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Hypokalemia in children
Authors: Michael J Somers, MD, Avram Z Traum, MD
Section Editor: Tej K Mattoo, MD, DCH, FRCP
Deputy 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 3.5
mEq/L. However, symptoms are unlikely to occur in most healthy children until serum potassium is below 3
mEq/L.
The etiology, clinical findings, diagnosis, evaluation, and management of pediatric hypokalemia are reviewed
here. Hypokalemia in adults is discussed separately. (See "Clinical manifestations and treatment of hypokalemia
in 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 those
who are critically ill [13]. In one study of 667 children cared for in a singlecenter pediatric intensive care unit in
the United States during the calendar year 2006, 40 percent of the patients had a serum potassium level below
3.5 mEq/L [1]. This included patients with severe hypokalemia, defined as potassium level less than 2.5 mEq/L (4
percent); moderate hypokalemia, defined as potassium level 2.5 to less than 3 mEq/L (12 percent); and mild
hypokalemia, defined as potassium level from 3 to less than 3.5 mEq/L (24 percent). Hypokalemia was
associated 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 with
diarrhea 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 total
body potassium. Hypokalemia is defined as serum level below the normal value, which is usually defined as 3.5
mEq/L.
Homeostatic mechanisms — Homeostatic mechanisms regulate potassium balance in order to maintain high
intracellular levels required for cellular functions (metabolism and growth), and low extracellular concentration to
preserve the steep concentration gradient across the cell membrane needed for nerve excitation and muscle
contraction. In children, positive potassium balance is needed for growth, whereas in adults, homeostasis is
directed towards a zero potassium balance.
After a bolus of potassium intake, normal physiologic processes preserve the intra and extracellular balance via
intracellular potassium movement, which is regulated by cell membrane NaKATPase (mediated by insulin, and
alpha 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 in
adults, 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
®
®

(GFR) (table 1). (See "Causes and evaluation of hyperkalemia in adults", section on 'Brief review of potassium
physiology'.)
Pathogenesis of hypokalemia — Hypokalemia in children is caused by derangements of the hemostatic
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
hypokalemia.
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 underlying
pathophysiologic 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 the
kidney or gastrointestinal tract can lead to significant potassium depletion.
Increased intracellular uptake — As noted above, the normal distribution of potassium between cells and the
extracellular fluid is primarily maintained by the NaKATPase pump in the cell membrane. Increased activity of
the NaKATPase pump and/or alterations in other potassium transport pathways can result in transient
hypokalemia 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 in
response to the increase in extracellular pH. In general, serum potassium concentration falls by less than 0.4
mEq/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 in
plasma bicarbonate concentration, resulting in a filtered bicarbonate load above its reabsorptive threshold, which
leads 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 of
the NaKATPase pump, and is used therapeutically to treat severe hyperkalemia [5]. In particular, insulin
administration in children with diabetic ketoacidosis results in a fall in serum potassium due to the increased
insulinmediated intracellular movement of potassium. One small study also reported that insulin increased renal
potassium 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 refeeding
syndrome after prolonged starvation, or in children and adolescents with eating disorders [7]. (See "Anorexia
nervosa 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 'Nutritional
recovery 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 Na
KATPase pump activity. The use of these agents in children can decrease serum potassium levels, and in some
Decreased potassium intake●
Increased intracellular movement of potassium●
Excessive loss of potassium via the gastrointestinal tract, kidney, or skin●

