <15 mEq/g creatinine (<1.5mEq/mmol creatinine) when hypokalemia is due to GI losses, poor intake, cellular shift, or diuretic use.Ratios >15 mEq/g creatinine in the setting of a low serum potassium suggest pathologic urinary losses eitherdue to increased mineralocorticoid activity or tubular dysfunction. (See "Evaluation of the adult patient withhypokalemia", section on 'Urine potassium­to­creatinine ratio'.)

For hypertensive patients, plasma renin and aldosterone are obtained.

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MANAGEMENT

Overview — The acuity and degree of the hypokalemia influence the clinical approach to therapy. The goals oftherapy are to prevent or treat life­threatening complications (arrhythmias, paralysis, rhabdomyolysis, anddiaphragmatic weakness) associated with severe hypokalemia, replace the potassium deficit, and correct theunderlying cause. The urgency of therapy depends upon the severity of hypokalemia, and the rate of decline inserum potassium concentration. Lower grade hypokalemia (serum/plasma potassium between 2.5 and 3 mEq/L)or chronic hypokalemia at lower levels tend to be better tolerated by the patient and are less likely to requireurgent interventions.

The management of pediatric hypokalemia includes:

Low renin and high aldosterone levels are suggestive of primary hyperaldosteronism (adrenalabnormalities). Metabolic alkalosis is also observed in these patients.

•

Low renin and low aldosterone are suggestive of one of the following:•

Increased activity of another mineralocorticoid that is not aldosterone (eg, apparentmineralocorticoid excess and some forms of congenital adrenal hyperplasia) (see 'Other etiologies'above)

­

Liddle syndrome due to enhanced sodium tubular resorption (see 'Liddle syndrome' above and"Genetic disorders of the collecting tubule sodium channel: Liddle's syndrome andpseudohypoaldosteronism type 1")

­

For normotensive patients, evaluation focuses on the acid­base status of the patient as determined byvenous pH and serum electrolytes (table 5).

For patients with metabolic acidosis, diagnostic possibilities include types I and II RTA and diabeticketoacidosis.

•

For patients with metabolic alkalosis, diagnostic possibilities include chronic diuretic use, persistentvomiting, and the genetic tubulopathies of Bartter and Gitelman syndromes. Measurement of urinarychloride concentration may be helpful in differentiating among these disorders.

•

Urinary chloride concentration is normal in Bartter or Gitelman syndromes (see "Bartter andGitelman syndromes")

­

Urinary chloride concentration is low in patients with vomiting.­

Urinary chloride concentration is variable with diuretic therapy depending on whether tubularfunction is still responsive to diuretic activity.

­

In patients who have no underlying acid­base disorders, diagnostic possibilities include magnesiumdepletion or osmotic diuresis. (See "Clinical manifestations of magnesium depletion", section on'Hypokalemia'.)

•

Although genetic testing can be performed for the rare genetic potassium­wasting disorders of Bartter,Gitelman, and Liddle syndromes, other clinical findings that are suggestive of these diagnoses should bepresent prior to genetic testing. These entities are discussed in greater detail separately. (See "Bartter andGitelman syndromes" and "Genetic disorders of the collecting tubule sodium channel: Liddle's syndrome andpseudohypoaldosteronism type 1".)

Ascertaining the need for potassium replacement.

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Potassium supplementation — When the decision is made that potassium supplementation is needed, choicesregarding the route, formulation, and rate of replacement therapy are based on the clinical setting.

Route — Potassium can be administered either enterally or intravenously. Whenever possible, potassiumsupplementation should be given enterally. Data in children cared for in a cardiac intensive care unit have shownthat enteral administration has comparable efficacy and fewer side effects than IV administration [27].

The main concern about the use of IV potassium supplementation is the inadvertent administration of a largeamount of potassium in a short period of time, resulting in hyperkalemia. Safety measures to prevent thiscomplication include limiting the absolute amount of potassium in any single container or bag of fluid, and usingan infusion pump. IV potassium administration is also associated with pain and phlebitis when administeredthrough a peripheral vein, which can be minimized if the potassium content of the infusion is less than 20 mEq/L.Central venous access is needed if the potassium concentration exceeds 40 mEq/L.

Formulation — Potassium supplementation commonly comes in four preparations: potassium chloride,potassium phosphate, potassium citrate, and potassium bicarbonate.

Our approach based on severity — The rapidity of potassium supplementation is dependent on the severityof hypokalemia based on the presence or absence of symptoms.

