Body Composition: Salt and Water

Jennifer L. Ruth and Steven J. Wassner

Pediatr. Rev. 2006;27;181-188
DOI: 10.1542/pir.27-5-181

The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http://pedsinreview.aappublications.org/cgi/content/full/27/5/181

Pediatrics in Review is the official journal of the American Academy of Pediatrics. A monthly
publication, it has been published continuously since 1979. Pediatrics in Review is owned,
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 back to basics

BACK TO Body Composition:

Salt and Water
BASICS Jennifer L. Ruth, MD,* Steven J. Wassner, MD†

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

1. Recognize the different body fluid compartments and the percentage of

A review of the scientific
foundations of current clinical
practice
Author Disclosure
Drs Ruth and Wassner did not
disclose any financial relationships
relevant to this article.
body fluid with different ages.
2. Know how the equilibrium between extracellular fluid and intracellular
fluid is maintained.
3. Describe how to calculate the plasma osmolality by using electrolytes, blood
urea nitrogen, and glucose concentration.
4. List the daily requirements for sodium.
5. Discuss the relationship between serum sodium concentration and total
body sodium content.
6. Understand the relationship between chronic sodium depletion and
intravascular volume depletion.
Introduction
Primitive, single-celled organisms
began their ocean life continually
surrounded by water and a steady
supply of nutrients. As more complex
organisms developed and finally left
the oceans for dry land, the external
sea had to be internalized. The great
19th century physiologist Claude
Bernard coined the term “milieu in-
terior” to describe that internal envi-
ronment. He said that our escape
from the sea was due to our ability to
control our internal environment, a
concept we now call homeostasis.
Humans have developed sophisti-
cated homeostatic mechanisms that
control salt and water metabolism.
This dynamic process changes with
age and sex and in response to a
variety of disturbances. In this article,
we discuss fluid and electrolyte
homeostasis as well as selected fluid
*Resident in Pediatrics, Pennsylvania State
University Children’s Hospital, Hershey, Pa.
†
Professor of Pediatrics; Chief, Division of Pediatric
Nephrology and Hypertension, Pennsylvania State
Children’s Hospital, Hershey, Pa.
and electrolyte problems seen within
the pediatric age group.
Body Fluid Compartments
and Growth
Water is the most abundant com-
pound within the human body. It
can be found within cells, around
cells, within the blood vessels, and in
smaller amounts within ligaments
and bones. The percentage of body
water changes with age and body
composition. Early in gestation, al-
most 90% of a fetus’s body weight is
water. This ratio falls to 80% in se-
verely preterm infants, 70% in term
infants, 65% in young children, and
approximately 60% in older children
and adolescents. Body water is dis-
tributed into two main compart-
ments: the intracellular and the ex-
tracellular. In the average adult,
intracellular water makes up approx-
imately 40% of body weight or two
thirds of total body water. Water
comprises approximately 80% of a
cell’s weight. Adipose tissue is an ex-
ception that essentially is free of in-
tracellular water. Because obese per-

Pediatrics in Review Vol.27 No.5 May 2006 181

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back to basics

nous end of the capillary, the contin-

ued decrease in hydrostatic pressure,
coupled with increasing oncotic
Figure 1. Starling forces. Kⴝcapillary filtration coefficient, Pcⴝcapillary hydrostatic
pressure, alters the balance of forces
pressure, Piⴝinterstitial hydrostatic pressure, IIcⴝcapillary oncotic pressure,
IIiⴝinterstitial oncotic pressure. to favor fluid reabsorption into the
capillary lumen. Approximately 90%
of the fluid initially filtered into the
sons have a higher ratio of adipose able for filtration. For example, the interstitium at the arteriolar end of a
tissue, they have a lower percentage glomerular capillaries have a much capillary bed is reabsorbed back into
of total body water. higher capillary filtration coefficient the intravascular space; the other
In addition to the water within than other capillaries, a necessity for 10% is returned to the circulation by
cells, water circulates between and adults who produce more than 150 L the lymphatic system. When the nor-
around cells as well as within blood of glomerular filtrate each day. If the mal state of homeostasis has been
vessels. The water bathing the cells is capillaries in the feet were as perme- disrupted, as in dehydration or other
called interstitial fluid and comprises able as those in the glomeruli, every- causes of decreased blood pressure,
approximately 15% to 20% of body one would have pedal edema. the net flow of fluid is from the inter-
weight; the serum, or water part of Figure 2 depicts the Starling stitial compartment into the intravas-
the blood, comprises another 4% to
forces acting along a typical muscle cular compartment, thus maintain-
5% of body weight. Collectively, the
capillary. At the arteriolar end of the ing blood pressure and restoring
interstitial and intravascular fluid vol-
capillary, the net hydrostatic pressure homeostasis. Conversely, both intra-
umes are termed extracellular water
gradient minus the net oncotic pres- vascular volume overload (by in-
(ECW). As a whole, ECW makes up
sure gradient favors the movement of creasing the capillary hydrostatic
approximately one third of total
body water, or 20% to 25% of body water out of the capillary and into the pressure) and hypoalbuminemia (by
weight (depending on age). interstitium. As water leaves the cap- decreasing the capillary oncotic pres-
illary, the hydrostatic pressure falls, sure) lead to the net movement of
Transfer of Water Between and the oncotic pressure begins to fluid out of blood vessels and into the
Compartments rise. At some point toward the ve- interstitium.
Starling Forces
Exchange of water between the in-
terstitial and intravascular compart-
ments is rapid and governed by the
balance of forces known as Starling
forces, named after the physiologist
who first described their operation.
According to the Starling formula
(Fig. 1), the net movement of fluid
across a capillary membrane is a func-
tion of that membrane’s innate per-
meability as well as the difference in
hydrostatic and oncotic pressures on
the two sides of the membrane. Both
act to maintain intravascular volume
and blood pressure. As might be ex-
pected, some capillary beds are in-
nately more permeable than others
(have a higher capillary filtration co-
efficient). The capillary filtration co- Figure 2. Starling forces at work. The balance of Starling forces along a muscle
efficient takes into account, and is capillary. At the arterial end, the direction of the net force is out of the capillary and
proportional to, the permeability of into the interstitium. At the venular end, the balance of forces is reversed, and fluid
the capillary wall and the area avail- moves back into the capillary.