cases, result in hypokalemia [8,9]. (See "Acute asthma exacerbations in children: Inpatient management", section
on 'Laboratory'.)
Hypokalemic periodic paralysis — Hypokalemic periodic paralysis is a rare neuromuscular condition that
presents with sudden episodes of severe muscle weakness associated with hypokalemia. In these patients, the
potassium level can drop rapidly to below 2 mEq/L. Symptoms may be triggered by events associated with
increased adrenergic tone, such as exercise, stress, and highcarbohydrate meals.
Hypokalemic periodic paralysis is due to defects in muscle calcium and sodium channels. Most cases are
hereditary and are primarily associated with a mutation in the gene that codes for the alpha1 subunit of the
dihydropyridinesensitive calcium channel in skeletal muscle. These patients typically present in late childhood or
adolescence. Acquired cases have been reported in patients with hyperthyroidism (referred to as thyrotoxic
periodic paralysis), and typically present in older patients between 20 and 30 years of age. (See "Hypokalemic
periodic 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 is
relatively low (5 to 10 mEq/L). However, the loss of gastric secretions results in metabolic alkalosis that leads to
increased urinary potassium losses. As noted above, metabolic alkalosis leads to increased distal delivery of
sodium bicarbonate, which in combination with hypovolemiainduced hyperaldosteronism results in enhanced
potassium 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 distal
nephron by the principal cells in the connecting tubule and cortical collecting tubule. In the distal tubule, sodium is
reabsorbed under the influence of mineralocorticoids (primarily aldosterone) and potassium is exchanged to
preserve electroneutrality. Increased urinary potassium loss contributing to hypokalemia is typically due to one or
both of the following mechanisms:
Heavy metals: Barium toxicity is a rare cause of hypokalemia, caused by blockade of potassium channels
limiting their efflux from cells. Barium salts are found in fireworks and rodent toxins [10,11]. Barium sulfate is
the formulation used in radiographic procedures and is not absorbed from the gut. Cesium has been
reported as a rare cause of hypokalemia in adults due to its use as an alternative therapy for cancer, but has
not been reported in children [12].
●
Antipsychotic drugs: Hypokalemia has been reported in association with the use of risperidone and
quetiapine in adults. Given the increasing use of this medication in children and adolescents, a high index of
suspicion should be present in children with hypokalemia or cardiac arrhythmias who are prescribed these
medications. (See "Causes of hypokalemia in adults", section on 'Antipsychotic drugs'.)
●
Chloroquine intoxication due to intracellular movement of potassium is an uncommon cause of severe
hypokalemia in children [1316].
●
Increased delivery of sodium and water to the distal nephron●
Increased mineralocorticoid activity●

Increased distal delivery of sodium and water — In children, the following conditions are associated with
urinary 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 proximal
nephron segments leading to distal delivery of sodium. In addition, volume depletion leads to increased
aldosterone activity.
Nonreabsorbable ions — Nonreabsorbable anions are accompanied by sodium, resulting in distal
delivery of sodium, which is exchanged with potassium. Pediatric settings, in which the presence of
nonreabsorbable anions results in increased distal delivery of sodium, include excess filtered bicarbonate in
patients with excessive vomiting or with proximal (type 2) renal tubular acidosis (RTA), betahydroxybutyrate in
patients with diabetic ketoacidosis, and hippurate following toluene abuse (gluesniffing). (See 'Gastrointestinal
losses' 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 in
hypokalemia. This is most commonly seen in children with diabetic ketoacidosis who have glucose osmotic
diuresis 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 may
also result from osmotic diuresis if there is inadequate fluid replacement, which leads to increased aldosterone
activity and enhanced distal potassium secretion. (See 'Increased mineralocorticoid activity' below.)
Genetic tubular disorders — Bartter and Gitelman syndromes are autosomal recessive diseases that are
caused by mutations in genes encoding tubular transport proteins involved in sodium reabsorption. In these
patients, sodium absorption is disrupted leading to increased distal delivery of sodium, resulting in metabolic
alkalosis 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 urinary
potassium losses. (See "Bartter and Gitelman syndromes".)
Tubular injury — Tubular injury due to tubulointerstitial diseases or cisplatin results in decreased sodium
reabsorption in more proximal nephron segments, leading to distal delivery of sodium, where potassium is
exchanged for sodium. In one small case series of pediatric patients, tubulopathy due to cisplatin, which resulted
in reduced potassium, persisted for months to years following completion of chemotherapy [19]. (See "Cisplatin
nephrotoxicity", section on 'Salt wasting'.)
Distal (type 1) renal tubular acidosis (RTA) — In distal (type 1) RTA, increased urinary potassium loss is
due to enhanced potassium secretion needed to maintain electroneutrality because of the impaired distal
acidification (ie, defective secretion of protons) (table 3). In addition, tubular cellular membrane permeability is
also 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 therapy●
Nonreabsorbable anions (eg, mannitol or bicarbonate)●
Osmotic diuresis●
Genetic tubular disorders (ie, Bartter and Gitelman syndromes)●
Tubular injury due to interstitial nephritis or cisplatin●
Prolonged administration (several days) or a large amount of intravenous (IV) fluid with no potassium
supplementation
●

