Received: 2 October 2021 | Revised: 25 October 2021 | Accepted: 28 October 2021

DOI: 10.1111/apa.16170

MINI REVIEW

Diagnosis and management of hypernatraemia in children

Jakub Zieg

Department of Paediatrics, Second

Medical Faculty, Motol University Abstract
Hospital, Charles University, Prague,
Hypernatraemia is most commonly caused by excessive loss of solute-­free water or
Czech Republic
decreased fluid intake; less often, the aetiology is salt intoxication. Especially infants,
Correspondence
young children and individuals with a lack of access to water are at risk of develop-
Jakub Zieg, Department of Paediatrics,
Second Faculty of Medicine, Motol ing hypernatraemia. Diagnosis is based on detailed history, physical examination and
University Hospital, Charles University,
basic laboratory tests. Correction of hypernatraemia must be slow to prevent cerebral
V Úvalu 84, 150 06 Prague 5, Czech
Republic. oedema and irreversible brain damage. This article reviews the aetiology, differential
Email: jakubzieg@hotmail.com
diagnosis and management of conditions associated with paediatric hypernatraemia.
Funding information Distinguishing states with water deficiency from states with salt excess is important
This work was supported by the project
for proper management of hypernatraemic patients.
(Ministry of Health, Czech Republic) for
conceptual development of research
organization 00064203 (University KEYWORDS
Hospital Motol, Prague, Czech Republic) children, hypernatraemia, plasma osmolality, salt excess, water loss

1 | I NTRO D U C TI O N
Hypernatraemia is defined as a serum concentration of sodium
above 145 mmol/L. This electrolyte abnormality is encountered less
frequently in children compared to hyponatraemia; however, rapid
diagnosis of hypernatraemia is necessary to prevent neurologic in-
jury due to a decrease in the intracellular water content of brain cells.
The most common aetiology is dehydration secondary to gastroen-
teritis or systemic infection, and insufficient breastfeeding may also
result in hypernatraemic dehydration, but cases of salt poisoning can
occur, mainly in young infants.1,2 Hypernatraemia may also be a pre-
senting sign of a urine concentration defect. Generally, infants and
young children are at higher risk of developing hypernatraemia due
to their small mass-­to-­surface ratio.3 Most cases are mild, but espe-
cially sodium levels of 160 mmol/L and higher require rapid clinical
assessment, a differential diagnostic process and adequate treat-
ment, because improper management can lead to severe complica-
4
tions. This mini review discusses the common aetiology, diagnostics
and management strategies in paediatric hypernatraemic states.
2 | R EG U L ATI O N O F PL A S M A
OS M O L A LIT Y A N D S E RU M S O D I U M LE V E L S
Water is essential for the human body to function. Approximately
60% of body weight in adults is attributable to water. While the in-
tracellular compartment (ICC) is the largest and represents about
two-­thirds of total body water, the extracellular compartment (ECC)
comprising plasma, interstitial and transcellular fluid contains the
remaining one-­third. Children have higher body water content was
compared to adults. Water comprises 75% of term newborns and
even more in preterm infants. Unlike adults, water is distributed
equally between the ICC and ECC in term neonates.5 Adult values
of the ICC and ECC proportions are reached by the age 1–­3 years.6
The water in the human body is moved across semipermeable
membranes via special channels called aquaporins and by osmosis.
Thus, the content of water is determined by osmotically active par-
ticles creating tonicity in individual compartments. There are two
major sources of water: the water content in the diet and metabolic
water produced by the oxidation of ingested food. Urine, faeces,

Abbreviations: ADH, antidiuretic hormone; DIDMOAD, diabetes insipidus, diabetes mellitus, optic atrophy, deafness; ECC, extracellular compartment; FENa, sodium fractional
excretion; GFR, glomerular filtration rate; ICC, intracellular compartment; RAA, renin–­angiotensin–­aldosterone.

