ARTICLE

Hypokalemia/Hyperkalemia and
Hyponatremia/Hypernatremia
Diane H. Brown, MD,* Neil J. Paloian, MD*
*Department of Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, WI

PRACTICE GAP

It is vital that pediatricians understand how to evaluate and treat common

electrolyte derangements. With thorough understanding of the fundamental
physiologic systems that regulate sodium and potassium homeostasis,
pediatricians will have the knowledge to manage children with any variety of
electrolyte disorders.

OBJECTIVES After completing this article, readers should be able to:

Describe the signs and treatment for a patient with hypokalemia.

Describe the signs and treatment for a patient with hyperkalemia.
Describe the signs and treatment for a patient with hyponatremia.
Describe the signs and treatment for a patient with hypernatremia.

ABSTRACT
Electrolyte disorders are very common in the pediatric population.
Derangements in serum sodium and potassium concentrations are among the
most frequently seen given the risk factors and comorbidities unique to
AUTHOR DISCLOSURE: Drs Brown and
children. Pediatricians, in both outpatient and inpatient settings, should be Paloian have disclosed no financial
comfortable with the evaluation and initial treatment of disturbances in these relationships relevant to this article. This
electrolyte concentrations. However, to evaluate and treat a child with commentary does not contain a
discussion of an unapproved/
abnormal serum concentrations of sodium or potassium, it is critical to
investigative use of a commercial
understand the regulatory physiology that governs osmotic homeostasis and product/device.
potassium regulation in the body. Comprehension of these basic physiologic
processes will allow the provider to uncover the underlying pathology of these
ABBREVIATIONS
electrolyte disturbances and devise an appropriate and safe treatment plan.
ADH antidiuretic hormone
BUN blood urea nitrogen
ECF extracellular fluid
ECG electrocardiogram
OVERVIEW OF SODIUM IN THE CELLULAR SPACES FENa fractional excretion of sodium
Sodium is an essential electrolyte in the human body. Sodium is responsible for GI gastrointestinal
IV intravenous
neuro-electrical activity (depolarization of neurons and other excitable cells) and SIADH syndrome of inappropriate
regulates the extracellular fluid (ECF) volume. antidiuretic hormone