reduced proximal tubule's absorptive capacity for bicarbonate. (See "Etiology and clinical manifestations of renal
tubular acidosis in infants and children" and 'Increased distal delivery of sodium and water' above.)
Increased mineralocorticoid activity — Increased mineralocorticoid activity enhances potassium urinary
excretion.
Hypovolemia — In children, the most common cause of increased mineralocorticoid activity is due to
secretion 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 membranes
and increasing membrane permeability. Potassium flows down its concentration gradient out of tubular epithelial
cells into the lumen. A large study in adults comparing conventional amphotericin with the liposomal form found a
significant reduction in hypokalemia from 11.6 to 6.7 percent [20]. A review of children outside of the neonatal
period receiving amphotericin found hypokalemia to be present in 47 percent of those measured, but none of
those receiving liposomal amphotericin [21]. (See "Amphotericin B nephrotoxicity".)
Liddle syndrome — Liddle syndrome is caused by an autosomal dominant, gainoffunction mutation in
subunits of the epithelial sodium channel (ENaC) that presents in childhood as hereditary hypokalemic metabolic
alkalosis 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 pseudohypoaldosteronism
type 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 the
promoter of the gene encoding aldosterone synthase in the adrenal zona fasciculata (involved in cortisol
synthesis) with the coding region of the related gene in the zona glomerulosa (involved in aldosterone
synthesis). This mutation increases the production of aldosterone, which can be suppressed by
glucocorticoid administration. GRA typically presents with hypertension before 21 years of age. The
potassium 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 glucocorticoid
remediable aldosteronism (GRA)'.)
●
Apparent mineralocorticoid excess (AME) is an autosomal recessive disorder due to mutations of the gene
that encodes 11betahydroxysteroid dehydrogenase type 2 isoform, which normally breaks down cortisol to
cortisone. This genetic defect results in increased levels of renal cortisol, which binds to the mineralocorticoid
receptor. AME typically presents in infancy or early childhood with severe hypertension, failure to thrive, and
muscle weakness due to hypokalemia. Chronic ingestion of licorice containing glycyrrhetinic acid has a
similar effect. (See "Apparent mineralocorticoid excess syndromes (including chronic licorice ingestion)".)
●
Although the most common form of congenital adrenal hyperplasia (21hydroxylase deficiency) leads to
decreased aldosterone synthesis and hyperkalemia, other rarer forms of congenital adrenal hyperplasia are
associated with increased mineralocorticoid synthesis and hypokalemia. These include 17alphahydroxylase
deficiency, which presents with hypertension, hypokalemia, and hypogonadism at puberty, and 11beta
hydroxylase deficiency, which presents in neonates with virilization, hypertension, and hypokalemia. (See
"Uncommon congenital adrenal hyperplasias", section on 'CYP17A1 deficiencies' and "Uncommon
congenital adrenal hyperplasias", section on '11betahydroxylase deficiency'.)
●