© 2021 Foundation Acta Pædiatrica. Published by John Wiley & Sons Ltd

Acta Paediatrica. 2022;111:505–510.  wileyonlinelibrary.com/journal/apa | 505

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506
sweating, breathing and insensible perspiration are the main routes
of water elimination. Importantly, urine output represents the major
mechanism of external water balance.7
Plasma osmolality and blood pressure are the main determi-
nants of water homoeostasis. On the other hand, impaired ability
of kidneys to excrete sodium and to control extracellular volume
is an important risk factor for hypertension.8 Plasma osmolality is
defined as the concentration of all the solutes in a given weight of
water. It is maintained by osmoregulation within normal limits (275–­
290 mmol/L) and is primarily determined by the sodium (Na) concen-
tration. Plasma osmolality may be directly measured or calculated
using serum values of sodium, glucose and urea. Under physiological
conditions, an increase in plasma osmolality stimulates thirst and ar-
ginine vasopressin, also known as antidiuretic hormone (ADH) se-
cretion.9 In contrast, plasma hypoosmolality causes the suppression
of ADH release. Tonicity is the effective osmolality and reflects the
content of effective osmoles providing the driving force for water
movement into the compartment of greater tonicity. Hypotonic
plasma causes cellular swelling (e.g. brain oedema), while on the other
hand hypertonic plasma leads to cell shrinkage. Significant changes
in osmolality may lead to life-­threatening conditions affecting brain
cells. The pre-­prohormone of ADH is synthetized in the hypothala-
mus, and ADH is then stored in the posterior hypophysis. It regulates
body water retention by reducing the water lost to the urine. Apart
from hyperosmolality, hypovolemia also stimulates AVP release to a
lesser extent by the action of baroreceptors that sense the intravas-
cular pressure and respond to stretching of the vessel wall, providing
information to the central nervous system and regulating the release
of ADH. While low-­pressure receptors are located in larger veins, the
atria and lungs, high-­pressure receptors reside in the carotid sinus
and aortic arch.10 Stimulation of both types of baroreceptors leads to
ADH secretion in states with extracellular depletion.
Intravascular dehydration also causes the activation of the
renin–­angiotensin–­aldosterone (RAA) axis, which results in water
retention and an increase in blood pressure by increasing sodium
and water reabsorption and arteriolar tone.11,12 ADH contributes to
blood pressure maintenance not only by water reabsorption but also
13
by its direct vasopressor effect. Small decreases in blood pressure
have little effect, but more significant falls in blood pressure will sac-
rifice concentration for volume and release ADH, even in patients
with hypoosmolar plasma. There are other non-­osmotic stimuli that
promote ADH release, such as nausea, hypoxia, acute hypoglycae-
14
mia, motion sickness, alcohol, morphine and nicotine. In the kid-
neys, ADH acts through V2 receptors on the principal cells of the
renal distal tubules and collecting ducts by increasing the number
of aquaporin 2 receptors, i.e. molecular water channels in the apical
membranes.
There are only very discreet variations in plasma osmolality de-
spite changes in water intake and excretion. The amount of water
loss varies on a daily basis depending on body temperature, physi-
cal activity and environmental conditions. The kidneys can regulate
urine osmolality within a large range, from 50 to 900–­1400 mmol/L
15
in adults.
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ZIEG
Key Notes
• Hypernatraemia is an uncommon electrolyte abnormal-
ity, which may lead to severe neurologic damage.
• Distinguishing states with water deficiency from the
states of salt excess is important for the adequate
therapy.
• The review summarizes the current view of the physi-
ology of water and sodium homoeostasis and practical
approach to diagnosis and management of a hyper-
natraemic child.
A well-­preserved thirst mechanism that stimulates the desire to
drink is very important in disorders of urinary concentration as it
prevents dehydration. Central osmoreceptors are neurons located
in the organum vasculosum of the lamina terminalis and in subfor-
nical organ in hypothalamus outside the hemato-­encephalic barrier.
These cells are able to transform osmotic stimuli to electric signals
and to send the information to neurons responsible for the produc-
tion of ADH.16 Central osmoreceptors are very sensitive; even a 1%
variation in plasmatic osmolarity is sufficient to determine signifi-
cant modifications in ADH secretion. The threshold for cessation
of ADH release corresponds to a plasma osmolarity <275 mmol/kg,
while for plasma osmolarity >284 mmol/kg or higher, the ADH con-
centration rises linearly.17 The brain generates efferent neural out-
put via the sympathetic nervous system, and outgoing stimuli can
change the heart rate, cardiac output and peripheral vascular tone.
Recently, peripheral osmoreceptors were discovered in the thoracic
dorsal root ganglia that innervate hepatic blood vessels in mice.18
Other receptors that play an important role in maintaining body
fluid balance are flow receptors in the juxtaglomerular apparatus.
Upon stimulation, these receptors are able to moderate blood flow in
the afferent arteriole by a mechanism of tubuloglomerular feedback.
Increased tubular flow causes vasoconstriction of the afferent arte-
riole with a decreased glomerular filtration rate (GFR). This prevents
water loss in conditions with increased GFR. Increased tubular flow
also inhibits renin release. Atrial and brain natriuretic peptide both
produced in the heart play an important role in natriuresis. They act
directly on tubules to decrease sodium tubular reabsorption, facil-
itate sodium excretion and block the effect of the RAA system.14
3 | A E TI O LO G Y O F H Y PE R N ATR A E M I A
As hyponatraemia is commonly caused by an excess of water, hy-
pernatraemia is usually associated with water deficiency. The abil-
ity to concentrate the urine and an intact thirst mechanism along
with unrestricted free access to water are the main protective
measures of the body against the development of hypernatrae-
mia. 2 Hypernatraemia rarely develops in children with an adequate
thirst response and free access to water. Two main causes of