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 The human body is composed of 50% to 75% water,
with two-thirds of the water being intracellular and the re-
maining one-third being extracellular. Cell membranes are
generally permeable to water and allow water to move be-
tween the intracellular and extracellular space. Because of
this, it is necessary to be able to regulate the volume of
the water spaces. Osmolality gradients between the ECF
and intracellular fluid will cause water to move from one
compartment to the other. The intracellular volume is
controlled by regulating ECF osmolality (water balance),
and ECF volume maintenance is accomplished by modi-
fying total body sodium load (sodium balance). These 2
processes often occur simultaneously but are distinct
processes.
SODIUM AND WATER REGULATION
The intracellular fluid volume is regulated by maintaining
plasma osmolality within a certain range, usually 280 to
290 mOsm/kg H2O (280–290 mmol/kg H2O). Under
normal circumstances, plasma osmolality is determined
primarily by the serum sodium concentration ([Na1]),
demonstrated in the following equation for calculating
plasma osmolality: (2 × [Na1]) 1 ([Glucose]/18) 1 ([BUN]/2.8)
(with Glucose and BUN measured in mg/dL). Note that many
cell membranes in the body are permeable to blood urea nitro-
gen (BUN), and, therefore, BUN does not play a large role in
effective plasma osmolality. Plasma osmolality (sodium con-
centration) is controlled by modifying water balance using 2
important methods: thirst modification (regulating water input)
and antidiuretic hormone (ADH) secretion (regulating water
output). An increasing plasma osmolality stimulates thirst and
ADH secretion to increase total body water, and a decreasing
plasma osmolality depresses thirst and ADH secretion to de-
crease total body water. When ADH is released in response to
a higher osmolality, it recruits aquaporin 2 channels in the
renal collecting duct and allows for free water to be reab-
sorbed. The absence of ADH removes those water chan-
nels, and free water is excreted. In a healthy state, the body
maintains serum sodium concentrations between 135 and
145 mEq/L (135–145 mmol/L).
The ECF volume is regulated by altering the total body
sodium content. When ECF volume becomes too low, re-
nin is released and activates the synthesis of angiotensin
II and aldosterone. Aldosterone stimulates renal sodium
reabsorption and potassium secretion in the distal tubule
and collecting duct. Suppression of aldosterone when ECF
volume is elevated causes renal sodium excretion and low-
ers the total body sodium content. Primary disturbances
in total body sodium amount do not necessarily translate
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to changes in the serum sodium concentration but rather
contribute to changes in the ECF volume. Sodium defi-
ciency causes hypovolemia, and sodium excess causes
edema and hypertension. Although these are common pa-
thologies seen by pediatric providers, they are outside the
scope of this review.
HYPONATREMIA
Overview
Hyponatremia is defined as a serum sodium concentra-
tion less than 135 mEq/L (<135 mmol/L) and is a common
electrolyte issue, occurring in up to 34% of hospitalized
patients. (1) When children develop hyponatremia, it is
often because of an inherent or acquired condition that
impairs the kidney’s ability to excrete free water. Rarely,
excess free water intake can lead to hyponatremia; how-
ever, the occurrence of acute iatrogenic hyponatremia due
to hypotonic intravenous (IV) fluid administration is in-
creasingly recognized. (2) Last, low effective arterial blood
volume or volume depletion from impaired renal sodium
reabsorption will stimulate ADH secretion to preserve end
organ perfusion, causing hyponatremia.
Clinical Implications
When a patient develops hyponatremia, the resulting
decrease in serum osmolality promotes fluid to shift from
the extracellular space to the intracellular space. This can
result in cellular swelling; in brain cells this can lead to
cerebral edema and encephalopathy. The symptoms of hy-
ponatremic encephalopathy can vary among patients and
can include headache, nausea/vomiting, and weakness.
The symptoms of hyponatremic cerebral edema can pre-
sent as behavioral changes and decreased consciousness,
and if the edema becomes more advanced, the patient can
develop signs of cerebral herniation and the Cushing triad
(bradycardia, irregular breathing, hypertension). In addi-
tion, decreasing plasma sodium causes neurons to depo-
larize more easily and subsequently lowers the seizure
threshold. Importantly, children are at greater risk for hy-
ponatremic-induced encephalopathy at a higher serum
sodium concentration than adults. (3) It is believed that
this occurs because of the higher brain-to-skull ratio in
children, with less space in the skull if swelling occurs.
Furthermore, hyponatremia can lead to the development
of hypoxemia. This primarily occurs due to the develop-
ment of pulmonary edema because the hypoosmolality
causes ECF fluid shifting into the pulmonary cells. Severe
hyponatremia, with severe cerebral edema, can lead to
 Table 1. Etiologies of Hyponatremia
Hypovolemia
Gastrointestinal losses
Diuretic induced
Exercise: marathons
Excess salt loss
Cerebral salt wasting
Adrenal disorders: 21-hydroxylase deficiency, hypoaldosteronism
Cystic fibrosis
Primary renal tubular disorders: Bartter and Gitelman syndromes
Chronic kidney disease: obstructive uropathy, bilateral renal
dysplasia
Euvolemia
Syndrome of inappropriate antidiuretic hormone secretion
Pulmonary: pneumonia, bronchiolitis, intubation (positive
pressure ventilation)
Medications: carbamazepine, vincristine, cyclophosphamide,
narcotics, many others
Primary polydipsia/psychogenic polydipsia
Hypervolemia
Reduced effective circulating volume
Nephrotic syndrome
Heart failure
Liver failure
Renal dysfunction
decreased cerebral blood flow and eventual centrally medi-
ated respiratory arrest, amplifying existing hypoxemia.
Causes
When evaluating the cause of hyponatremia, understanding
the fluid status of the patient is essential. The underlying
etiologies of hyponatremia (Table 1) can often be deter-
mined by assessing the child’s volume status. (4) The most
common cause of hyponatremia, often seen in the hospital
setting, is syndrome of inappropriate antidiuretic hormone
(SIADH). SIADH occurs when a patient is euvolemic or
even hypervolemic and ADH is inappropriately secreted.
This situation can occur secondary to many different ill-
nesses, but most often occurs in patients with pulmonary
disorders or infections (such as pneumonia), patients who
have undergone surgery, patients with central nervous system
disorders including head trauma, patients with malignancies
with ectopic ADH production, or patients taking certain medi-
cations. Although many medications are known to cause
SIADH, common medications include carbamazepine, cyclo-
phosphamide, and selective serotonin reuptake inhibitors.
Hypovolemic hyponatremia is caused by conditions
that decrease the ability of the renal tubule to reabsorb so-
dium. This is seen in hereditary conditions with excess
urinary sodium losses via the kidney, such as Bartter syn-
drome (a genetic disorder that impairs sodium reabsorp-
tion in the loop of Henle), Gitelman syndrome (a genetic
disorder that impairs sodium reabsorption in the distal
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tubule), and the salt-wasting forms of congenital adrenal
hyperplasia. In addition, diuretics (especially thiazide diu-
retics) can cause hyponatremia in this manner. Finally,
scenarios in which the total body volume is high but the
effective arterial blood volume is low (heart failure, liver
failure, nephrotic syndrome) can lead to hyponatremia. In
these scenarios, ADH synthesis is increased to try and
maintain ECF volume and organ perfusion, at the expense
