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Hypernatremia in children - UpToDate 15/08/18 19(54
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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: Melanie S Kim, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2018. | This topic last updated: Mar 10, 2017.
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 (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 'Excessive weight loss'). In older 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
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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 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 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. (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
renal 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 "Clinical features and diagnosis of diabetic ketoacidosis in children and adolescents", 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 "Emergency care of moderate
and severe thermal burns in children", 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 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 'Excessive weight loss'.)
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:
● 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 [13-16]. Infants and young children are especially susceptible due to their
inability to communicate their thirst, and their reliance on others for access to water. A teaspoon of salt
contains 100 mEq of sodium (Na), which can increase the serum sodium concentration in a 10 kg child by 17
mEq/L. The unpleasant salty taste of such preparations should limit their voluntary ingestion, but in situations
of intentional poisoning these children 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, 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 [17]. (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 [16,18]. (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 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 [1,18]. (See 'Laboratory evaluation' below.)
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 [19]. 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 [14,20].
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'.)
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 [21,22]. 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 [23]. 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.
● 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 "Diagnosis of polyuria and diabetes insipidus", section on '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 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 [1,18]. (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?
● 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 [24]. (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)
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 [25]. 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) [24].
● 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 [26].
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 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 = 1000 mL
● Free water deficit – 6 L [(156/140 mEq/L) - 1] = 686 mL
● Isotonic loss – Total fluid deficit - Water deficit = 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 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.)
● 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 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.
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. 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.
18. Coulthard MG, Haycock GB. Distinguishing between salt poisoning and hypernatraemic dehydration in
children. BMJ 2003; 326:157.
19. Finberg L. Hypernatremic (hypertonic) dehydration in infants. N Engl J Med 1973; 289:196.
20. FINBERG L. Pathogenesis of lesions in the nervous system in hypernatremic states. I. Clinical
ovservations of infants. Pediatrics 1959; 23:40.
21. 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.
22. 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.
23. 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.
24. 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.
25. El-Bayoumi MA, Abdelkader AM, El-Assmy MM, et al. Normal saline is a safe initial rehydration fluid in
children with diarrhea-related hypernatremia. Eur J Pediatr 2012; 171:383.
26. 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 12.0
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
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
Renal disease
Obstructive uropathy
Sickle cell nephropathy
Nephronophthisis
Cystinosis
Osmotic diuresis
Mannitol use
Hyperglycemia
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.
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.
Contributor Disclosures
Michael J Somers, MD Nothing to disclose Avram Z Traum, MD Nothing to disclose Tej K Mattoo, MD,
DCH, FRCP Nothing to disclose Melanie S Kim, MD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a 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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Hypernatremia in children - UpToDate 15/08/18 19(54

Official reprint from UpToDate®

Authors: Michael J Somers, MD, Avram Z Traum, MD

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

● 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)

● Water loss that is not replaced

● Excessive salt intake relative to water ingestion

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

Urinary concentration defects — Impaired urinary concentration is typically due to antidiuretic

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

Other medications associated with drug-induced nephrogenic DI include amphotericin,

Iatrogenic causes — Iatrogenic causes of hypernatremia include the administration of sodium

Nonspecific initial manifestations of hypernatremia include irritability, restlessness, weakness, vomiting,

Other laboratory studies that may be included:

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

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

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

● Total fluid deficit – 10 percent of 10 kg = 1000 mL

● Free water deficit – 6 L [(156/140 mEq/L) - 1] = 686 mL

● Isotonic loss – Total fluid deficit - Water deficit = 314 mL

● 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

SUMMARY AND RECOMMENDATIONS

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

Use of UpToDate is subject to the Subscription and License Agreement.

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

Topic 14276 Version 12.0

Osmotic regulation of ADH release and thirst

ADH: antidiuretic hormone.

Graphic 65195 Version 5.0

Pediatric causes of hypernatremia due to free urinary water losses

Conditions with urinary concentration defects

Central diabetes insipidus

Nephrogenetic diabetes insipidus

Other inherited disorders or syndromes

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis

Sickle cell nephropathy

Graphic 88819 Version 2.0

Utility of urine and plasma osmolality in the evaluation of

In cases when the cause of pediatric hypernatremia remains uncertain,

Graphic 88818 Version 1.0

Total body water and its major subdivisions as a function of age

Graphic 56512 Version 2.0

Conflict of interest policy

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