Identifying and, if possible, treating the underlying cause of hypokalemia (eg, hypomagnesemia).

Use of potassium­sparing diuretic therapy for patients with chronic renal wasting conditions, for which there isno treatment for the underlying disorder (Bartter or Gitelman syndrome).

Electrocardiographic monitoring for symptomatic children and those in whom there is a concern for cardiacarrhythmia.

In patients receiving intravenous (IV) fluid, use of saline solution without dextrose. Dextrose­containingsolution should be avoided since the administration of dextrose stimulates the release of insulin, which drivesextracellular potassium into the cells.

Potassium chloride tends to result in quicker potassium repletion per dose than phosphate or citrate [28] andis the most common pharmacologic supplement. It is also preferred in patients with concomitanthypochloremia or metabolic alkalosis.

Potassium phosphate is often used in the setting of proximal tubule dysfunction, such as Fanconi syndromeor cystinosis, where there is loss of both potassium and phosphorus.

Potassium citrate or bicarbonate is generally used in children with hypokalemia and acidosis, as seen intypes I and II renal tubular acidosis (RTA).

In symptomatic patients (arrhythmias, marked muscle weakness, or paralysis), rapid potassiumsupplementation should be provided. In some cases, this requires IV administration of potassium chloride,particularly in those who are unable to take oral medications. In this setting, an infusion with a potassiumconcentration of no more than 40 mEq/L is given at a rate not to exceed 0.5 to 1 mEq/kg of body weight perhour. The goal is to raise the potassium level by 0.3 to 0.5 mEq/L. These patients require continuouselectrocardiographic (ECG) monitoring to detect changes due to hypokalemia, and also possibly reboundhyperkalemia during replacement therapy. (See 'Clinical manifestations' above and "Causes, diagnosis, andevaluation of hyperkalemia in children", section on 'Cardiac conduction abnormalities'.)

In asymptomatic patients with potassium levels less than 3 mEq/L, replacement of potassium stores isgenerally needed. Oral therapy is preferred and IV supplementation should be reserved for those who are

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Other interventions

Magnesium depletion — Hypomagnesemia may accompany hypokalemia. Magnesium can be lost at thesame time as potassium with gastrointestinal (GI) losses or with diuretic use. Hypomagnesemia can also promoterenal potassium wasting directly in the distal tubule, and can also prevent reabsorption of filtered potassium at theloop of Henle [24]. (See "Clinical manifestations of magnesium depletion", section on 'Hypokalemia'.)

Potassium­sparing diuretics — Potassium supplementation by itself is less effective in tubulopathies suchas Bartter or Gitelman syndromes, where there is ongoing renal wasting of potassium. Use of a potassium­sparing diuretic such as amiloride may attenuate these losses. (See "Bartter and Gitelman syndromes", sectionon 'NSAIDs and drugs that block distal tubule sodium­potassium exchange'.)

Children with hyperaldosteronism may benefit from spironolactone or eplerenone therapy to reduce the urinarypotassium effect of aldosterone. (See "Treatment of primary aldosteronism", section on 'First line:Mineralocorticoid antagonists'.)

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SUMMARY AND RECOMMENDATIONS

unable to take oral medications. The amount of replacement therapy is dependent on the cause of thehypokalemia, presence of any acid­base disorder, and ongoing excessive losses. In particular,supplementation may not be needed in patients whose hypokalemia was caused by cellular uptake (eg, beta­adrenergic agents or exogenous insulin), as correction of the underlying cause results in resolution ofhypokalemia.

In asymptomatic patients with acute hypokalemia and potassium levels between 3 and 3.5 mEq/L, correctionof the underlying cause and dietary potassium are usually sufficient without the need for additional potassiumsupplementation.

In asymptomatic patients with chronic hypokalemia, potassium supplementation may be needed, particularlyif the underlying cause is not amenable to correction (eg, types I and II RTA). (See "Treatment of distal (type1) and proximal (type 2) renal tubular acidosis".)

th th

th th

Basics topic (see "Patient education: Hypokalemia (The Basics)")

Hypokalemia is defined as a serum or plasma potassium level below the normal value, which is usuallydefined as 3.5 mEq/L. Normal serum potassium concentrations in children and adolescents are similar tolevels in adults. However, infants have a higher normal range of potassium because of their reduced urinarypotassium excretion, caused by their relatively increased aldosterone insensitivity and decreased glomerularfiltration rate (table 1).