of plasma osmolality. Cerebral salt wasting is a poorly under-
stood entity, related to SIADH, seen in patients recovering
from neurosurgery; however, these patients have polyuria
and can become volume depleted. The pathophysiology of
cerebral salt wasting is unclear but is identified by hyponatre-
mia and excessive urinary sodium losses in patients with
neurologic disease.
Excess water intake rarely causes hyponatremia, al-
though it can be seen when water intake exceeds the kid-
ney’s ability to dilute the urine even when ADH is
maximally suppressed. In infants, this can be caused by
dilute formula or supplemental feedings with water in
families with food insecurities. This can also occur in
older children who are gastrostomy tube fed and are given
excessive free water, in the case of the child with a near-
drowning event who ingests large amounts of fresh water,
or in the case of a child with psychogenic polydipsia.
Hyponatremia can be seen when other osmotically
active substances, such as glucose or endogenous toxins,
are in such excess that they increase the extracellular os-
molality. Appropriately, to compensate, the serum sodium
level decreases to decrease the plasma osmolality.
Pseudohyponatremia was once a common cause of
hyponatremia, due to a laboratory anomaly seen when
serum levels of lipids or proteins are elevated. Improve-
ments in laboratory techniques have rendered this finding
uncommon in most medical centers today; the provider
should inquire with their local laboratory to determine
whether pseudohyponatremia is a possibility based on the
assay used.
Evaluation
Evaluation of hyponatremia starts with a thorough history
and physical examination. Obtaining a detailed history
may reveal dehydration from gastrointestinal (GI) losses,
excess free water intake, or signs of pathologies or medica-
tions that can cause SIADH. Low urine output can be
indicative of impairment of the kidneys to excrete free wa-
ter, recognizing that infants’ urine-concentrating capability
is less than that of older children. The physical examina-
tion can identify vital sign changes consistent with
Vol. 44 No. 7 JULY 2023 351
 hypovolemia (tachycardia and hypotension) and skin find-
ings of decreased skin turgor.
Obtaining a basic metabolic panel to assess for hyper-
glycemia, renal function, and potassium concentration
is essential. Hyperglycemia can cause a decrease in the
serum sodium level by 1.6 mEq/L (1.6 mmol/L) for
every 100 mg/dL (5.55 mmol/L) of glucose higher than
100 mg/dL (5.55 mmol/L). This is often seen in diabetic
ketoacidosis. BUN/creatinine can give information on
the patient’s renal function because renal dysfunction
may impair the kidney’s ability to excrete free water. Hy-
perkalemia, discussed elsewhere in this review, can be a
marker of adrenal insufficiency or hypoaldosteronism.
Hypokalemia often accompanies excessive diuretic use or
Bartter or Gitelman syndrome.
Urine studies are also important in evaluating hyponatre-
mia. A urine specific gravity can give information about the
release of ADH. A high specific gravity suggests elevated
ADH production, consistent with SIADH or low effective
blood volume. A low specific gravity suggests excessive
free water intake. Note that an infant’s ability to concentrate
urine is limited and can result in misinterpretation of the spe-
cific gravity in this age group; the ability to concentrate urine
to that of adults occurs 6 months to 1 year after birth. Assess-
ing urine and serum osmolality can help to confirm SIADH,
where serum osmolality is lower than urine osmolality despite
ongoing hyponatremia.
Treatment
Treatment of hyponatremia depends on the etiology, signs
and symptoms, and chronicity. In the child with SIADH,
the offending pathology or medication should be identified
and treated or discontinued. If the underlying cause
cannot be remedied, the main treatment strategy is fluid
restriction. Trying to correct with normal saline or hyper-
tonic fluid is not first-line treatment in this situation be-
cause this is not a disease of sodium deficiency. In fact,
sodium balance is preserved, and any excess sodium will
be promptly excreted. Typically, restricting patients to two-
thirds of their daily fluid needs will allow the kidney to re-
move more water than is ingested, and the serum sodium
level will normalize.
In patients with hypovolemic hyponatremia, supportive
care with normal saline fluid (if total body volume deple-
tion) or treatment of the heart failure/liver failure/ne-
phrotic syndrome is the mainstay of action. If a patient
has hyponatremia due to either hyperglycemia or another
intoxication, correcting the underlying etiology will help
resolve the hyponatremia.
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Patients with neurologic complications, such as increasing
cerebral edema or seizures, indicate a medical emergency and
require treatment immediately with hypertonic saline. Increas-
ing serum sodium by 3 to 5 mEq/L (3–5 mmol/L) is usually
enough to help reverse severe symptoms, and this can be
done by using 3 to 5 mL/kg of 3% sodium chloride.
One of the concerns with correcting hyponatremia is
that correcting too fast could cause osmotic demyelination
syndrome (central pontine myelinolysis), seen when rapid
normalization of the serum sodium concentration leads to
damage of neuronal myelin sheaths, with subsequent cere-
bellar dysfunction, paralysis, or additional neurologic signs
and symptoms. After the emergency correction phase of
fluid and electrolyte resuscitation, the sodium level should
be corrected by less than 10 mEq/L (10 mmol/L) in a
24-hour period to safely avoid that process. Correction
should be based on the child’s sodium deficit, calculated
as 0.6 × weight (kg) × (desired Na – patient’s Na). The flu-
ids used to treat these patients should include the correct
amount of sodium and water that delivers the needed ex-
tra sodium considering the amount of free water and so-
dium given in the emergency phase and their ongoing
maintenance needs; the rate is calculated to raise the
sodium level by no more than 10 mEq/L (10 mmol/L)
per day.
HYPERNATREMIA
Overview
Hypernatremia is defined as a serum sodium concentration
greater than 145 mEq/L (145 mmol/L). Because sodium is
the dominant extracellular osmolyte, hypernatremia often
develops when osmotic regulation is impaired.
Clinical Implications
With increasing extracellular osmolality, there will be shifts
of fluid from the intracellular space to the extracellular space.
This can lead to shrinkage of cells, which can cause rupture
of bridging veins in the brain and lead to intracranial or in-
tracerebral hemorrhages. Hypernatremia can present with
increased irritability and agitation, and a neurologic examina-
tion may reveal increased tone and brisk reflexes. Patients
can also develop venous sinus thrombosis, which can lead to
infarctions of the brain. In muscle cells, severe hypernatre-
mia can cause rhabdomyolysis. The mortality rate of children
with hypernatremia is estimated to be approximately 15%. (5)
Clinical findings of hypernatremia are correlated with the de-
gree and rate of rise of sodium elevation; children with mild
or chronic hypernatremia may be asymptomatic.
 Table 2. Etiologies of Hypernatremia
Excess water loss
Gastrointestinal loss
Urinary water loss
Urinary concentration defect
Central diabetes insipidus
Nephrogenic diabetes insipidus: congenital, acquired/drug-induced (lithium, amphotericin, demeclocycline, ifosfamide, foscarnet, and cidofovir)
Hypercalcemia and hypokalemia
Renal disease: obstructive uropathy, sickle cell disease, nephronophthisis, cystinosis
Osmotic diuresis: diabetic ketoacidosis
Skin loss: excessive sweating, febrile illness
Inadequate water intake
Decreased access to water: infants, neuromotor disease
Impaired thirst mechanism: holoprosencephaly, craniopharyngioma
Iatrogenic: saline or total parenteral nutrition infusion
Salt poisoning: incorrect mixing of formula

