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Hypernatremia in children
Authors: Michael J Somers, MD, Avram Z Traum, MD
Section Editor: Tej K Mattoo, MD, DCH, FRCP
Deputy Editor: Laurie Wilkie, MD, MS

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Dec 2022. | This topic last updated: Oct 12, 2020.

INTRODUCTION

Hypernatremia is typically defined as a serum or plasma sodium greater than 150 mEq/L.
Although pediatric hypernatremia is an uncommon electrolyte abnormality, there can be
significant neurologic injury in patients with severe hypernatremia, especially those with
acute and rapid changes in serum sodium.

The etiology, clinical findings, diagnosis, and evaluation of pediatric hypernatremia are
reviewed here.

EPIDEMIOLOGY

The true incidence of pediatric hypernatremia is unknown, as published data are based on
hospitalized children.

As an example, a Scottish study reported an overall incidence of hypernatremia (defined as a

plasma sodium >150 mEq/L) of 0.04 percent for all pediatric hospitalizations in pediatric
patients over two weeks of age over a study period from 1996 to 2006 [1]. However, the risk
of hypernatremia was 10 times greater in neonates less than two weeks of age, with an
incidence of 0.4 percent. Neonatal hypernatremia was almost exclusively seen in breastfed
infants with excessive weight loss (water loss). Of note, the incidence of neonatal
hypernatremia in breastfed infants was higher than reported in previous studies (0.03 to 0.07
percent) (see "Initiation of breastfeeding", section on 'Assessment of intake'). In older

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patients between two weeks and 17 years of age, the most common cause of hypernatremia
on admission was excess water loss due to gastroenteritis or systemic infection. However, in
this cohort, it was more common for hypernatremia to develop during hospitalization,
particularly in patients with systemic infection or those who underwent cardiac surgery. In
addition, approximately one-third of the patients had an underlying neurologic condition.

In an earlier study from a tertiary children's hospital in Texas from 1992 to 1994,
hypernatremia (defined as a serum sodium greater than 150 mEq/L) was detected in 1.4
percent of sodium values in a laboratory database, but only 0.2 percent of patients were
discharged with a diagnosis of hyperosmolality due to hypernatremia [2]. Of the 68 children
with a final discharge diagnosis of hyperosmolality/hypernatremia, two-thirds of the children
developed hypernatremia during hospitalization, and the most common cause of
hypernatremia was inadequate fluid intake.

PATHOPHYSIOLOGY

Hypernatremia is caused by an imbalance in the body's handling of water, resulting in a

relative excess of effective plasma osmolality (tonicity) to total body water. The plasma
tonicity is defined as the concentration of solutes that do not easily cross the cell membrane,
which is primarily due to sodium salts in the extracellular space. As a result, serum or plasma
sodium is used as a surrogate for assessing tonicity. (See "General principles of disorders of
water balance (hyponatremia and hypernatremia) and sodium balance (hypovolemia and
edema)", section on 'Plasma tonicity'.)

The formulas used to estimate plasma tonicity are similar to those for the plasma osmolality,
with the one exception that the contribution of urea (an ineffective osmole) is not included.
The multiplier factor of "2" accounts for the osmotic contributions of the anions that
accompany sodium, the primary extracellular cation:

● Plasma tonicity = 2 x [Na] + [glucose]/18 (if glucose is measured in mg/dL)

● Plasma tonicity = 2 x [Na] + [glucose] (if glucose is measured in mmol/L)

Plasma tonicity is tightly regulated by the release of antidiuretic hormone (ADH) from the
posterior pituitary promoting water retention, and by thirst-prompting water ingestion
( figure 1). These homeostatic mechanisms that mediate plasma tonicity and water
balance are similar in adults and children, resulting in a normal range of plasma sodium
between 135 and 145 mEq/L that does not vary by age. (See "General principles of disorders

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of water balance (hyponatremia and hypernatremia) and sodium balance (hypovolemia and
edema)", section on 'Regulation of plasma tonicity'.)

Hypernatremia is most often caused by the failure to replace water losses, which, in children,
are most commonly due to gastrointestinal fluid loss. In these patients, the sodium plus
potassium concentration in the fluid that is lost is less than the plasma sodium
concentration. As a result, water is lost in excess of sodium plus potassium, which will tend to
increase the plasma sodium concentration. In individuals with intact thirst mechanisms, the
intake of free water promptly corrects any increase in plasma sodium. However, when water
losses cannot be replaced because of a lack of free access to water, excessive loss in acute
illnesses, or impaired thirst mechanism, sodium concentration increases and may result in
hypernatremia. Infants and children who are significantly neurodevelopmentally impaired
are at particular risk for hypernatremia, as they may be unable to communicate their thirst
and are dependent on others for fluid repletion. Pediatric hypernatremia also may result
from urinary or skin loss of free water without adequate water replacement.

Less commonly, pediatric hypernatremia may be caused by intake of sodium in excess of

water (eg, administration of a hypertonic salt solution). In this setting, patients also are
unable to access free water to correct the plasma tonicity.