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Pediatric hypokalemia is caused by derangements of the normal hemostatic mechanisms that regulatepotassium balance, and include the following (table 2):

Decreased dietary potassium intake is unlikely to cause hypokalemia in healthy children. However,prolonged decreased intake can contribute to potassium depletion caused by other disorders.

•

Intracellular potassium uptake results in transient hypokalemia. Increased potassium entry into the cellsis promoted by the following conditions: alkalosis, increased insulin activity (eg, exogenous insulinadministration) and beta­adrenergic activity (eg, albuterol administration), and hypokalemic periodicparalysis. (See 'Increased intracellular uptake' above.)

•

Increased gastrointestinal loss is the most common cause of pediatric hypokalemia.•

Increased urinary losses is usually due to either increased delivery of sodium to the distal nephron inexchange for potassium (eg, diuretic therapy, genetic tubular disorders [Bartter and Gitelmansyndromes], and osmotic diuresis) or increased mineralocorticoid activity (eg, hyperaldosteronism due tohypovolemia). (See 'Increased urinary losses' above.)

•

Clinical manifestations vary depending on the severity and acuity of hypokalemia. Symptoms generally donot become manifest until the serum potassium is below 3 mEq/L unless there is a rapid significant fall inserum potassium. Clinical findings include muscle weakness and paralysis, cardiac arrhythmias andelectrocardiogram (ECG) changes, and polyuria due to impaired urinary concentration. (See 'Clinicalmanifestations' above.)

The diagnosis of hypokalemia is made by the detection of a serum or plasma potassium level that is belowthe normal range of 3.5 mEq/L. In many instances, the diagnosis is made incidentally when serum or plasmaelectrolytes are obtained during an evaluation for another condition, especially in children with levels between3 and 3.5 mEq/L, whereas levels below 3 mEq/L are more often associated with clinical signs and symptoms.(See 'Diagnosis' above.)

After acute management of symptomatic severe hypokalemia, further evaluation focuses on determining theetiology, as subsequent care is based on the underlying cause of hypokalemia. The assessment includes afocused history and physical examination. In most cases, the history is sufficient to determine the underlyingcause. However, additional laboratory testing may be needed in patients in whom the diagnosis remainsuncertain (algorithm 1). (See 'Evaluation to determine underlying etiology' above.)

The acuity and degree of the hypokalemia influence the clinical approach to therapy. The goals of therapyare to prevent or treat life­threatening complications (arrhythmias, paralysis, rhabdomyolysis, anddiaphragmatic weakness) associated with severe hypokalemia, replace the potassium deficit, and correct theunderlying cause. (See 'Management' above.)

For symptomatic patients with hypokalemia (arrhythmias, marked muscle weakness, or paralysis), werecommend that potassium supplementation be administered (Grade 1B). In some cases, this requiresintravenous (IV) administration of potassium chloride, particularly in those who are unable to take oralmedications. In this setting, an infusion with a potassium concentration of no more than 40 mEq/L is given ata rate not to exceed 0.5 to 1 mEq/kg of body weight per hour. The goal is to raise the potassium level by 0.3to 0.5 mEq/L. These patients require continuous ECG monitoring to detect changes due to hypokalemia, andalso possibly rebound hyperkalemia during replacement therapy. (See 'Our approach based on severity'above.)

In asymptomatic patients, the need for potassium supplementation is based on the underlying cause and theseverity of hypokalemia. If potassium supplementation is needed, we recommend that oral potassium

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REFERENCES

1. Cummings BM, Macklin EA, Yager PH, et al. Potassium abnormalities in a pediatric intensive care unit:frequency and severity. J Intensive Care Med 2014; 29:269.

2. Singhi S, Marudkar A. Hypokalemia in a pediatric intensive care unit. Indian Pediatr 1996; 33:9.

3. Thomas B. Electrolyte abnormalities in children admitted to pediatric intensive care unit. Indian Pediatr2000; 37:1348.

4. Talbert A, Thuo N, Karisa J, et al. Diarrhoea complicating severe acute malnutrition in Kenyan children: aprospective descriptive study of risk factors and outcome. PLoS One 2012; 7:e38321.

5. Moore RD. Stimulation of Na:H exchange by insulin. Biophys J 1981; 33:203.

6. Carlotti AP, St George­Hyslop C, Bohn D, Halperin ML. Hypokalemia during treatment of diabeticketoacidosis: clinical evidence for an aldosterone­like action of insulin. J Pediatr 2013; 163:207.