Causes replaced. Initial questioning can focus on a history of GI

Hypernatremia is typically the result of free water losses
or deficits (Table 2). (6)(7) Hypernatremia is generally not
due to sodium excess in isolation and requires some de-
gree of free water deficit. Diabetes insipidus is a primary
cause of loss of free water absorption in the distal tubule
and is either central (due to decreased ADH production in
the posterior pituitary) or nephrogenic (ADH resistance).
Other types of losses of free water include osmotic diure-
sis due to hyperglycemia/glucosuria or mannitol therapy.
In addition, excess insensible losses can lead to hypernatre-
mia seen with intense exercise, sweating, fevers, respiratory
illnesses causing tachypnea, and burns. Finally, water losses
from GI causes, including gastroenteritis, diarrhea, malab-
sorption, or vomiting, can lead to hypernatremia if free
water losses exceed sodium losses. Iatrogenic causes of hy-
pernatremia include excess sodium administration often in
the form of sodium ingestion, high-calorie formula inges-
tion, and administration of hypertonic fluid or blood prod-
ucts. Note that in children with normal neurologic status
and free access to water, hypernatremia will not develop be-
cause hyperosmolality will trigger the thirst mechanism.
Hypernatremia is, therefore, seen in children and small in-
fants who are reliant on their caregivers to feed them and
provide them with water, when caregivers are restricting ac-
cess to water, or in children with underlying neuromotor
disease who cannot obtain water themselves or who cannot
vocalize thirst. Hypernatremia is also common in hospital-
ized children with acute illness and mental status changes
or who have imposed fluid restrictions.
Evaluation
Evaluation of hypernatremia starts with a good history and
physical examination. Often in pediatrics, hypernatremia
is due to hypotonic fluid loss, which is not adequately
losses (vomiting, diarrhea, gastrostomy tube losses) and
intake. It is important to determine the child’s urine out-
put volume, including whether output is low versus exces-
sive and whether it is dilute versus concentrated. Knowing
whether the child is unable to access free water when
thirsty is important, as is any history of neurologic impair-
ment, which could alter a patient’s thirst mechanism. And
last, obtaining a good breastfeeding or formula history is
critical in the infant; knowing whether the baby is latching
well, whether the mother is producing enough milk, how
the formula is being made and how much the baby takes,
and whether the baby appears “full” after feeding can all
help determine causes of hypernatremia.
Obtaining the following laboratory values can help dif-
ferentiate the cause of the hypernatremia: urine osmolal-
ity, urine sodium, urine creatinine, plasma osmolality, and
a basic metabolic profile. Comparing urine osmolality
with plasma osmolality can help differentiate whether the
hypernatremia is due to a concentrating defect such as di-
abetes insipidus, in which urine osmolality will be low, or
due to volume depletion, in which urine osmolality should
be high. When looking at the urine sodium level, most pa-
tients with hypernatremia due to hypovolemia will have a
sodium level less than 25 mEq/L (<25 mmol/L). A urine
sodium level greater than 200 mEq/L (>200 mmol/L) is
more suggestive of excessive sodium intake. Urine sodium
(UNa), urine creatinine (UCr), plasma sodium (PNa) and
plasma creatinine (PCr) levels can be used to calculate the
fractional excretion of sodium (FENa). FENa greater than
2% suggests excessive salt intake without fluid replace-
ment, and FENa less than 1% suggests that the hyperna-
tremia is due to water loss. FENa can be calculated as
[(PCr × UNa)/(PNa × UCr)] × 100. In the setting of comorbid