ZIEG
hypernatraemia are excessive water losses and excessive sodium in-
take. Less frequently, insufficient water intake and mineralocorticoid
overproduction may be responsible for hypernatraemia. Patients
with hypernatraemia usually present with non-­specific symptoms
such as nausea, vomiting, irritability, restlessness, weakness and
hyperthermia. Spasticity, convulsions, absence seizures, coma and
other neurologic symptoms may occur. A rapid rise in serum sodium
can result in hyperthermia, intracranial haemorrhage, venous sinus
thrombosis or demyelination. Rhabdomyolysis may be a complica-
3,19,20
tion of severe hypernatraemia.
4 | D I AG N OS I S
A diagnosis of hypernatraemia is suspected in the presence of symp-
toms and confirmed by an elevated serum sodium concentration.
A detailed history is the first step, and states with too little water
need to be distinguished from states with too much salt. 5 The fluid
intake and output, weight dynamics and composition of oral fluids
or infusions should be assessed. Evaluation of water and electrolyte
losses and their replacement along with medication history are im-
portant. A renal concentrating defect is suspicious in children with
inadequately high urine output and low urine osmolality in hyper-
natraemic states. While hypovolemic hypernatraemia is usually as-
sociated with weight loss, weight gain is seen in salt intoxication.
Serum and urinary sodium, creatinine, and osmolality levels are labo-
ratory markers used for the differential diagnosis of hypernatraemia.
Calculation of the sodium excretion fraction is very helpful. While
fractional excretion of sodium (FENa) ≤1% is characteristic for water
21
loss, FENa of ≥2% will typically be seen in salt-­poisoned children.
Ion-­selective electrode assays are used in most of the laboratories
for sodium assessment; however, pseudohypernatraemia-­falsely
increased sodium serum levels may occur in children with hypo-
proteinemia due to increased plasma water fraction if indirect ion-­
elective electrode assays are used. 22 Image 1 shows an algorithm for
the differential diagnosis of hypernatraemia (Figure 1).
F I G U R E 1 Practical approach to
differential diagnosis of paediatric
hypernatraemia. FENa, sodium fractional
excretion; Posm, plasma osmolality; Uosm,
urine osmolality
|
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507
5 | C LI N I C A L S TATE S W ITH FR E E WATE R
LOS S
The most common mechanism leading to a high serum sodium
concentration is increased loss of solute-­
free water, which ex-
ceeds the sodium wasting in children with acute gastroenteritis.
Hypernatraemic dehydration most frequently affects young infants
receiving insufficient water replacement for losses. Fluid shifts from
the cells to the hypertonic intravascular space result in cell dehy-
dration and shrinkage. Hypernatraemic dehydration is usually clini-
cally less apparent as general signs of dehydration are mitigated,
which may delay the diagnosis. Brain cell dehydration may result in
severe neurological injury such as intracranial haemorrhage and is
associated with significant morbidity and mortality. Mainly children
with a serum sodium concentration of more than 160 mmol/L and
those with fast correction of sodium are at the greatest risk of com-
plications. 23 Decreased body water content is caused by excessive
water losses from the urinary tract in children with diabetes insipi-
dus centralis and renalis, states characterized by a renal concentra-
tion defect related to decreased ADH or resistance to its effects.
Patients typically present with polydipsia, polyuria, dehydration and
hypoosmolar urine. Genetic causes, trauma, infection, tumours and
autoimmune processes are the most common cause of diabetes in-
sipidus centralis. Genetic and acquired aetiologies are responsible
for nephrogenic diabetes insipidus. A disturbed kidney concentra-
tion mechanism may be associated with certain electrolyte abnor-
malities (hypokalaemia, hypercalcaemia), chronic kidney disease or
drug exposure. 24 The aetiology of diabetes insipidus is summarized