ETIOLOGY

The causes of pediatric hypernatremia can be separated into the two previously discussed
mechanisms that result in pediatric hypernatremia (see 'Pathophysiology' above):

● Water loss that is not replaced

● Excessive salt intake relative to water ingestion

Excess water losses — Loss of body fluids with a sodium plus potassium concentration that
is less than serum or plasma sodium (hypotonic fluids) will result in an increase in sodium
concentration if the water losses are not replaced. Sources of hypotonic body fluid losses
include gastrointestinal fluids, dilute urine, and skin loss due to sweat or burns. In addition,
inadequate water intake that fails to replace ongoing normal fluid losses will result in excess
water loss and increases in serum or plasma sodium.

Gastrointestinal loss — In children, the most common cause of hypernatremia is

hypotonic gastrointestinal losses without replacement, which result in effective water loss. In
particular, gastroenteritis due to rotavirus can present with profuse watery diarrhea and

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hypernatremia [3]. In addition, losses due to vomiting or nasogastric drainage can lead to
excess free water loss and hypernatremia.

Urinary water loss — Excessive urinary free water loss may be caused by disorders with
impaired urinary concentration (eg, diabetes insipidus [DI]) or osmotic diuresis. Without
adequate water replacement, sodium concentration will rise and may result in
hypernatremia ( table 1).

Urinary concentration defects — Impaired urinary concentration is typically due to

antidiuretic hormone (ADH) deficiency or resistance, which leads to excretion of a dilute urine
(urine osmolality less than plasma osmolality) and excessive urinary free water loss.

● Central DI – Central DI is caused by inadequate production or release of ADH. Central DI

has multiple etiologies, including congenital central nervous system (CNS)
malformations and genetic syndromes with associated CNS anomalies, and acquired
causes due to CNS tumors, infiltrative processes of the hypothalamic-pituitary stalk, and
sequelae from neurosurgery and trauma. (See "Clinical manifestations and causes of
central diabetes insipidus", section on 'Causes'.)

● Nephrogenic DI – Nephrogenic DI is caused by an inadequate renal tubular response to

circulating ADH. The multiple causes of pediatric nephrogenic DI can be further divided
into the following categories (see "Clinical manifestations and causes of nephrogenic
diabetes insipidus", section on 'Causes'):

• Congenital nephrogenic DI – Congenital nephrogenic DI is most often the result of

mutations in the vasopressin type 2 receptor (AVPR2), found at the locus Xp28. In this
X-linked disorder, male infants typically present in the first weeks of life with
fussiness, low-grade fever, and polyuria with hypernatremia. In addition, hereditary
nephrogenic DI may be caused by a mutation in the aquaporin-2 gene (AQP2) at
12q13, which encodes the ADH-sensitive water channels. Congenital nephrogenic DI
is also observed in other inherited disorders, including Bardet-Biedl and Bartter
syndromes, nephronophthisis, cystinosis, and familial hypomagnesemia with
hypercalciuria and nephrocalcinosis.

• Acquired nephrogenic DI – Drug toxicity is the most common cause of acquired DI.
Lithium toxicity is the most frequent cause of drug-induced nephrogenic DI, and its
use has increased in children and adolescents with mood disorders. Lithium also can
cause interstitial nephritis and fibrosis, further exacerbating urinary concentrating
capacity. The effects of lithium on urinary concentrating ability can be permanent.

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(See "Renal toxicity of lithium", section on 'Nephrogenic diabetes insipidus'.)

Other medications associated with drug-induced nephrogenic DI include

amphotericin, demeclocycline, ifosfamide, foscarnet, and cidofovir.

Hypercalcemia and hypokalemia also can produce functional defects in water

reabsorption that are usually reversible once the electrolyte perturbation resolves.
(See "Clinical manifestations and causes of nephrogenic diabetes insipidus", section
on 'Hypercalcemia' and "Hypokalemia-induced kidney dysfunction", section on
'Impaired urinary concentrating ability'.)

• Renal disease – In children, impaired urinary concentration is seen in a variety of

renal diseases, including obstructive uropathy, sickle cell disease, nephronophthisis,
cystinosis, and acute or chronic kidney disease. In these disorders, the decline in
urinary concentrating ability may be due to a number of different factors, including
resistance to ADH, impairment of the renal medulla countercurrent mechanism,
and/or decrease in the number of functioning nephrons, which can lead to osmotic
diuresis as the ability to reabsorb the increasing solute load is exceeded.

Osmotic diuresis — Hypernatremia can also occur from urinary water losses due to
renal excretion of nonelectrolyte, nonreabsorbed solutes, such as mannitol or glucose (eg,
patients with diabetic ketoacidosis and hyperglycemia). While the urine osmolality is
augmented with the presence of these substances, the urinary concentration of sodium plus
potassium is below plasma levels. If there is inadequate water repletion, the enhanced
urinary free water loss leads to an increase in sodium concentration, and potentially
hypernatremia. (See "Complications of mannitol therapy", section on 'Volume depletion and
hypernatremia' and "Diabetic ketoacidosis in children: Clinical features and diagnosis",
section on 'Serum sodium'.)

Skin loss — The sodium plus potassium content of sweat is less than half that of plasma,
but normal sweating causes only modest overall free water losses and does not typically lead
to hypernatremia. However, with vigorous or sustained exercise, or significant febrile illness,
water losses from sweat can become more substantial and can result in hypernatremia if not
corrected with water intake. Increased insensible water losses due to burns can also lead to
hypernatremia [4]. (See "Moderate and severe thermal burns in children: Emergency
management", section on 'Fluid resuscitation'.)