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 acute kidney injury, FENa can help differentiate between
prerenal disorders and acute tubular necrosis.
Treatment
Providing the needed amount of free water to correct the
serum sodium level is the mainstay in treatment of hyper-
natremia. Adequately assessing the free water deficit in
children can be approximated as follows: Free water deficit
(mL) 5 lean body weight (kg) × 0.6([patient’s [Na]/140] 1).
The free water deficit is added to the ongoing maintenance
fluid needs to equal the total correction fluid volume. Cor-
recting hypernatremia too quickly can lead to cerebral edema
due to the production of intracellular idiogenic osmoles. Be-
cause of this, it is reasonable to correct the sodium at a rate
that is not more than 0.5 to 1 mEq/L (0.5–1 mmol/L) per
hour, usually over at least 48 hours. In cases of extreme hy-
pernatremia (sodium level >170 mEq/L [>170 mmol/L]), it
is recommended to not correct the sodium level below
150 mEq/L (150 mmol/L) in the first 48 to 72 hours.
OVERVIEW OF POTASSIUM IN THE CELLULAR
SPACES
Opposite to sodium, little potassium exists extracellularly.
Approximately 2% of total body potassium is extracellular;
the remaining 98% of potassium in the body is intracellu-
lar, predominantly in the myocytes. The ratio of intracellu-
lar to extracellular potassium preserves the cellular resting
membrane potential necessary for the functioning of the
nervous system and muscle cells. Small changes in the ex-
tracellular potassium concentration can considerably alter
this ratio, causing disruption of the cell resting membrane
potential.
POTASSIUM REGULATION
Total body potassium content is maintained by balancing
intake and output. Potassium is found in many foods,
with high quantities in fruits and vegetables. Output is
controlled mainly by the kidney, with a small amount
(<5%) excreted through the GI tract. Unlike adults, in
whom potassium intake should equal output, children re-
quire a positive potassium balance. This correlates with
Table 3. Normal Serum Potassium Levels by Age
AGE POTASSIUM, mEq/L (mmol/L)
Premature infant 4.0–6.5 (4.0–6.5)
Newborn 3.9–5.9 (3.9–5.9)
Infant 4.1–5.3 (4.1–5.3)
Child 3.4–4.7 (3.4–4.7)
Adult 3.5–5.0 (3.5–5.0)
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higher serum potassium concentrations in children, most
notable in preterm infants (Table 3). (8)
Serum potassium regulation is achieved via 2 methods.
The first is by transferring potassium between the intracel-
lular and extracellular spaces. Insulin and epinephrine
cause net cellular uptake of potassium. In addition, alkalo-
sis produces a net intracellular uptake of potassium. Con-
versely, acidosis results in a net shift of potassium from
the intracellular space to the extracellular space.
The second mechanism to regulate serum potassium is
by balancing the total body potassium concentration, ac-
complished via renal potassium handling. The final urine
potassium concentration is determined by modifying the
amount of tubular secretion. An increasing serum potas-
sium concentration, an increased aldosterone level, a high-
potassium diet, and higher tubular sodium content increase
potassium secretion. Angiotensin II and a low-potassium
diet inhibit potassium secretion. Healthy kidneys can maxi-
mally conserve potassium when the total body potassium
level is low and can excrete excess potassium when the total
body potassium level is high.
HYPOKALEMIA
Overview
Hypokalemia is characterized by a serum potassium concen-
tration below normal, recognizing that very young children
have higher normal serum potassium concentrations. Mild
hypokalemia (potassium level >3 mEq/L [>3 mmol/L]) is
often well tolerated; as the level falls below 3 mEq/L
(<3 mmol/L), the likelihood of developing signs and symp-
toms increases, especially if the drop in potassium is acute.
Clinical Implications
With hypokalemia, the cell membrane becomes hyperpolar-
ized, impairing the ability of the myocytes to contract. This ini-
tially causes weakness and eventual paralysis, often starting in
the lower extremities and progressing proximally. The smooth
muscles of the GI tract and lungs can become involved, leading
to ileus and respiratory failure. (9) In addition, prolonged and
severe hypokalemia (<2.5 mEq/L [<2.5 mmol/L]) can lead to
rhabdomyolysis. (10) Hyperpolarization of the cardiac cells can
disrupt cardiac conduction, causing characteristic changes on
electrocardiogram (ECG), including ST depression, decreased
amplitude of T waves, increased amplitude of U waves, and
prolongation of the PR and QT intervals. Subsequently,
these changes lead to arrhythmias, including premature
atrial and ventricular beats, bradycardia, tachycardia, atrio-
ventricular block, and ventricular tachycardia or fibrilla-
tion. (11) Rarely, prolonged hypokalemia can cause
 Table 4. Causes of Hypokalemia in Children
MECHANISM CAUSE
Total body potassium depletion
Gastrointestinal losses Severe malnutrition
Eating disorders
Diarrhea
Renal losses
Increased distal tubular sodium Diuretics (loop and thiazide)
Osmotic diuresis
Tubular injury (cisplatin, aminoglycosides, cidofovir, foscarnet)
Increased mineralocorticoid activation Volume depletion
Corticosteroids
Bartter syndrome
Gitelman syndrome
Cystinosis
Familial hyperaldosteronism/glucocorticoid-remediable aldosteronism
Apparent mineralocorticoid excess
Licorice intoxication
Congenital adrenal hyperplasia (17-alpha-hydroxylase deficiency
and 11-beta-hydroxylase deficiency)
Primary aldosteronism
Increased tubular potassium membrane permeability Amphotericin B
Increased distal tubular sodium absorption Liddle syndrome
Imbalance of tubular electroneutrality Type 1 renal tubular acidosis
Type 2 renal tubular acidosis
Skin losses Cystic fibrosis
Shifting of potassium intracellularly
Alkalosis Metabolic alkalosis
Respiratory alkalosis
Insulin Exogenous insulin administration
Congenital hyperinsulinism
Refeeding syndrome
b-Adrenergic receptors Epinephrine
Albuterol
Terbutaline
Periodic paralysis Familial
Thyrotoxicosis