Cystic fibrosis and skin losses — Electrolyte abnormalities including hypokalemia have been reported in
patients with cystic fibrosis [22]. These findings typically occur in young children less than 2.5 years of age with
volume depletion, and often prior to making the diagnosis of cystic fibrosis.
CLINICAL MANIFESTATIONS — Clinical manifestations vary depending on the severity and acuity of
hypokalemia. Symptoms generally do not become manifest until the serum potassium is below 3 mEq/L unless
there 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 the
action potential, which is dependent on the transcellular potassium gradient. (See "Clinical manifestations and
treatment 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 if
there is a sudden precipitous drop in potassium. Muscle weakness typically starts in the proximal muscles of the
lower extremities and progresses upwards to the trunk and upper extremities. As the potassium drops below 2
mEq/L, severe weakness progresses, involving respiratory muscles, which may result in respiratory failure and
death.
Hypokalemia can also induce smooth muscle weakness, which is manifested as ileus [23]. Affected patients may
complain 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) can
lead to muscle cramps and/or fasciculations, rhabdomyolysis, and myoglobinuria. A potential diagnostic problem
is that the release of potassium from the cells with rhabdomyolysis can mask the severity of the underlying
hypokalemia 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 including
premature atrial and ventricular beats, sinus bradycardia, paroxysmal atrial or junctional tachycardia,
atrioventricular block, and ventricular tachycardia or fibrillation. Hypokalemia is also associated with characteristic
ECG changes including PR prolongation, flattening of T waves, and ST depression. With more profound
hypokalemia, U waves can emerge after the T waves, as best seen in the precordial leads [23,24]. (See "Clinical
manifestations and treatment of hypokalemia in adults", section on 'Cardiac arrhythmias and ECG abnormalities'.)
Renal manifestations — Prolonged hypokalemia can cause renal dysfunction, particularly impaired
concentrating 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 that
is below the normal range, usually 3.5 mEq/L. In infants, the normal range of potassium is greater than in older
children and adults because of their reduced urinary potassium excretion (table 1). In many instances, the
diagnosis is made incidentally when plasma or serum electrolytes are obtained during an evaluation for another
condition, especially in children with levels between 3 and 3.5 mEq/L, whereas levels below 3 mEq/L are more
often associated with clinical signs and symptoms.
Muscle weakness and paralysis●
Cardiac arrhythmias and electrocardiogram (ECG) changes●
Impaired urinary concentrating ability and other renal abnormalities●

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 one study in
children, 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 [25]. However, in another study that evaluated
samples from adult patients, there was no difference in levels between the two techniques [26]. These differing
results may be due to the use of different blood gas analyzers. Clinicians should be aware of these differences in
their 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 is
intracellular. Settings in which there is a transcellular movement of potassium into the cell can lead to the false
assumption of total body potassium depletion. This may lead to unnecessary potassium repletion rather than
correcting the underlying cause of increased intracellular potassium uptake (eg, alkalosis or administration of
insulin). 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 and
paralysis are differentiated from hypokalemia by the finding of an abnormally low potassium level. These include
myositis 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 life
threatening condition, initial management takes precedence over any diagnostic evaluation. The urgency and
type 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 extensive
diagnostic evaluation.
Historical clues include the following:
Physical examination — Once hypokalemia has been discerned, the initial physical assessment should include
the following:
Acute gastrointestinal (GI) illness with diarrhea or vomiting is the most common cause of hypokalemia in
otherwise healthy children.
●
Decreased dietary potassium intake is typically not the main cause of hypokalemia, but may be an
exacerbating 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] or
exogenous 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 periodic
paralysis. (See "Hypokalemic periodic paralysis".)
●
A diagnosis of thyrotoxic periodic paralysis should be considered in any patient with concomitant or
preceding 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 warrants
further evaluation.
●
Cardiac rate and rhythm by auscultation to screen for arrhythmias.●

Laboratory studies — In symptomatic cases or if there is any concern for a cardiac arrhythmia, an
electrocardiogram (ECG) should be performed, and treatment should be immediately started to address any
clinically significant findings.
In the child with relatively mild hypokalemia with a history of present illness that suggests a clear etiology such as
viral 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 whether
or not there is excessive renal potassium loss (table 4 and algorithm 1).
Urinary potassium excretion — The most common pediatric cause of increased urinary potassium excretion
is hypovolemia, which results in increased mineralocorticoid activity due to secretion of aldosterone
(hyperaldosteronism). In these children, hypokalemia and increased urinary potassium renal excretion resolve
with 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 rapid
improvement to a normal potassium level with replacement therapy. In addition, unless the underlying etiology is
addressed (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 and
treatment 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, these
are difficult to perform in many children and delay establishment of a diagnosis.
Further evaluation — For those children with hypokalemia and excessive urinary potassium excretion without
an apparent etiology, further evaluation is warranted and is based on the presence or absence of an elevated
blood pressure (algorithm 1).
Muscle strength and tone.●
Reflexes.●
Evaluation of the effective circulating volume and respiratory status. These factors influence initial
management strategies and can prove useful in clarifying acidbase and volume balance in children with
unclear 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 of
decreased urine flow, random levels may appear >20 mmol/L even though overall daily potassium excretion
is being appropriately conserved.
●
Spot potassiumtocreatinine ratios correct for any variations in urine volume in patients with stable
glomerular filtration rate. A urine potassiumtocreatinine ratio should be <15 mEq/g creatinine (<1.5
mEq/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 either
due to increased mineralocorticoid activity or tubular dysfunction. (See "Evaluation of the adult patient with
hypokalemia", section on 'Urine potassiumtocreatinine ratio'.)
●
For hypertensive patients, plasma renin and aldosterone are obtained.●