7. Fuentebella J, Kerner JA. Refeeding syndrome. Pediatr Clin North Am 2009; 56:1201.

8. Habashy D, Lam LT, Browne GJ. The administration of beta2­agonists for paediatric asthma and its adversereaction in Australian and New Zealand emergency departments: a cross­sectional survey. Eur J EmergMed 2003; 10:219.

9. Krebs SE, Flood RG, Peter JR, Gerard JM. Evaluation of a high­dose continuous albuterol protocol fortreatment of pediatric asthma in the emergency department. Pediatr Emerg Care 2013; 29:191.

10. Deepthiraju B, Varma PR. Barium toxicity a rare presentation of fireworks ingestion. Indian Pediatr 2012;49:762.

11. Glauser J. Cardiac arrhythmias, respiratory failure, and profound hypokalemia in a trauma patient. CleveClin J Med 2001; 68:401, 405.

12. Melnikov P, Zanoni LZ. Clinical effects of cesium intake. Biol Trace Elem Res 2010; 135:1.

13. Yanturali S, Aksay E, Demir OF, Atilla R. Massive hydroxychloroquine overdose. Acta Anaesthesiol Scand2004; 48:379.

14. Marquardt K, Albertson TE. Treatment of hydroxychloroquine overdose. Am J Emerg Med 2001; 19:420.

15. Jordan P, Brookes JG, Nikolic G, Le Couteur DG. Hydroxychloroquine overdose: toxicokinetics andmanagement. J Toxicol Clin Toxicol 1999; 37:861.

16. McKenzie AG. Intensive therapy for chloroquine poisoning. A review of 29 cases. S Afr Med J 1996;86:597.

17. Molla AM, Rahman M, Sarker SA, et al. Stool electrolyte content and purging rates in diarrhea caused byrotavirus, enterotoxigenic E. coli, and V. cholerae in children. J Pediatr 1981; 98:835.

18. Butler T, Islam M, Azad AK, et al. Causes of death in diarrhoeal diseases after rehydration therapy: anautopsy study of 140 patients in Bangladesh. Bull World Health Organ 1987; 65:317.

19. Bianchetti MG, Kanaka C, Ridolfi­Lüthy A, et al. Persisting renotubular sequelae after cisplatin in childrenand adolescents. Am J Nephrol 1991; 11:127.

therapy be given (Grade 1B). The formulation of potassium is also dependent on the underlying condition.(See 'Our approach based on severity' above and 'Formulation' above.)

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20. Walsh TJ, Finberg RW, Arndt C, et al. Liposomal amphotericin B for empirical therapy in patients withpersistent fever and neutropenia. National Institute of Allergy and Infectious Diseases Mycoses StudyGroup. N Engl J Med 1999; 340:764.

21. Dutta A, Palazzi DL. Risk factors of amphotericin B toxicty in the nonneonatal pediatric population. PediatrInfect Dis J 2012; 31:910.

22. Scurati­Manzoni E, Fossali EF, Agostoni C, et al. Electrolyte abnormalities in cystic fibrosis: systematicreview of the literature. Pediatr Nephrol 2014; 29:1015.

23. Linshaw MA. Potassium homeostasis and hypokalemia. Pediatr Clin North Am 1987; 34:649.

24. Schaefer TJ, Wolford RW. Disorders of potassium. Emerg Med Clin North Am 2005; 23:723.

25. Chhapola V, Kanwal SK, Sharma R, Kumar V. A comparative study on reliability of point of care sodium andpotassium estimation in a pediatric intensive care unit. Indian J Pediatr 2013; 80:731.

26. Morimatsu H, Rocktäschel J, Bellomo R, et al. Comparison of point­of­care versus central laboratorymeasurement of electrolyte concentrations on calculations of the anion gap and the strong ion difference.Anesthesiology 2003; 98:1077.

27. Moffett BS, McDade E, Rossano JW, et al. Enteral potassium supplementation in a pediatric cardiacintensive care unit: evaluation of a practice change. Pediatr Crit Care Med 2011; 12:552.

28. Sanguinetti MC, Jurkiewicz NK. Role of external Ca2+ and K+ in gating of cardiac delayed rectifier K+currents. Pflugers Arch 1992; 420:180.