decreased responsiveness to ADH, thereby causing poly-
uria. (12)
Causes
Hypokalemia in children represents disturbances in potas-
sium regulation (Table 4). (13)(14)(15)(16) These disorders
reflect either a decrease in total body potassium concentra-
tion or excessive movement of extracellular potassium into
the intracellular space. Shifting of too much potassium in-
tracellularly is brought about by conditions with high lev-
els of insulin or epinephrine or by any primary pathology
causing an alkalosis (metabolic or respiratory). (13)(14)(15)
In addition, genetic defects in skeletal muscle calcium or
sodium channels or hyperthyroidism can interfere with
potassium movement between the extracellular and intra-
cellular space, causing hypokalemic periodic paralysis.
This results in acute and severe hypokalemia often trig-
gered by activities that increase adrenergic tone or by the
intake of meals with a high carbohydrate content. (16)
Pathologies that deplete the total body potassium stores
will also cause hypokalemia. Dietary deficiency of potas-
sium can cause hypokalemia, but this is rare and generally
seen only in children with severe malnourishment. In-
stead, decreased total body potassium concentration is pre-
dominantly due to excessive losses. Urinary potassium
losses are usually due to either an excess of tubular sodium
delivered to the distal tubule or increased mineralocorticoid
activity. (17)(18) Causes of increased distal tubular sodium
levels include diuretic therapy, osmotic diuresis, hereditary
disorders of tubular sodium reabsorption, and medications
causing proximal tubular injury. In addition, pathologies
that increase secretion or activation of mineralocorticoids/
aldosterone will cause hypokalemia. In children, this is
most commonly seen with volume depletion, either from
GI losses or in the setting of poor oral intake and increased
insensible fluid loses. Less common causes of elevated aldo-
sterone activity in children include hereditary disorders of
mineralocorticoid activity and aldosterone-secreting tumors.
Other unique causes of urinary potassium losses include

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 amphotericin B, types 1 and 2 renal tubular acidosis, and
Liddle syndrome (a genetic disorder characterized by hyper-
tension with hypokalemic metabolic alkalosis and inhibited
aldosterone secretion).
Potassium losses in the GI tract are a common cause
of hypokalemia in children. (19) Any cause of diarrhea,
either acute or chronic, can result in hypokalemia due
to the high amount of potassium secretion from the co-
lon seen in diarrheal illness. Upper GI tract losses of
potassium are much less pronounced, although persis-
tent emesis can cause hypokalemia due to the combina-
tion of alkalosis and volume depletion. Finally, certain
pathologic states, such as cystic fibrosis, can result in
significant potassium losses through sweat with subse-
quent hypokalemia.
Evaluation
To diagnose hypokalemia, the clinician must be aware of
the local laboratory assays and reference ranges. In addi-
tion, it is important to be aware of the different normal val-
ues for age. In a patient with severe (potassium level, <2.5
mEq/L [<2.5 mmol/L]) or symptomatic hypokalemia, further
diagnostics should be deferred until the potassium level has
been raised to a safe range. A physical examination should
focus on vital sign abnormalities and the presence of weak-
ness, paralysis, or respiratory distress/failure. An ECG should
be obtained promptly to evaluate for arrhythmias.
After diagnosing a child as having hypokalemia, it is
imperative to discover the cause of the hypokalemia, and
this begins with a thorough history and physical examina-
tion. The cause may become obvious based on a history of
gastroenteritis, contributory medication use, or a family
history of an inherited form of hypokalemia. Physical exam-
ination may reveal tachycardia or hypotension, Kussmaul
breathing, or hypertension. Further laboratory evaluation,
Table 5. Doses of Supplemental Potassium Salts
Potassium chloride
IV single dose
IV daily dose
Oral
Potassium phosphate
IV single dose
IV daily dose
Oral
Potassium acetate
IV single dose
IV daily dose
Potassium citrate/citric acid, oral
IV5intravenous.
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dependent on the differential diagnosis, may include a full
chemistry panel, blood gas, renin and aldosterone levels,
and genetic testing.
Urine potassium testing is not often necessary but can
be useful if there is difficulty in determining whether hy-
pokalemia is renal in origin. If a child has hypokalemia
from extrarenal loses or from the shifting of potassium in-
tracellularly, renal excretion of potassium should be mini-
mal. In the setting of hypokalemia, a urinary potassium-
to-creatinine ratio less than 15 mEq/g creatinine indicates
extrarenal loses or cellular shifting, whereas a ratio greater
than or equal to 15 mEq/g creatinine indicates renal potas-
sium wasting.
Treatment
If the child with hypokalemia is symptomatic or at very high
risk for symptoms, potassium chloride should be IV adminis-
tered, with a goal of raising the potassium concentration
enough that symptoms abate or until the potassium concen-
tration is at least 2.5 mEq/L ($2.5 mmol/L). Continuous ECG
monitoring should be performed in these settings.
If the child is asymptomatic and the potassium level is
mildly to moderately low, treatment is based on the under-
lying cause of the hypokalemia. If it is caused by potas-
sium shifting, correcting the underlying pathology may
allow potassium to move back to the extracellular space. If
the patient has a loss of potassium but the underlying
source is easily correctable and the child can resume oral
intake of food, supplemental potassium may not be re-
quired (ie, mild volume depletion).
If the underlying source of the hypokalemia cannot be cor-
rected, supplemental potassium must be provided. Oral potas-
sium is preferred over IV potassium due to an increased risk
of causing hyperkalemia when given IV and because IV potas-
sium can injure peripheral veins: concentrations of potassium
PEDIATRIC DOSE MAXIMUM/ADULT DOSE
0.5–1 mEq/kg per dose 40 mEq per dose
1–4 mEq/kg per day None
2–5 mEq/kg per day 1–4× daily 40 mEq 4× daily
0.08–0.64 mmol/kg None
0.5–2 mmol/kg per day 10–40 mmol/d
2–3 mmol/kg per day 2–4× daily 8–16 mmol 4× daily
0.5–1 mEq/kg per dose 40 mEq per dose
1–4 mEq/kg per day None
2–4 mEq/kg per day 2–4× daily 100 mEq/d (30 mEq 3× daily)
 greater than 40 mEq/L (>40 mmol/L) should be adminis-
tered only via a central venous catheter. Doses are listed in Ta-
ble 5 and are offered as a starting point only; final doses are
titrated to maintain a normal serum potassium concentration.
(20)
The formulation of a potassium supplement can vary
based on the causal pathology, although potassium chlo-
ride is used in most cases of hypokalemia. Potassium
chloride is typically readily available in IV, oral suspen-
sion, and tablet forms. Potassium phosphate can be used
when there is comorbid hypophosphatemia. IV potassium
acetate or oral potassium citrate can be provided in circum-
stances of hypokalemia and acidosis.
There are certain situations in which adjunct therapies
can be used to treat hypokalemia. These adjunct therapies
are typically used to augment urinary potassium excretion
in either chronic distal tubular sodium delivery (ie, Bartter
syndrome) or hyperaldosteronism. The most common
medications suggested in these instances include the
potassium-sparing diuretics (spironolactone, amiloride),
although angiotensin-converting enzyme inhibitors or an-
giotensin receptor blockers are occasionally used. These
adjunct treatments should be prescribed cautiously given
the risk of worsening preexisting volume depletion.
HYPERKALEMIA
Overview
Mild to moderate elevations (<6 mEq/L [<6 mmol/L]) in
serum potassium concentration typically cause no signs
and symptoms in children, but as the potassium exceeds
7 mEq/L (7 mmol/L), the risk of life-threatening clinical
manifestations increases rapidly. Rarely, rapid increases in
serum potassium above 6 mEq/L (6 mmol/L) may cause
signs and symptoms in a child at high risk.
Clinical Implications
Hyperkalemia causes an imbalance in the cell resting mem-
brane potential by altering the intracellular-to-extracellular
potassium ratio and depolarizing the cell membrane. In
muscle cells, this process causes ascending muscle weak-
ness and paralysis. In addition, depolarization in cardiac
cells causes a variety of cardiac conduction issues, which
present as palpitations and syncope. On ECG, cardiac depo-
larization appears as peaked T waves and shortening of the
QT interval when the serum potassium level is greater than
5.5 to 6.0 mEq/L (>5.5–6.0 mmol/L), prolonged PR interval
and decrease in the frequency of the P wave with potassium
level greater than 6.5 to 7.0 mEq/L (>6.5–7.0 mmol/L), and
disappearance of the P wave with widening of the QRS