Inadequate water intake — Hypernatremia can develop if normal free water losses are
not replaced, either because of lack of access to water or lack of thirst. Infants and children

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who are dependent on others for fluid intake or who have an impaired thirst mechanism are
more vulnerable to hypernatremic hypovolemia.

Infants and young children — Compared with older children and adults, infants and
young children are at increased risk for hypernatremic hypovolemia because they have a
higher ratio of surface area to volume, resulting in greater insensible water losses from the
skin; and, while their thirst mechanism is intact, they are unable to communicate their need
for fluids and cannot independently access fluids to replenish fluid losses.

In neonates, the most common cause of hypernatremia is inadequate intake in infants who
are breastfed [1,5-8]. Careful attention to weight loss and breastfeeding adequacy has been
shown to prevent this potentially devastating complication [9]. (See "Initiation of
breastfeeding", section on 'Assessment of intake'.)

Impaired thirst mechanism — Children with structural midline brain abnormalities

may have an impaired or no thirst mechanism (adipsia or hypodipsia), which may result in
chronic hypernatremia. These lesions include congenital abnormalities, such as
holoprosencephaly [10,11], acquired lesions (eg, craniopharyngioma), and infiltrative
processes of the hypothalamic-pituitary stalk. These patients may have concomitant central
DI, and careful attention to both water intake and the use of desmopressin therapy makes
their management especially challenging. (See "Etiology and evaluation of hypernatremia in
adults", section on 'Hypothalamic lesions affecting thirst or osmoreceptor function'.)

Excess salt intake — Hypernatremia can be a consequence of salt intake out of proportion

to water. In children, excessive salt intake is generally due to iatrogenic administration of
excess sodium (eg, hypertonic saline solution), or due to salt poisoning. In either setting,
patients are unable to access free water in order to restore plasma tonicity and correct
hypernatremia.

Iatrogenic causes — Iatrogenic causes of hypernatremia include the administration of

sodium bicarbonate infusions for metabolic acidosis or hypertonic saline, which may be used
in the acute management of increased intracranial pressure. (See "Evaluation and
management of elevated intracranial pressure in adults", section on 'Hypertonic saline
bolus'.)

In addition, the administration of isotonic saline to replete hypotonic losses can also lead to
increased sodium, and potentially hypernatremia, by net sodium gain in the following
settings:

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● Uncontrolled diabetes, in which the free water lost in an osmotic diuresis from
nonreabsorbed glucose is replaced with isotonic saline.

● Recovery from acute kidney injury, in which the free water lost in an urea-induced
osmotic diuresis is replaced with isotonic saline.

● Nasogastric suction, in which patients receive isotonic saline to replace hypotonic

intestinal fluid losses with a sodium plus potassium concentration well below that of
plasma.

● Edematous, critically ill patients who have received large volumes of saline and then
receive loop diuretic therapy, which impairs renal concentrating ability, resulting in
inappropriately high water losses [12].

Salt poisoning — Salt poisoning has been described both from incorrect formula
preparation and as an intentional form of child abuse [13-17]. Infants, young children, and
individuals with significant developmental delay are especially susceptible due to their
inability to communicate their thirst, their reliance on others for access to water, and smaller
volume of distribution. A teaspoon of salt contains 100 mEq of sodium (Na), which can
increase the serum sodium concentration in a 10 kg child by 15 mEq/L. The unpleasant salty
taste of such preparations should limit their voluntary ingestion, but in situations of
intentional poisoning these individuals are often subjected to limited access to other fluids,
thereby ensuring the ingestion of the hypertonic preparations.

Salt poisoning causes a rapid onset of hypernatremia and tonicity, often resulting in cerebral
hemorrhage and irreversible neurologic injury. Osmotic demyelination can occur, similar to
the injury caused by a rapid elevation in serum sodium in patients with chronic hyponatremia
[18]. (See "Osmotic demyelination syndrome (ODS) and overly rapid correction of
hyponatremia".)

Salt poisoning has a number of distinguishing features from excessive water loss, which, as
noted above, is the most common cause of hypernatremia [16,19]. (See 'Excess water losses'
above.)

● Salt poisoning is initially associated with weight gain due to the stimulation of both
thirst, which increases fluid intake, and ADH release, which diminishes water loss. In
contrast, unreplaced water losses severe enough to produce hypernatremia are usually
associated with weight loss.

● Total urinary sodium excretion is appropriately increased with salt poisoning, and is

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appropriately reduced with hypovolemia due to unreplaced water losses. The fractional
excretion of sodium (FENa) may be useful in a patient with hypernatremia, as a FENa
greater than 2 percent in a volume-replete (well hydrated) patient is strongly suggestive
of salt poisoning, whereas a FENa less than 1 percent is suggestive of dehydration
caused by water loss [1,19]. (See 'Laboratory evaluation' below.)

More rapid correction has been safely reported for patients with acute salt poisoning who
present within 24 hours of ingestion than for those with hypernatremia due to other causes
[17].

CLINICAL MANIFESTATIONS

Acute hypernatremia — Clinical findings in acute pediatric hypernatremia are generally

manifested by neurological symptoms as water moves out of brain cells leading to cerebral
contraction. The presence and severity of symptoms correlate with the degree of plasma
sodium elevation and its rate of rise.