MANAGEMENT
Overview — The acuity and degree of the hypokalemia influence the clinical approach to therapy. The goals of
therapy are to prevent or treat lifethreatening complications (arrhythmias, paralysis, rhabdomyolysis, and
diaphragmatic weakness) associated with severe hypokalemia, replace the potassium deficit, and correct the
underlying cause. The urgency of therapy depends upon the severity of hypokalemia, and the rate of decline in
serum 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 require
urgent interventions.
The management of pediatric hypokalemia includes:
Low renin and high aldosterone levels are suggestive of primary hyperaldosteronism (adrenal
abnormalities). 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, apparent
mineralocorticoid 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 and
pseudohypoaldosteronism type 1")

For normotensive patients, evaluation focuses on the acidbase status of the patient as determined by
venous pH and serum electrolytes (table 5).
●
For patients with metabolic acidosis, diagnostic possibilities include types I and II RTA and diabetic
ketoacidosis.
•
For patients with metabolic alkalosis, diagnostic possibilities include chronic diuretic use, persistent
vomiting, and the genetic tubulopathies of Bartter and Gitelman syndromes. Measurement of urinary
chloride concentration may be helpful in differentiating among these disorders.
•
Urinary chloride concentration is normal in Bartter or Gitelman syndromes (see "Bartter and
Gitelman syndromes")

Urinary chloride concentration is low in patients with vomiting.
Urinary chloride concentration is variable with diuretic therapy depending on whether tubular
function is still responsive to diuretic activity.

In patients who have no underlying acidbase disorders, diagnostic possibilities include magnesium
depletion 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 be
present prior to genetic testing. These entities are discussed in greater detail separately. (See "Bartter and
Gitelman syndromes" and "Genetic disorders of the collecting tubule sodium channel: Liddle's syndrome and
pseudohypoaldosteronism type 1".)
●
Ascertaining the need for potassium replacement.●

Potassium supplementation — When the decision is made that potassium supplementation is needed, choices
regarding 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, potassium
supplementation should be given enterally. Data in children cared for in a cardiac intensive care unit have shown
that 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 large
amount of potassium in a short period of time, resulting in hyperkalemia. Safety measures to prevent this
complication include limiting the absolute amount of potassium in any single container or bag of fluid, and using
an infusion pump. IV potassium administration is also associated with pain and phlebitis when administered
through 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 severity
of 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 is
no treatment for the underlying disorder (Bartter or Gitelman syndrome).
●
Electrocardiographic monitoring for symptomatic children and those in whom there is a concern for cardiac
arrhythmia.
●
In patients receiving intravenous (IV) fluid, use of saline solution without dextrose. Dextrosecontaining
solution should be avoided since the administration of dextrose stimulates the release of insulin, which drives
extracellular potassium into the cells.
●
Potassium chloride tends to result in quicker potassium repletion per dose than phosphate or citrate [28] and
is the most common pharmacologic supplement. It is also preferred in patients with concomitant
hypochloremia or metabolic alkalosis.
●
Potassium phosphate is often used in the setting of proximal tubule dysfunction, such as Fanconi syndrome
or 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 in
types I and II renal tubular acidosis (RTA).
●
In symptomatic patients (arrhythmias, marked muscle weakness, or paralysis), rapid potassium
supplementation 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 potassium
concentration of no more than 40 mEq/L is given at a rate not to exceed 0.5 to 1 mEq/kg of body weight per
hour. The goal is to raise the potassium level by 0.3 to 0.5 mEq/L. These patients require continuous
electrocardiographic (ECG) monitoring to detect changes due to hypokalemia, and also possibly rebound
hyperkalemia during replacement therapy. (See 'Clinical manifestations' above and "Causes, diagnosis, and
evaluation of hyperkalemia in children", section on 'Cardiac conduction abnormalities'.)
●
In asymptomatic patients with potassium levels less than 3 mEq/L, replacement of potassium stores is
generally needed. Oral therapy is preferred and IV supplementation should be reserved for those who are
●