in Table 1. Moreover, osmotic diuresis, e.g. in diabetic ketoacidosis
and acute kidney injury due to glucose and urea-­induced solute diu-
resis or after mannitol administration, may result in hypernatraemia if
water losses are not adequately replaced. Hypernatraemia may also
occur in individuals with excessive sweating due to prolonged physi-
cal activity, fever or exposure to high temperatures. Interestingly,
although sweat is hypotonic compared to plasma, endurance sport
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508
TA B L E 1 Aetiology of diabetes insipidus in children
Central diabetes insipidus Familial
Acquired
Cerebral malformations
Nephrogenic diabetes insipidus Familial
Acquired
Abbreviation: DIDMOAD, diabetes insipidus, diabetes mellitus, optic atrophy, deafness.
activities may also cause hyponatraemia due to increased ADH se-
25
cretion and high water intake.
6 | C LI N I C A L S TATE S W ITH S O D I U M
E XC E S S
High sodium consumption, inappropriate rehydration by enteral or
parenteral hypernatraemic solutions and salt poisoning lead to hy-
pernatraemia from sodium excess. Cases of salt poisoning in children
have been reported, both unintentional and intentional. Salt toxicity
is dangerous and associated with significant (>50%) mortality due to
irreversible neurological damage. 26 Renal impairment and the inabil-
ity of children to communicate the need for fluids represent the main
risk factors for salt toxicity. A high serum sodium content leads to
rapidly increased tonicity and excretion of water without electrolyte
loss. A variety of neurological symptoms may occur.
7 | C LI N I C A L S TATE S W ITH I N S U FFI C I E NT
WATE R I NTA K E
Intact thirst sensation is an important regulator of body water
homoeostasis. Children with adipsia or hypodipsia due to a con-
genital or acquired hypothalamic defect are at a particular risk of
16512227, 2022, 3, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/apa.16170 by Mahidol University Library and Knowledge Center, Wiley Online Library on [03/06/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
ZIEG
Autosomal dominant
Autosomal recessive
X-­linked
Wolfram syndrome, DIDMOAD
Tumors—­germinoma, craniopharyngioma, glioma, metastasis
Langerhans cell histiocytosis
Vascular/hypoxic
Infectious—­meningitis, encephalitis, tuberculosis, sarcoidosis
Traumatic/post-­surgery
Autoimmune
Drug-­induced
Hypocalaemia, hypercalcaemia
Holoprosencephaly, genesis of corpus callosum, septo-­optic
dysplasia
X-­linked
Autosomal recessive
Autosomal dominant
Drug-­induced—­lithium, amphotericin B, rifampicin, clozapine,
methicillin, demeclocycline, cyclophosphamide,
ifosfamide, vinblastine, furosemide
Primary kidney disease: obstructive uropathy, polycystic
kidney disease, nephronophthisis, cystinosis, Bartter
syndrome, sickle cell disease, Sjögren syndrome
Mineralocorticoid excess
hypernatraemia development. Also, small infants and children with-
out free access to water may encounter hypernatraemia. The serum
sodium concentration may increase mainly if the restricted access
to water is also combined with water ongoing losses. Ineffective
breastfeeding-­associated hypernatraemia was reported in several
studies. Poor feeding secondary to lactation failure and excessive
weight loss are the main presenting signs. 2,27 Unlike other forms of
hypernatraemic dehydration, there is usually mild or no neurologic
damage. 28
8 | C LI N I C A L S TATE S W ITH
M I N E R A LO CO RTI CO I D OV E R PRO D U C TI O N
Hypernatraemia may accompany states with endogenous and
exogenous mineralocorticoid excess. Conditions associated with
mineralocorticoid excess include primary hyperaldosteronism,
deoxycorticosterone-­
s ecreting tumours and congenital adre-
nal hyperplasia due to 11-­
hydroxylase deficiency. The sodium
concentration in patients with primary hyperaldosteronism is
typically higher than the normal range or only mildly elevated
due to resetting of the osmostat. Patients usually also pre-
sent with hypokalaemia, suppressed renin activity and hy-
pertension. High renin activity is associated with secondary
hyperaldosteronism. 29