Nonspecific initial manifestations of hypernatremia include irritability, restlessness,

weakness, vomiting, muscular twitching, fever, and, in infants, high-pitched cry and
tachypnea [20]. Severe symptoms are observed with an acute rise of sodium above 160
mEq/L and include altered mental status, lethargy, coma, and seizures. In the most severe
cases, such as salt poisoning, the rapid rise in sodium leads to acute brain shrinkage,
resulting in vascular rupture with cerebral and subarachnoid hemorrhage, demyelination,
and irreversible neurologic injury [14,21].

Because the most common cause of pediatric hypernatremia is excessive fluid losses,
patients may also have manifestations of hypovolemia, including tachycardia, orthostatic
blood pressure changes or decreased blood pressure, dry mucous membranes, and
decreased peripheral perfusion with a delay in capillary refill. (See "Clinical assessment and
diagnosis of hypovolemia (dehydration) in children", section on 'Clinical assessment'.)

Chronic hypernatremia — It appears that patients with chronic hypernatremia (defined as

hypernatremia that is present more than one day) are asymptomatic due to cerebral
adaption, which occurs within one to three days. This process involves restoration of brain
volume by water movement from the cerebrospinal fluid into the brain, and generation and
uptake of intracellular solutes (osmolytes) that promote water movement into the brain cells.
(See "Manifestations of hyponatremia and hypernatremia in adults", section on 'Cerebral
adaptation to hypernatremia'.)

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In addition, it may be difficult to appreciate nonspecific findings, as many of these patients

have underlying neurologic conditions (midline brain abnormalities) [10,11]. (See 'Inadequate
water intake' above.)

DIAGNOSIS

The diagnosis of hypernatremia is made by the detection of an elevated plasma or serum

sodium level above 150 mEq/L. Clinicians need to be aware that sodium values in capillary
and non-capillary whole blood samples tend to be 2 to 3 mEq/L lower than measurements
using venous samples [22,23]. Measurements obtained via blood gas analyzers may be even
lower [24], necessitating familiarity with the technique used in a clinical setting. For patients
in whom ongoing monitoring of sodium is needed, this variation based on sampling
technique and method of analysis should be kept in mind while managing patients with
abnormal sodium values.

Transient hypernatremia (in which the serum sodium concentration can rise by as much as
10 to 15 mEq/L within a few minutes due to water loss into cells) can be induced by severe
exercise or seizures. Sodium returns to normal within 5 to 15 minutes after the cessation of
exercise or seizures. (See "Etiology and evaluation of hypernatremia in adults", section on
'Water loss into cells'.)

In addition, spuriously falsely elevated sodium values have been observed in ill neonates
with hypoalbuminemia (plasma albumin <30 g/L) in whom sodium is measured by indirect
ion-selective electrodes, commonly utilized in main laboratory analyzers [25]. This artifact is
circumvented by measurements using direct ion-selective electrodes found in point-of-care
blood analyzers.

EVALUATION

The evaluation in pediatric hypernatremia is focused on determining the underlying etiology.

However, evaluation should be delayed in the severely ill patient who requires fluid
resuscitation.

Clinical evaluation — The underlying etiology of hypernatremia is usually evident from the

history. Because pediatric hypernatremia is most often due to unreplaced hypotonic fluid
losses, the history focuses on whether there are increased body fluid losses (eg, diarrhea) or
inadequate fluid intake.

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● History of excess gastrointestinal losses because of the presence of watery stools with
documentation of the frequency and amount, or loss from nasogastric or colostomy
drainage.

● History of impaired urinary concentration based on excessive urine output (polyuria)

and dilute appearance. Urinary concentrating defect is suggested in infants who
regularly and frequently soak through their diapers every few hours, and in older
children with increased frequency of voiding, including nighttime voiding. In addition,
questions about the appearance of the urine may be helpful, as a child with impaired
concentration typically has urine that looks like water with little or no odor (dilute), and
does not ever have a concentrated urine typically characterized by a yellow appearance,
which may be accompanied by a strong ammonia odor.

● Neurologic impairment, particularly with midline brain defect, which is associated with
impaired thirst mechanism, or inability to independently access free water.

● In breastfed infants, history of intake is assessed by whether there is successful latch-

on, the frequency of feeding, mother's feeling of milk release, and whether the infant
appears satiated following feeding. (See "Initiation of breastfeeding".)

Laboratory evaluation — Laboratory studies should preferably be obtained before

significant fluid intervention has taken place, although fluid therapy should never be delayed
in the severely ill patient.

When the underlying diagnosis remains uncertain, comparing the urine with plasma
osmolality may be helpful in establishing the underlying mechanism and diagnosis
( algorithm 1).

● Urine osmolality less than plasma osmolality is consistent with a urinary concentrating
defect (ie, diabetes insipidus [DI]), which is usually due to a defect in either the release
or response to antidiuretic hormone (ADH). Further evaluation to delineate between
central and nephrogenic DI is based on the child's urinary response to water
deprivation and the subsequent administration of desmopressin, which is discussed
elsewhere. (See "Evaluation of patients with polyuria", section on 'Protocol in infants
and children'.)

● Urine osmolality greater than plasma osmolality demonstrates that the secretion and
response to ADH is intact. In this setting, hypernatremia is typically caused by free
water loss from the gastrointestinal tract or skin and inadequate water intake, and less

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frequently by osmotic diuresis or excess salt intake (ie, iatrogenic causes or salt
poisoning).