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GRAPHICS

Normal serum potassium levels in children*

Age Range (mEq/L or mmol/L)

Premature infant 4 to 6.5

Newborn 3.7 to 5.9

Infant 4.1 to 5.3

Child >1 year old 3.5 to 5

* Local laboratory reference ranges for normal may vary depending on laboratory and assay technique. Clinical implicationsof variation from normal or reference range levels must be considered individually.

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Pediatric causes of hypokalemia

Gastrointestinal

Increased losses (diarrhea, vomiting, nasogastric drainage)

Decreased intake (anorexia, bulimia)

Increased potassium intracellular uptake

Alkalosis

Increased insulin activity

Beta adrenergic agents (eg, albuterol, epinephrine, dopamine)

Periodic paralysis

Genetic etiology

Hyperthyroidism

Other Drugs

Barium

Antipsychotic drugs

Chloroquine

Increased urinary losses

Increased distal delivery of sodium to distal nephron

Diuretics

Osmotic diuretics (mannitol, hyperglycemia)

Non­reabsorbed anions (elevated serum bicarbonate level)

Tubular injury (Cisplatin)

Types I and II renal tubular acidosis

Increased mineralocorticoid activity

Hyperaldosteronism due to hypovolemia

Glucocorticoid remediable aldosteronism (GRA)

Apparent mineralocorticoid excess (AME)

Rare forms of congenital adrenal hyperplasia (17­alpha­hydroxylase deficiency and 11­beta­hydroxylasedeficiency)

Tubulopathies (Bartter syndrome, Gitelman syndrome)

Amphotericin

Enhanced sodium reabsorption (Liddle syndrome)

Increased skin loss

Cystic fibrosis

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Characteristics of the different types of renal tubular acidosis

Type 1 RTA Type 2 RTA

Hyperkalemic RTA –Type 4 RTA

(hypoaldosteronism)and distal tubulevoltage defects

Primary defect Impaired distalacidification

Reduced proximalbicarbonatereabsorption

Decreased aldosteronesecretion or aldosteroneresistance. Reduced sodiumreabsorption in the distaltubule (voltage defect).

Plasma bicarbonate Variable, may bebelow 10 meq/L

Usually 12 to 20 meq/L Variable (greater than 17meq/L in hypoaldosteronism)

Urine pH Greater than 5.3 Variable, greater than5.3 if the serum HCO3exceeds the tubule'sbicarbonatereabsorptive threshold.Less than 5.3 when theserum HCO3 isreduced to levels thatcan be largelyreabsorbed despitedefective proximaltubule reabsorptivemechanisms.

Variable, greater than 5.3with voltage defects, andusually less than 5.3 withhypoaldosteronism

Plasma potassium Usually reduced buthyperkalemic formsexist; hypokalemialargely corrects withalkali therapy

Reduced, made worseby bicarbonaturiainduced by alkalitherapy

Increased; correcting thehyperkalemia alone willimprove the acidosis byincreasing ammoniumavailability

Urine anion gap Positive Negative Positive

Urine calcium/creatinine ratio Increased Normal Normal

Nephrolithiasis/nephrocalcinosis Yes No No

HCO3: bicarbonate; RTA: renal tubular acidosis.

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Laboratory testing for pediatric hypokalemia of unknown etiology

Blood tests

Chemistries (sodium, potassium, chloride, bicarbonate, magnesium, creatinine)

Venous pH

Plasma renin activity

Plasma aldosterone

Urine tests

Chemistries (sodium, potassium, chloride, calcium, creatinine)

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Diagnostic approach to determine the etiology of pediatric hypokalemia

K: potassium; Cr: creatinine; GI: gastrointestinal; RTA: renal tubular acidosis; DKA: diabetic ketoacidosis; Aldo: aldosterone;AME: apparent mineralocorticoid excess; NG: nasogastric.

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Pediatric causes of concomitant hypokalemia and acid­base disorders based onurinary potassium loss

Low urinary potassiumlosses

High urinary potassiumlosses

Metabolic acidosis Diarrhea Fanconi syndrome

Cystinosis

Types I and II RTA

Ketoacidosis

Metabolic alkalosis Vomiting

Chronic diuretic use

With high blood pressure:

Hyperaldosteronism

With normal blood pressure:

DiureticsVomitingBartter syndromeGitelman syndrome

RTA: renal tubular acidosis.

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Contributor Disclosures

Michael J Somers, MD Nothing to disclose Avram Z Traum, MD Nothing to disclose Tej K Mattoo, MD, DCH,FRCP Nothing to disclose Melanie S Kim, MD Nothing to disclose

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