Other interventions
Magnesium depletion — Hypomagnesemia may accompany hypokalemia. Magnesium can be lost at the
same time as potassium with gastrointestinal (GI) losses or with diuretic use. Hypomagnesemia can also promote
renal potassium wasting directly in the distal tubule, and can also prevent reabsorption of filtered potassium at the
loop of Henle [24]. (See "Clinical manifestations of magnesium depletion", section on 'Hypokalemia'.)
Potassiumsparing diuretics — Potassium supplementation by itself is less effective in tubulopathies such
as Bartter or Gitelman syndromes, where there is ongoing renal wasting of potassium. Use of a potassium
sparing diuretic such as amiloride may attenuate these losses. (See "Bartter and Gitelman syndromes", section
on 'NSAIDs and drugs that block distal tubule sodiumpotassium exchange'.)
Children with hyperaldosteronism may benefit from spironolactone or eplerenone therapy to reduce the urinary
potassium effect of aldosterone. (See "Treatment of primary aldosteronism", section on 'First line:
Mineralocorticoid antagonists'.)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and
"Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5 to 6 grade
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the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written
at the 10 to 12 grade reading level and are best for patients who want indepth information and are
comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or email these
topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on
"patient info" and the keyword(s) of interest.)
SUMMARY AND RECOMMENDATIONS
unable to take oral medications. The amount of replacement therapy is dependent on the cause of the
hypokalemia, 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, beta
adrenergic agents or exogenous insulin), as correction of the underlying cause results in resolution of
hypokalemia.
In asymptomatic patients with acute hypokalemia and potassium levels between 3 and 3.5 mEq/L, correction
of the underlying cause and dietary potassium are usually sufficient without the need for additional potassium
supplementation.
●
In asymptomatic patients with chronic hypokalemia, potassium supplementation may be needed, particularly
if the underlying cause is not amenable to correction (eg, types I and II RTA). (See "Treatment of distal (type
1) 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 usually
defined as 3.5 mEq/L. Normal serum 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 (table 1).
●

Pediatric hypokalemia is caused by derangements of the normal hemostatic mechanisms that regulate
potassium 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 cells
is promoted by the following conditions: alkalosis, increased insulin activity (eg, exogenous insulin
administration) and betaadrenergic activity (eg, albuterol administration), and hypokalemic periodic
paralysis. (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 in
exchange for potassium (eg, diuretic therapy, genetic tubular disorders [Bartter and Gitelman
syndromes], and osmotic diuresis) or increased mineralocorticoid activity (eg, hyperaldosteronism due to
hypovolemia). (See 'Increased urinary losses' above.)
•
Clinical manifestations vary depending on the severity and acuity of hypokalemia. Symptoms generally do
not become manifest until the serum potassium is below 3 mEq/L unless there is a rapid significant fall in
serum potassium. Clinical findings include muscle weakness and paralysis, cardiac arrhythmias and
electrocardiogram (ECG) changes, and polyuria due to impaired urinary concentration. (See 'Clinical
manifestations' above.)
●
The diagnosis of hypokalemia is made by the detection of a serum or plasma potassium level that is below
the normal range of 3.5 mEq/L. In many instances, the diagnosis is made incidentally when serum or plasma
electrolytes are obtained during an evaluation for another condition, especially in children with levels between
3 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 the
etiology, as subsequent care is based on the underlying cause of hypokalemia. The assessment includes a
focused history and physical examination. In most cases, the history is sufficient to determine the underlying
cause. However, additional laboratory testing may be needed in patients in whom the diagnosis remains
uncertain (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 therapy
are to prevent or treat lifethreatening complications (arrhythmias, paralysis, rhabdomyolysis, and
diaphragmatic weakness) associated with severe hypokalemia, replace the potassium deficit, and correct the
underlying cause. (See 'Management' above.)
●
For symptomatic patients with hypokalemia (arrhythmias, marked muscle weakness, or paralysis), we
recommend that potassium supplementation be administered (Grade 1B). In some cases, this requires
intravenous (IV) administration of potassium chloride, particularly in those who are unable to take oral
medications. In this setting, an infusion with a potassium concentration of no more than 40 mEq/L is given at
a rate not to exceed 0.5 to 1 mEq/kg of body weight per hour. The goal is to raise the potassium level by 0.3
to 0.5 mEq/L. These patients require continuous ECG monitoring to detect changes due to hypokalemia, and
also 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 the
severity 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 Pediatr
2000; 37:1348.
4. Talbert A, Thuo N, Karisa J, et al. Diarrhoea complicating severe acute malnutrition in Kenyan children: a
prospective 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 diabetic
ketoacidosis: 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 adverse
reaction in Australian and New Zealand emergency departments: a crosssectional survey. Eur J Emerg
Med 2003; 10:219.
9. Krebs SE, Flood RG, Peter JR, Gerard JM. Evaluation of a highdose continuous albuterol protocol for
treatment 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. Cleve
Clin 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 Scand
2004; 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 and
management. 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 by
rotavirus, 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: an
autopsy 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 children
and 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.)