Other laboratory studies that may be included:

● Serum BUN and creatinine to determine renal function. Serum creatinine is also used to
calculate the fractional excretion of sodium (FENa).

● Serum/plasma and urine measurements of sodium and creatinine.

• Urine sodium is typically low (<25 mEq/L) in patients with hypernatremic

hypovolemia, generally due to gastrointestinal losses.

• In contrast, urine sodium exceeds 200 mEq/L in patients with salt poisoning [1].

• Fractional excretion of sodium (FENa) may be useful, as a FENa greater than 2

percent is strongly suggestive of salt poisoning, whereas a FENa less than 1 percent
is suggestive of hypernatremia caused by water loss [1,19]. (See "Acute kidney injury
in children: Clinical features, etiology, evaluation, and diagnosis", section on
'Fractional excretion of sodium'.)

TREATMENT

General principles — Correction of hypernatremia requires both the administration of dilute

fluids to correct the water deficit and, when appropriate, interventions to limit further water
loss. Many pediatric patients also have a concurrent volume isotonic deficit usually due to
gastrointestinal losses. Such patients with hypernatremia will require replacement of both
water and electrolyte deficits. In these patients, it is important to assess the volume status as
in the setting of significant hypovolemia, because in patients with moderate to severe
hypovolemia, fluid resuscitation with isotonic fluid to restore intravascular volume and tissue
perfusion takes precedence over correction of the hypernatremia. (See "Treatment of
hypovolemia (dehydration) in children", section on 'Emergent fluid repletion phase'.)

In cases where hypernatremia alone is the primary abnormality, therapy is aimed at

correcting the plasma sodium by providing free water and determining a rate of desired
correction. Issues that need to be addressed when treating pediatric hypernatremia are:

● What is the volume status of the patient? Is there an emergent need for fluid
resuscitation to restore intravascular volume and tissue perfusion?

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● What is the magnitude of the water deficit that needs to be restored?

● At what rate should the hypernatremia be corrected (as lowering the sodium
concentration too rapidly may lead to neurologic injury)?

● Is there a concurrent ongoing fluid loss that needs to be addressed?

● What is the underlying cause of hypernatremia and are there specific interventions that
need to be considered?

Management also includes ongoing monitoring of the patient's fluid status with frequent
clinical examinations and follow-up laboratory evaluation, including subsequent assessment
of sodium levels. Based on these data, the initial fluid prescription may need to be revised.

Volume status and emergent fluid resuscitation — In any child with significant volume
depletion, first management steps should be directed toward ensuring cardiovascular
stability. In patients with moderate to severe hypovolemia, emergent fluid resuscitation with
isotonic fluid is administered to restore intravascular volume and tissue perfusion. However,
overzealous fluid resuscitation needs to be avoided to prevent inadvertent volume overload,
which may be associated with cerebral edema [26]. (See "Treatment of hypovolemia
(dehydration) in children", section on 'Emergent fluid repletion phase'.)

Calculating the free water deficit — With the restoration of effective intra-arterial volume,
or in cases where there is no need for urgent volume expansion, the focus turns to providing
the fluid necessary to correct any existing hypovolemia, and enough free water to correct the
hypernatremia.

The volume of free water to be provided can be calculated using one of two common
approaches:

● Free water deficit in milliliters = Current total body water x ([current plasma Na/140] - 1)

For this equation, estimating total body water (TBW) as 60 percent of the child's weight in
kilograms (0.6 L/kg) is a reasonable starting point for the purposes of calculating fluid
replacement. The exact proportion varies as a child progresses from infancy to adolescence,
and is lower in obese individuals ( figure 2). Thus, in a 6 kg infant with a plasma sodium of
160, the free water deficit is: (0.6 L/kg) x (6 kg) x ([160/140] – 1) = 0.51 liters or 510 mL.

● Free water deficit in milliliters = (4 mL/kg) x (weight in kg) x (desired change in plasma
Na)

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This approach uses the estimate that the provision of 4 mL/kg of free water will lower plasma
sodium by approximately 1 mEq/L. For the 6 kg infant described above with plasma sodium
elevated 20 mEq/L above desired, his or her water deficit would be: (4 mL/kg) x (6 kg) x (20
mEq/L change) = 480 mL.

The variation in free water needed between the two calculations is generally clinically
negligible and, in any case, the equations are used as estimates with follow-up laboratory
results and clinical exams guiding ongoing changes.

Prescribed fluid — Free water calculations provide for an estimate of the amount of water
without sodium needed to return plasma sodium to a normal concentration. However, in
most clinical settings, the administered fluid typically contains sodium, but is hypotonic to
the patient's plasma, thereby providing free water. As an example, the 500 mL free water
deficit in the example above could be delivered with the administration of 1 liter of 0.45
percent saline. In addition, normal saline (0.9 percent saline) is isotonic in patients with
normal plasma sodium; however, it is a hypotonic fluid for children with hypernatremia, and
accordingly can be used as initial rehydration fluid for patients with hypernatremic
hypovolemia [27]. Enteral fluids including oral rehydration therapy are also typically
hypotonic fluids.