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9 | M A N AG E M E NT
Once the aetiology of hypernatraemia is clarified (deficiency of
water vs. excess of salt), the goal of treatment is the administration
of free water to correct the water deficit using formula3:
Free water deficit (ml) = 4 ml × weight (kg) × desired change in sodium in mmol∕L.
Maintenance of the circulatory volume by isotonic solution or
colloids should precede the administration of a hypotonic solution
to dehydrated children. Although 0.9% NaCl is an isosmotic solution
commonly used in fluid resuscitation, it cannot be considered physio-
logic because of its higher content of sodium and chloride. However, it
30
is the preferred intravenous fluid for acutely ill children. As in hypo-
natraemic states, the correction of hypernatraemia should be gradual
to prevent the development of cerebral oedema. Insensible losses,
urine output and other fluid wasting should be added to the calcu-
lated free water deficit. The serum sodium level should not decrease
by more than 1 mmol/L/h and 15 mmol/24 h to prevent brain swelling.
So, it may take more than 48 h in some cases to reach the desired
natraemia. Hypernatraemia with serum sodium >170 mmol/L should
not be corrected to below 150 mmol/L in the first 48–­72 h. Strict and
regular monitoring of serum sodium levels (1–­4 h) and fluid intake
and output is important.3,4 Isotonic solution (10–­20 mL/kg) should be
administered initially in a hypovolemic hypernatraemic child for the
restoration of vascular volume, followed by rehydration therapy in-
cluding water deficit and fluid maintenance requirements. The free
water content of the solution can be calculated by the formula:
% free water = 1 − (i. v. fluid sodium∕serum sodium) .
In a child with hypernatraemia of 180 mmol/L, 0.9% normal
saline with 154 mmol/L of sodium provides 19% of solute-­
free
water. Therefore, in children with extremely high serum sodium
(>175 mmol/L), the sodium content of the initial solution to ensure
hemodynamic stability needs to be increased so that the final so-
dium concentration of the solution is approximately 10–­15 mmol/L
lower. While for the subsequent rehydration phase in mild hyperna-
traemia 30 mmol/L sodium solution may be used, in children with
severe hypernatraemia, a solution with 75 mmol/L sodium should be
administered to prevent a rapid decrease in serum sodium levels.31
Importantly, vital functions including regular blood pressure measure-
ments need to be monitored during the correction of hypernatraemia.
The amount of free water deficit is calculated using the formula above,
TA B L E 2 Water maintenance requirements in children (adapted
from Ref. 27)
Weight Water requirements
≤10 kg 100 ml/kg
>10–­20 kg 1000 ml + 50ml for every kg over 10
>20–­8 0 kg 1500 ml + 20 ml for every kg over 20
>80 kg 2700 ml
|
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509
and maintenance requirements including sensible and insensible
losses need to be added.32 (Table 2) Of note, management of children
with impaired urinary concentration ability differs, and 5% glucose is
appropriate initial rehydration fluid for these patients, because sodium
containing solutions may further worsen their hypernatraemia.33
10 | CO N C LU S I O N
Understanding and respecting the physiologic principles of sodium
and water homoeostasis is essential in the adequate management
of children with hypernatraemia. Although this electrolyte abnor-
mality is quite rare in clinical practice, a differential diagnosis and
correct therapeutic strategy may be challenging in some cases. Slow
correction of serum sodium levels along with frequent monitoring
of natraemia are the mainstay of therapy. Improper treatment may
cause irreversible and severe neurologic complications.
C O N FL I C T O F I N T E R E S T
None.
ORCID
Jakub Zieg https://orcid.org/0000-0001-6077-9536
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How to cite this article: Zieg J. Diagnosis and management of
hypernatraemia in children. Acta Paediatr. 2022;111:505–­
510. https://doi.org/10.1111/apa.16170