Table 6. Causes of Hyperkalemia in Children

MECHANISM CAUSE
Total body potassium overload
Excess intake Iatrogenic
Large blood cell transfusions
Decreased renal clearance
Low effective arterial blood volume Dehydration
Nephrotic syndrome
Heart failure
Liver failure
Low glomerular filtration rate Acute kidney injury
Chronic kidney disease
Tubular dysfunction Type 4 renal tubular acidosis
Pyelonephritis
Sickle cell disease
Decreased mineralocorticoid activation Congenital adrenal hyperplasia
Adrenal insufficiency
Pseudohypoaldosteronism
Potassium-sparing diuretics
Angiotensin-converting enzyme inhibitors/angiotensin receptor blockers
Calcineurin inhibitors
Shifting of potassium extracellularly
Acidosis Metabolic acidosis
Respiratory acidosis
Decreased insulin Diabetes mellitus/diabetic ketoacidosis
b-Blockers
Cell breakdown Rhabdomyolysis
Tumor lysis
Hemolysis
Periodic paralysis Familial

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 complex and an eventual sinusoidal QRST complex with potas-
sium level greater than 8 mEq/L (>8 mmol/L). (21) Eventually
the child will develop ventricular fibrillation or asystole. Spe-
cific patients may experience different signs and symptoms at
variable levels of hyperkalemia.
Causes
Hyperkalemia is caused by either an excess of total body po-
tassium or increased movement of potassium from intracel-
lular to extracellular spaces (Table 6). (20) In contrast to
hypokalemia, insulin deficiency and acidosis allow potas-
sium to move extracellularly. Unique to hyperkalemia, how-
ever, are causes of cell injury that allow intracellular
solutes, including potassium, to flow into the extracellular
space. Any source of cell injury or lysis in children can
cause hyperkalemia. Hyperkalemic periodic paralysis, an
autosomal dominant sodium channel disorder that results
in acute excess shifting of potassium extracellularly, is a
rare form of hyperkalemia, and episodes of paralysis can be
triggered by anesthesia, cold temperatures, or fasting. (20)
Due to the large amount of intracellular potassium, trans-
cellular movement of potassium into the extracellular space
can cause acute symptomatic hyperkalemia; however, these
conditions do not typically cause chronic hyperkalemia
given the capacity of the kidney to remove large quantities
of potassium.
An excessive intake of potassium alone rarely causes
sustained hyperkalemia given the kidney’s ability to ex-
crete potassium. Hyperkalemia due to excessive intake of
potassium is typically only seen when very high doses of
parenteral potassium or blood products are delivered to a
patient who cannot excrete the excess potassium, such as
a neonate whose glomerular filtration rate is relatively
lower than that of older children or a child with kidney
disease.
Hyperkalemia due to total body overload is more often
secondary to decreased elimination of potassium, often
caused by impaired urinary excretion of potassium. The
most common cause of this in children is a decreased ar-
terial blood volume, typically from loss of sodium and wa-
ter via GI losses or insensible losses. The decreased
sodium in the distal nephron impairs potassium secretion
in the collecting duct; hyperkalemia is compounded by
possible comorbid acidosis from poor tissue perfusion or
administration of potassium-containing medications and
fluids. Any etiology of acute or chronic kidney disease can
lead to hyperkalemia when a low glomerular filtration rate
causes decreased filtration of both potassium and sodium,
which limits the ability of the collecting duct to secrete
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potassium. In addition, any cause of aldosterone resis-
tance or deficiency can also cause hyperkalemia by impair-
ing potassium secretion at the collecting duct.
Finally, pseudohyperkalemia is one cause of hyperkale-
mia that the clinician should be familiar with because is it
is very common in children, although it is very distinct
from other causes of hyperkalemia. Pseudohyperkalemia
is due to movement of potassium out of the cells in labo-
ratory tubes but outside of the child. In these situations,
cell lysis occurs in the laboratory specimen due to a diffi-
cult blood draw or poor handling of the sample. (22) In
pseudohyperkalemia, the laboratory result is not equal to
the child’s serum potassium level.
Evaluation
Hyperkalemia is diagnosed on routine electrolyte testing.
Before extensive evaluation of the cause of hyperkalemia,
it is critical to assess the child for cardiac or neurologic
symptoms or for risk of developing signs and symptoms.
An ECG should be obtained urgently in these cases. Once
the patient has been stabilized or the potassium level low-
ered to a safer range, further evaluation must be per-
formed to identify the cause of the hyperkalemia.
Unique to hyperkalemia is the need to exclude pseudo-
hyperkalemia. If pseudohyperkalemia is suspected, the
provider should analyze the laboratory draw technique. In
addition, a clinical history of leukemia may raise the suspi-
cion for pseudohyperkalemia as excess white blood cells
can cause release of potassium from the cell during the
clotting phase, and blood cell counts should be obtained
(noting that children with leukemia do have risks for true
hyperkalemia). Further evaluation requires assessing the
specimen for the presence of hemolysis and, if necessary,
retesting the child with a larger-gauge needle and from a
free-flowing vein without any local trauma, ideally without
the use of a tourniquet. Pseudohyperkalemia should be
suspected in asymptomatic children who have no risk fac-
tors for hyperkalemia.
After pseudohyperkalemia has been ruled out, the eval-
uation should be focused on determining the source of
the hyperkalemia. This may be apparent from the history
and physical examination findings; signs and symptoms
of severe volume depletion, polyuria/polydipsia with Kuss-
maul breathing, recent blood transfusions, intense exer-
cise, or use of contributory medications may all explain a
child’s hyperkalemia. Abnormal vital signs, including hy-
potension and tachycardia, would also raise concern for
volume depletion. In addition, a medical history of chronic
kidney disease, congenital anomalies of the urinary tract,
 or adrenal insufficiency also place a child at high risk for
hyperkalemia. If the underlying source of hyperkalemia is
not identified, further laboratory evaluation may be ex-
panded based on the patient evaluation to include BUN
and creatinine levels, serum glucose levels, blood gas, uri-
nalysis, albumin levels, liver transaminase levels, hemoglo-
bin and hematocrit levels with markers of cell breakdown,
lactate dehydrogenase and creatine kinase levels, white blood
cell counts, cortisol levels, renin levels, aldosterone levels,
and genetic testing. Furthermore, unexplained hyperkalemia
warrants imaging of the upper and lower urinary tracts and
echocardiography to evaluate for evidence of urinary obstruc-
tion, to rule out anatomic renal anomalies, and to assess for
cardiac abnormalities that could contribute to poor cardiac
output.
Urine testing is often unnecessary when evaluating
hyperkalemia but can assist in differentiating total body
potassium overload from extracellular shifting. In the
presence of hyperkalemia, the urinary potassium excretion
should be markedly elevated. Spot urine potassium level
exceeding 40 mEq/L (>40 mmol/L) is consistent with ap-
propriate urine potassium excretion and is suggestive of
excessive intake or cellular reallocation. In addition, low
urine sodium levels (<20 mEq/L [<20 mmol/L]) are con-
sistent with maximal renal sodium reabsorption seen in
severe volume depletion.
Treatment
A child with symptomatic hyperkalemia (including concern-
ing ECG changes) or a potassium concentration greater
than 7 mEq/L (>7 mmol/L) represents a medical
Table 7. Treatment of Hyperkalemia in Children
Acute hyperkalemia
Stabilize cardiac cell membrane
Calcium chloride (IV)
10% Calcium gluconate (IV)
Shift potassium intracellularly
Insulin (regular, IV)
10% Dextrose (with insulin, <5 years old, IV)
25% Dextrose (with insulin, >5 years old, IV)
Albuterol (neonate, inhaled)
Albuterol (children <25 kg, inhaled)
Albuterol (children 25–50 kg, inhaled)
Albuterol (children >50 kg, inhaled)
Sodium bicarbonate (IV)
Persistent hyperkalemia
Decrease total body potassium load
Furosemide (IV/PO) 0.5–1.0 mg/kg 1–4× daily
Sodium polystyrene sulfonate (PO/PR)
Dialysis
IV5intravenous, NA5not applicable, PO5by mouth, PR5by rectum.
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emergency. The goal of treatment in these patients is to
lower the serum potassium level to prevent life-threatening
arrhythmias. No matter the underlying pathology, treatment
in this case involves both decreasing the total body potas-
sium load and moving potassium intracellularly (Table 7).
(23) All nutrition, fluids, and medications containing potas-
sium should be discontinued. Medications that move potas-
sium intracellularly include insulin (administered with
glucose to prevent hypoglycemia), b-agonists (albuterol, ter-
butaline), and bicarbonate (noting that in the absence of
acidosis, the role of bicarbonate to treat hyperkalemia is
unclear). (24) Simultaneously, efforts should be made to
lower the total body potassium level with loop diuretics
(furosemide, bumetanide). Sodium polystyrene sulfonate,
an enteral cation exchange resin, is often used to increase
intestinal potassium excretion; however, it has a prolonged
onset of action, and its role in acute hyperkalemia is poorly
defined. If the previously mentioned therapies cannot lower
the potassium to a safer level, extracorporeal removal of po-
tassium by dialysis would be indicated; all forms of dialysis
efficiently remove total body potassium (hemodialysis, con-
tinuous renal replacement therapy, peritoneal dialysis), al-
though hemodialysis is typically the preferred modality due
to the ability to quickly obtain temporary vascular access
and the speed at which hemodialysis clears potassium. In
addition to addressing the hyperkalemia itself, emergency
treatment of hyperkalemia involves stabilization of the car-
diac membrane. This is achieved by IV administration of cal-
cium, usually in the form of calcium gluconate or calcium
chloride, which acts to decrease cardiac cell membrane excit-
ability and decrease the chance of a severe arrhythmia. This
PEDIATRIC DOSE MAXIMUM DOSE
20 mg/kg 1g
0.5 mL/kg 20 mL
0.1 U/kg 10 U
5 mL/kg NA
2 mL/kg 25 g
0.4 mg NA
2.5 mg NA
5 mg NA
10 mg NA
1 mEq/kg 50 mEq
40–80 mg 1–4× daily
1 g/kg 1–4× daily 15–30 g 1–4× daily
NA NA
Vol. 44 No. 7 JULY 2023 359
 effect is more notable in the setting of hypocalcemia; in addi-
tion, it is short-lived and may require repeated dosing for the
duration of time that the child is having an arrhythmia or is
at risk for cardiac conduction issues.
Once a child’s hyperkalemia has been determined to
be asymptomatic (and pseudohyperkalemia has been ex-
cluded), the next line of treatment depends on knowing
the underlying cause of the hyperkalemia and correcting
this cause if possible (ie, volume depletion, acidosis, use
of angiotensin-converting enzyme inhibitors or potassium-
sparing diuretics). Most cases of potassium shifting caus-
ing hyperkalemia are relatively short-lived because the re-
nal excretion of potassium can increase and the serum
potassium concentration will eventually normalize. If the
patient has a condition that cannot be corrected (chronic
kidney disease), the treatment is focused on maintaining a
normal serum potassium level by balancing intake and
output of potassium. In these cases, it is critical to work
with a registered dietitian to restrict potassium to an ap-
propriate amount without compromising nutrition. This
can be done with dietary modification or, if necessary, use
of low-potassium formulas. (23) Potassium excretion can
be augmented either by the urinary system with use of di-
uretics (loop or thiazides) or by increasing intestinal secre-
tion of potassium with the use of enteral cation exchange
resins (sodium polystyrene sulfonate), which are given
orally or rectally, or used to decant formula before admin-
istration. There are newer exchange resins available (pa-
tiromer, sodium zirconium cyclosilicate), but these are not
approved for use in pediatric patients. (25) If there are
comorbid conditions such as metabolic acidosis that are
compounding the hyperkalemia, these should be ad-
dressed with base replacement therapy. Most children
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who continue with hyperkalemia despite maximizing med-
ical treatments will have significant renal function impair-
ment; in these children, persistent hyperkalemia is an
indication for the initiation of chronic dialysis.
Summary
1. Electrolyte disorders are a common finding in
children in both the inpatient and outpatient
settings. (On the basis of research evidence
and expert opinion) (4)(7)(9)
2. Derangements of serum sodium and potassium
levels can cause significant comorbidity and
mortality. (On the basis of research evidence and
expert opinion) (3)(10)(11)(12)
3. Abnormalities of serum sodium should be
investigated as disorders of water balance, and
based on the causative pathophysiology, proper
steps should be taken to restore water
homeostasis. (On the basis of research evidence)
(1)(2)(5)
4. Abnormalities of serum potassium should
be investigated as disorders of potassium
movement and total body potassium load;
based on the causative pathophysiology, proper
steps should be taken to restore potassium
homeostasis. (On the basis of research evidence)
(9)(20)
References and teaching slides for this
article can be found at
https://doi.org/10.1542/pir.2021-005119.
 PIR QUIZ