Rate of correction — It is important to determine the chronicity of hypernatremia when

determining the rate of correction. As mentioned previously, in patients with chronic
hypernatremia, cerebral adaption to hypernatremia takes place over the first few days with
restoration of brain volume. In these patients, there is a risk of cerebral edema with rapid
provision of free water. Even in cases where hypernatremia is known to have occurred
acutely, similar rates of correction are generally used out of caution, especially with more
pronounced aberrations in plasma sodium.

For children with chronic hypernatremia (plasma sodium ≥150 mEq/L for greater than 24
hours) or those with acute severe hypernatremia (plasma sodium >160 mEq/L), we and other
experts recommend that a rate of correction does not exceed a fall of sodium greater than
0.5 mEq/L per hour (ie, 10 to 12 mEq/L per day). The following studies provide support for
this recommendation:

● In a retrospective case control study of 97 children with hypernatremia and dehydration

with a mean baseline serum sodium of 165 mEq/L, patients who developed cerebral
edema had a significantly faster rate of correction compared with those without
complications following correction of hypernatremia (1.0 versus 0.5 mEq/L per hour)

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[26].

● Similar findings were noted in another report in which the rate of reduction in serum
sodium was 1.0 mEq/L per hour in the nine infants who developed seizures compared
with 0.6 mEq/L per hour or less in 31 infants who did not develop seizures [28].

Ongoing losses and maintenance needs — The above calculations correct free water losses
that have occurred up to the time of presentation. Children have ongoing normal
maintenance needs and may also have excess free water losses not accounted for by
calculations for maintenance fluids (eg, continuing diarrhea or persistent fever), and should
receive replacement of these ongoing losses to prevent further electrolyte derangement.
Since ongoing losses can fluctuate over time, it can be challenging to try to estimate them
for inclusion in a fluid and electrolyte prescription that addresses current deficits as well.
Accordingly, many clinicians will prescribe fluid orders to address current needs and desired
rates of correction, and write separate orders to address ongoing losses. (See "Maintenance
intravenous fluid therapy in children".)

Treatment of specific etiologies — The initial evaluation and management of

hypernatremia usually occur concurrently. As noted above, obtaining additional laboratory
studies for evaluation should not delay initiation of fluid therapy for the critically ill child.
Although most young children develop hypernatremia related to acute illness or inability to
take in fluid, in cases where a chronic condition is identified, such as nephrogenic or central
diabetes insipidus, therapy directed to the underlying condition (eg, administration of
desmopressin) should be initiated in addition to providing free water replacement.

Clinical example — The following case synthesizes the information presented above in an

attempt to show how the principles are applied clinically. A 10 kg child (TBW 0.6 times body
weight) is estimated to have a 10 percent hypovolemic loss (approximately 1 liter of fluid) and
a serum/plasma sodium concentration of 156 mEq/L. The following calculations can be
made:

● Total fluid deficit: 10 percent of 10 kg = 1 L (1000 mL)

● Free water deficit: 6 L [(156/140 mEq/L) - 1] = 0.686 L (686 mL)
● Isotonic loss: Total fluid deficit - Water deficit = 1000 mL – 686 mL = 314 mL

During the emergent fluid phase, the patient received a 20 mL/kg bolus of normal saline (200
mL), replacing all but 114 mL of the isotonic fluid loss. Subsequent therapy includes
replacement of the free water deficit (686 mL) and remaining isotonic loss (114 mL),
maintenance of usual daily sodium and fluid needs (1000 mL/day of one-quarter isotonic

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saline in this case), and any excess ongoing loss of fluid and electrolyte. The water deficit
should be replaced over at least 36 hours so that the sodium is lowered at a rate below 0.5
mEq/L per hour. This is often accomplished by replacing two-thirds of the free water deficit
over the first 24 hours and the remainder over the next 12 or more hours.

Over the first 24 hours, the fluid regimen, which does not include replacement of excess
ongoing losses, would entail:

● Free water deficit (two-thirds of total water deficit) = 460 mL

● Remaining isotonic deficit = 114 mL of water and 17 mEq of sodium
● Maintenance needs = 1000 mL of water and 30 mEq of sodium

In this case, administration of one-quarter isotonic saline at 65 mL/hour would provide

adequate replacement of maintenance needs and remaining isotonic deficit, and would
provide free water at a rate lower than the maximum threshold rate of 0.5 mEq/L per hour.
Enteral fluids can also be used to replace free water deficits and provide maintenance needs.

SUMMARY AND RECOMMENDATIONS

● Hypernatremia is defined as a serum or plasma sodium greater than 150 mEq/L and is
an uncommon problem in children. Pediatric hypernatremia is most commonly seen in
the newborn period due to inadequate intake in breastfeeding neonates. In older
children, the most common cause of hypernatremia is excess water loss from
gastroenteritis or systemic infection. (See 'Epidemiology' above.)

● Hypernatremia is due to imbalance of the body's handling of water resulting in an

excess of plasma tonicity to total body water. In children, hypernatremia is usually
caused by loss of body fluids with a sodium plus potassium concentration that is less
than serum or plasma sodium. These losses are from the gastrointestinal tract, urine,
or skin. Less frequently, pediatric hypernatremia can be caused by excess salt intake,
including iatrogenic administration and salt poisoning. (See 'Pathophysiology' above
and 'Etiology' above.)

● Infants and small children are more vulnerable to hypernatremia than older individuals
because of greater insensible water losses and their inability to communicate their
need for fluids and access fluids independently. (See 'Infants and young children'
above.)