20. Walsh TJ, Finberg RW, Arndt C, et al. Liposomal amphotericin B for empirical therapy in patients with
persistent fever and neutropenia. National Institute of Allergy and Infectious Diseases Mycoses Study
Group. N Engl J Med 1999; 340:764.
21. Dutta A, Palazzi DL. Risk factors of amphotericin B toxicty in the nonneonatal pediatric population. Pediatr
Infect Dis J 2012; 31:910.
22. ScuratiManzoni E, Fossali EF, Agostoni C, et al. Electrolyte abnormalities in cystic fibrosis: systematic
review 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 and
potassium 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 laboratory
measurement 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 cardiac
intensive 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.
Topic 97159 Version 8.0

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 implications
of variation from normal or reference range levels must be considered individually.
Graphic 86501 Version 2.0

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 11betahydroxylase
deficiency)
Tubulopathies (Bartter syndrome, Gitelman syndrome)
Amphotericin
Enhanced sodium reabsorption (Liddle syndrome)
Increased skin loss
Cystic fibrosis

Characteristics of the different types of renal tubular acidosis
Type 1 RTA Type 2 RTA
Hyperkalemic RTA –
Type 4 RTA
(hypoaldosteronism)
and distal tubule
voltage defects
Primary defect Impaired distal
acidification
Reduced proximal
bicarbonate
reabsorption
Decreased aldosterone
secretion or aldosterone
resistance. Reduced sodium
reabsorption in the distal
tubule (voltage defect).
Plasma bicarbonate Variable, may be
below 10 meq/L
Usually 12 to 20 meq/L Variable (greater than 17
meq/L in hypoaldosteronism)
Urine pH Greater than 5.3 Variable, greater than
5.3 if the serum HCO3
exceeds the tubule's
bicarbonate
reabsorptive threshold.
Less than 5.3 when the
serum HCO3 is
reduced to levels that
can be largely
reabsorbed despite
defective proximal
tubule reabsorptive
mechanisms.
Variable, greater than 5.3
with voltage defects, and
usually less than 5.3 with
hypoaldosteronism
Plasma potassium Usually reduced but
hyperkalemic forms
exist; hypokalemia
largely corrects with
alkali therapy
Reduced, made worse
by bicarbonaturia
induced by alkali
therapy
Increased; correcting the
hyperkalemia alone will
improve the acidosis by
increasing ammonium
availability
Urine anion gap Positive Negative Positive
Urine calcium/creatinine ratio Increased Normal Normal
Nephrolithiasis/nephrocalcinosis Yes No No
HCO3: bicarbonate; RTA: renal tubular acidosis.

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)

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.

Pediatric causes of concomitant hypokalemia and acidbase disorders based on
urinary potassium loss

Low urinary potassium
losses
High urinary potassium
losses
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:
Diuretics
Vomiting
Bartter syndrome
Gitelman syndrome
RTA: renal tubular acidosis.

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
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multilevel review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to
UpToDate standards of evidence.
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