1. An 18-month-old previously healthy girl is evaluated in the emergency

department (ED) for dehydration. The family noticed mouth sores 3 days
earlier, and her physical examination reveals mouth ulcers as well as ulcers
on her hands and feet. She drank 8 oz of fluids during the past 24 hours and
is noted to have decreased wet diapers. Laboratory evaluation reveals serum
levels of sodium, 132 mEq/L (132 mmol/L); potassium, 4.2 mEq/L (4.2 mmol/L);
chloride, 105 mEq/L (105 mmol/L); bicarbonate, 16 mEq/L (16 mmol/L); blood
urea nitrogen (BUN), 9 mEq/L; creatinine, 0.42 mg/dL (37.13 mmol/L); and glucose,
86 mg/dL (4.77 mmol/L). Which of the following substances is most likely
responsible for this patient’s hyponatremia?
A. Aldosterone.
B. Angiotensin II. REQUIREMENTS: Learners can
take Pediatrics in Review quizzes
C. Antidiuretic hormone. and claim credit online only at:
D. Cortisol. http://pedsinreview.org.
E. Renin.
To successfully complete 2023
2. A 2-year-old child is being treated in the hospital for community-acquired Pediatrics in Review articles for
pneumonia. The child is refusing to eat or drink and is being treated with AMA PRA Category 1 Credit™,
maintenance intravenous fluids and intravenous antibiotics. A basic learners must demonstrate a
metabolic panel obtained on the second day of hospitalization shows the minimum performance level of
60% or higher on this
following values: serum sodium, 130 mEq/L (130 mmol/L); potassium,
assessment. If you score less
4.0 mEq/L (4.0 mmol/L); chloride, 103 mEq/L (103 mmol/L); bicarbonate, than 60% on the assessment,
20 mEq/L (20 mmol/L); BUN, 10 mEq/L; and creatinine, 0.37 mg/dL you will be given additional
(32.71 mmol/L). The child is noted to have mild periorbital edema. Vital signs opportunities to answer
show a heart rate of 120 beats/min and a respiratory rate of 20 breaths/min. questions until an overall 60%
or greater score is achieved.
The child is requiring 0.5 L/min of oxygen by nasal canula to maintain
normal oxygen saturations. The child’s weight today is 13 kg, and weight on This journal-based CME activity
admission was 12.7 kg. Which of the following is the most appropriate is available through Dec. 31,
treatment measure for this child’s hyponatremia? 2025, however, credit will be
recorded in the year in which
A. Intravenous normal saline bolus. the learner completes the quiz.
B. Intravenous 3% saline bolus.
C. Intravenous 5% dextrose and half-normal saline at 46 mL/h.
D. Intravenous 5% dextrose and normal saline at 30 mL/h.
E. Stop intravenous fluids.
3. A 3-year-old boy was evaluated in the ED for sepsis, and a basic metabolic
panel was obtained. The results were concerning for a serum potassium 2023 Pediatrics in Review is
approved for a total of 30
level of 5.7 mEq/L (5.7 mmol/L). As you describe causes and treatments of
Maintenance of Certification
hyperkalemia to the treating resident, you explain that this potassium shift (MOC) Part 2 credits by the
can occur as a result of which of the following? American Board of Pediatrics
(ABP) through the AAP MOC
A. Acidosis.
Portfolio Program. Pediatrics in
B. Albuterol. Review subscribers can claim up
C. Alkalosis. to 30 ABP MOC Part 2 points
D. Epinephrine. upon passing 30 quizzes (and
E. Insulin. claiming full credit for each
quiz) per year. Subscribers can
start claiming MOC credits as
early as October 2023. To learn
how to claim MOC points, go
to: https://publications.aap.org/
journals/pages/moc-credit.

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 4. A 6-year-old boy is being treated for a fungal infection with amphotericin B.
He is not on supplemental intravenous fluids. A basic metabolic panel is
ordered to monitor for electrolyte abnormalities while on treatment. Which
of the following electrolyte abnormalities is most likely to be seen in this
patient?
A. Hyperchloremia.
B. Hyperkalemia.
C. Hypernatremia.
D. Hypokalemia.
E. Hyponatremia.
5. A 12-month-old girl is being evaluated in the ED for dehydration. The infant
has been having emesis and poor oral intake for the past 48 hours and has
had 4 wet diapers today. On physical examination she is alert, awake, and
noncooperative with the examination. She is clinically dehydrated. A basic
metabolic panel is obtained from a capillary blood sample that showed a
serum sodium level of 137 mEq/L (137 mmol/L); potassium, 5.9 mEq/L
(5.9 mmol/L); chloride, 103 mEq/L (103 mmol/L); bicarbonate, 20 mEq/L
(20 mmol/L); BUN, 12 mEq/L; creatinine, 0.37 mg/dL (32.71 mmol/L); and
glucose, 84 mg/dL (4.66 mmol/L). Which of the following is the most
appropriate immediate next step in management?
A. Administer calcium gluconate.
B. Administer bicarbonate.
C. Administer insulin.
D. Obtain electrocardiogram.
E. Repeat potassium level from a venous specimen.

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