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● Clinical findings are generally manifested by neurological symptoms in patients with

acute hypernatremia as water moves out of brain cells leading to cerebral contraction.
The presence and severity of symptoms correlate with the degree of plasma or serum
sodium elevation and its rate of rise, and range from nonspecific findings (eg,
irritability, restlessness, weakness, vomiting, muscular twitching, fever, and, in infants,
high-pitched cry and tachypnea) to severe neurologic findings of altered mental status,
lethargy, coma, seizures, intracerebral and subarachnoid hemorrhage, and
demyelination. Most patients with chronic hypernatremia (defined as hypernatremia
that is present more than one day) are asymptomatic as cerebral adaption restores
brain volume. (See 'Clinical manifestations' above.)

● The diagnosis of hypernatremia is made by the detection of an elevated plasma or

serum sodium level above 150 mEq/L. (See 'Diagnosis' above.)

● The diagnostic evaluation of hypernatremia is focused on determining the underlying

cause of hypernatremia. However, it should be delayed in the severely ill patient who
requires fluid resuscitation. In most cases, the etiology of hypernatremia is evident
from the history. When the underlying diagnosis remains uncertain, comparing the
urine with plasma osmolality may be helpful in identifying children with urinary
concentrating defects (ie, diabetes insipidus [DI]) from those with water losses from the
skin or gastrointestinal tract. In addition, urinary sodium and fractional excretion of
sodium may help differentiate between hypernatremia due to water loss and salt
ingestion/poisoning ( algorithm 1 and table 1). (See 'Evaluation' above.)

● Treatment of hypernatremia consists of correcting hypernatremia with both the

administration of dilute fluids to correct the water deficit, and, when appropriate,
interventions to limit further water loss. Management of pediatric hypernatremia
includes determining the volume status of the patient, the magnitude of the water
deficit, and the safe rate of sodium correction; and identifying maintenance fluid needs,
excess ongoing losses not included in maintenance fluid calculation, and the etiology of
hypernatremia. In addition, readjustment of therapy is based on data from ongoing
monitoring of the patient's fluid status based on frequent clinical examinations and
follow-up laboratory evaluation, including subsequent assessment of sodium levels.
(See 'Treatment' above.)

• We recommend that the rate of correction in chronic pediatric hypernatremia or

severe acute hypernatremia (sodium greater than 160 mEq/L) does not exceed a fall
of 0.5 mEq/L per hour (ie, 10 to 12 mEq/L per day) (Grade 1B). Faster rates of

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correction are associated with a higher risk of cerebral edema. (See 'Rate of
correction' above.)

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REFERENCES

1. Forman S, Crofton P, Huang H, et al. The epidemiology of hypernatraemia in hospitalised

children in Lothian: a 10-year study showing differences between dehydration,
osmoregulatory dysfunction and salt poisoning. Arch Dis Child 2012; 97:502.

2. Moritz ML, Ayus JC. The changing pattern of hypernatremia in hospitalized children.
Pediatrics 1999; 104:435.

3. Kaiser P, Borte M, Zimmer KP, Huppertz HI. Complications in hospitalized children with
acute gastroenteritis caused by rotavirus: a retrospective analysis. Eur J Pediatr 2012;
171:337.

4. Namdar T, Stollwerck PL, Stang FH, et al. Transdermal fluid loss in severely burned
patients. Ger Med Sci 2010; 8:Doc28.

5. Cooper WO, Atherton HD, Kahana M, Kotagal UR. Increased incidence of severe
breastfeeding malnutrition and hypernatremia in a metropolitan area. Pediatrics 1995;
96:957.

6. Moritz ML, Manole MD, Bogen DL, Ayus JC. Breastfeeding-associated hypernatremia: are
we missing the diagnosis? Pediatrics 2005; 116:e343.

7. Oddie S, Richmond S, Coulthard M. Hypernatraemic dehydration and breast feeding: a

population study. Arch Dis Child 2001; 85:318.

8. Oddie SJ, Craven V, Deakin K, et al. Severe neonatal hypernatraemia: a population based
study. Arch Dis Child Fetal Neonatal Ed 2013; 98:F384.

9. Iyer NP, Srinivasan R, Evans K, et al. Impact of an early weighing policy on neonatal
hypernatraemic dehydration and breast feeding. Arch Dis Child 2008; 93:297.

10. Schaff-Blass E, Robertson GL, Rosenfield RL. Chronic hypernatremia from a congenital
defect in osmoregulation of thirst and vasopressin. J Pediatr 1983; 102:703.

11. König R, Beeg T, Tariverdian G, et al. Holoprosencephaly, bilateral cleft lip and palate and
ectrodactyly: another case and follow up. Clin Dysmorphol 2003; 12:221.

12. Hoorn EJ, Betjes MG, Weigel J, Zietse R. Hypernatraemia in critically ill patients: too little
water and too much salt. Nephrol Dial Transplant 2008; 23:1562.

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13. Paut O, André N, Fabre P, et al. The management of extreme hypernatraemia secondary
to salt poisoning in an infant. Paediatr Anaesth 1999; 9:171.

14. FINBERG L, KILEY J, LUTTRELL CN. Mass accidental salt poisoning in infancy. A study of a
hospital disaster. JAMA 1963; 184:187.

15. Meadow R. Non-accidental salt poisoning. Arch Dis Child 1993; 68:448.

16. Wallace D, Lichtarowicz-Krynska E, Bockenhauer D. Non-accidental salt poisoning. Arch

Dis Child 2017; 102:119.

17. Blohm E, Goldberg A, Salerno A, et al. Recognition and Management of Pediatric Salt
Toxicity. Pediatr Emerg Care 2018; 34:820.

18. Dobato JL, Barriga FJ, Pareja JA, Vela L. [Extrapontine myelinolyses caused by iatrogenic
hypernatremia following rupture of a hydatid cyst of the liver with an amnesic syndrome
as sequela]. Rev Neurol 2000; 31:1033.

19. Coulthard MG, Haycock GB. Distinguishing between salt poisoning and hypernatraemic
dehydration in children. BMJ 2003; 326:157.

20. Finberg L. Hypernatremic (hypertonic) dehydration in infants. N Engl J Med 1973;

289:196.

21. FINBERG L. Pathogenesis of lesions in the nervous system in hypernatremic states. I.

Clinical ovservations of infants. Pediatrics 1959; 23:40.

22. Levene I. Towards evidence based medicine for paediatricians. Question 1: Is

measurement of sodium from capillary blood accurate enough for clinical decision
making? Arch Dis Child 2014; 99:481.

23. Morimatsu H, Rocktäschel J, Bellomo R, et al. Comparison of point-of-care versus central

laboratory measurement of electrolyte concentrations on calculations of the anion gap
and the strong ion difference. Anesthesiology 2003; 98:1077.

24. 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.

25. King RI, Mackay RJ, Florkowski CM, Lynn AM. Electrolytes in sick neonates - which sodium
is the right answer? Arch Dis Child Fetal Neonatal Ed 2013; 98:F74.

26. Fang C, Mao J, Dai Y, et al. Fluid management of hypernatraemic dehydration to prevent
cerebral oedema: a retrospective case control study of 97 children in China. J Paediatr
Child Health 2010; 46:301.

27. El-Bayoumi MA, Abdelkader AM, El-Assmy MM, et al. Normal saline is a safe initial

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rehydration fluid in children with diarrhea-related hypernatremia. Eur J Pediatr 2012;

171:383.

28. Kahn A, Brachet E, Blum D. Controlled fall in natremia and risk of seizures in hypertonic
dehydration. Intensive Care Med 1979; 5:27.
Topic 14276 Version 18.0

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GRAPHICS

Osmotic regulation of ADH release and thirst

Relation between plasma ADH concentration and plasma osmolality in

normal humans in whom the plasma osmolality was changed by varying the
state of hydration. The osmotic threshold for thirst is a few mosmol/kg higher
than that for ADH.

ADH: antidiuretic hormone.

Data from Robertson GL, Aycinena P, Zerbe RL. Neurogenic disorders of osmoregulation. Am J
Med 1982; 72:339.

Graphic 65195 Version 5.0

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Pediatric causes of hypernatremia due to free urinary water losses

Conditions with urinary concentration defects

Central diabetes insipidus

Congenital

Central nervous system malformations (eg, holoprosencephaly)

Genetic causes

Acquired

Central nervous system tumors (eg, craniopharyngioma)

Infiltrative processes

Postneurosurgery

Trauma

Nephrogenetic diabetes insipidus

Congenital

X-linked (Xp28)

Autosomal (12q13)

Other inherited disorders or syndromes

Bardet-Biedl syndrome

Bartter syndrome

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis

Acquired

Drug induced

Lithium

Amphotericin

Demeclocycline

Ifosfamide

Foscarnet

Cidofovir

Electrolyte abnormalities

Hypercalcemia

Hypokalemia

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Renal disease

Obstructive uropathy

Sickle cell nephropathy

Nephronophthisis

Cystinosis

Osmotic diuresis
Mannitol use

Hyperglycemia

Graphic 88819 Version 2.0

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Utility of urine and plasma osmolality in the

evaluation of pediatric hypernatremia

In cases when the cause of pediatric hypernatremia remains

uncertain, comparing the urine osmolality (Uosm) with the plasma
osmolality (Posm) may be helpful in establishing the underlying
etiology. Uosm that is less than Posm suggests that the child has a
concentrating defect, which increases the likelihood of excess
urinary water loss. In contrast, children with Uosm greater than
Posm have an intact urinary concentrating mechanism and are more
likely to have hypernatremia due to excess gastrointestinal or skin
water loss, or excess salt intake.

Graphic 88818 Version 2.0

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Total body water and its major subdivisions as a function of

age

Data from: Friis-Hansen B. Body water compartments in children: changes during growth and
related changes in body composition. Pediatrics 1961; 28:169.

Graphic 56512 Version 2.0

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Contributor Disclosures
Michael J Somers, MD No relevant financial relationship(s) with ineligible companies to
disclose. Avram Z Traum, MD No relevant financial relationship(s) with ineligible companies to
disclose. Tej K Mattoo, MD, DCH, FRCP Consultant/Advisory Boards: Alnylam Pharmaceuticals [Primary
hyperoxaluria]. All of the relevant financial relationships listed have been mitigated. Laurie Wilkie,
MD, MS No relevant financial relationship(s) with ineligible companies to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level 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.

Conflict of interest policy

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