182 Pediatrics in Review Vol.27 No.5 May 2006

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Osmotic Equilibrium
Unlike the movement of water
within the extracellular compart-
ment, the transfer of water between
the extracellular and intracellular
compartments occurs in response to
osmolar gradients. Osmolality is de-
fined as the number of milliosmoles
of solute per kilogram of water. One
milliosmole is equal to one millimole
of solute. The osmolality of both the
intracellular and extracellular spaces
reflects the amounts and different
types of solutes within each compart-
ment. The kidney regulates solute
and water homeostasis in the extra-
cellular space, but the concentration
of these solutes within cells is care-
fully controlled by a variety of cellular
transport mechanisms. Because cells
are bounded by semipermeable
membranes, water flows across these
membranes to equalize extracellular
and intracellular osmolalities. The
major extracellular osmoles are so-
dium and its accompanying anion,
chloride. Other physiologic osmoles
within the ECW are glucose and urea
nitrogen (BUN). Serum osmolality
can be estimated by the following
equation:
2*Na (mEq/L) ⫹ [BUN (mg/dL)/
2.8] ⫹ [Glucose (mg/dL)/18]
Multiplying sodium concentration
by 2 reflects the presence of the an-
ions (predominantly chloride) that
accompany each sodium ion. Divid-
ing the BUN by 2.8 and glucose by
18 converts their units from mg/dL
to mmol (mOsm)/L. By conven-
tion, potassium usually is ignored in
the calculation of plasma osmolality
because its contribution is negligible.
As can be seen from the equation,
hypernatremia always is synonymous
with hyperosmolality, but hypona-
tremia does not necessarily imply
hypo-osmolality because urea (as in
acute or chronic renal failure), glu-
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cose (as in diabetes mellitus), or even
other unmeasured osmoles (such as
lactate, ethanol, or methanol) also
can contribute to total osmolality.
Total and effective osmolality
should be distinguished. Com-
pounds such as ethanol or methanol
rapidly diffuse across cell mem-
branes, so although they contribute
to the total osmolality, their presence
does not lead to the movement of
fluid across cell membranes. Urea
diffuses more slowly, and the acute
administration of urea has been used
to increase extracellular osmolality
and decrease cerebral swelling. How-
ever, when serum urea concen-
trations are chronically elevated,
intracellular and extracellular con-
centrations are equivalent, and urea
does not contribute to effective
osmolality.
Glucose, unlike the previous com-
pounds, diffuses poorly across cell
membranes. High serum glucose
concentrations always lead to the de-
velopment of an osmotic gradient
and the movement of fluid from the
intracellular to the extracellular com-
partment. This condition is seen
commonly in the hyperglycemia of
uncontrolled diabetes mellitus. The
movement of water from within cells
to the extracellular space leads to a
lower serum sodium concentration
(hyponatremia), which some authors
have incorrectly called “factitious hy-
ponatremia.” In truth, this is an ex-
ample of true hyponatremia because
the ECW content is increased for the
amount of sodium present. Lower-
ing blood glucose concentrations by
the administration of insulin de-
creases ECW osmolality, which leads
to diffusion of water back into the
intracellular space and an increase in
serum sodium concentration.
Rapid changes in ECW osmolality
always are associated with compensa-
tory changes within the intracellular
compartment. Cell function depends
back to basics
on a stable volume to keep the intra-
cellular concentration of enzymes,
cofactors, and ions at appropriate lev-
els. Therefore, the movement of wa-
ter and the resultant cellular swelling
(or contraction) can lead to cellular
dysfunction. The brain has limited
tolerance for either cellular swelling
or contraction, which explains why
disturbances in plasma osmolality
can be accompanied by central ner-
vous system dysfunction, including
lethargy, seizures, and coma. As
noted previously, the hyperosmolal-
ity of uncontrolled diabetes mellitus
leads to a shift of water out of cells
and into the extracellular fluid space.
In contrast, decreased plasma osmo-
lality (as sometimes occurs with vom-
iting, diarrhea, or the administration
of hypotonic intravenous fluids) is
associated with movement of water
into cells and the development of
cellular swelling. This swelling is of
most concern within the brain,
where the ability of brain cells to
expand is limited by the bony skull.
As a result, acute hypo-osmolality
(hyponatremia) can be associated
with the development of intracellular
cerebral edema, seizures, and death.
In addition to its presence within
a skull of defined volume, the brain is
tethered to the skull by membranes
that contain blood vessels. Condi-
tions that induce hyperosmolality
may cause brain cell volume to de-
crease acutely by as much as 10% to
15%. To reverse this shrinkage, the
brain has the unique ability to main-
tain intracellular volume by produc-
ing organic compounds such as tau-
rine, glycine, glutamine, sorbitol,
and inositol. Collectively, these com-
pounds are known as idiogenic os-
moles. An increase in the concentra-
tion of the idiogenic osmoles has
been detected as early as 4 hours after
the onset of hypernatremia, but does
not become significant until after
24 hours. If hyperosmolality devel-
Pediatrics in Review Vol.27 No.5 May 2006 183
back to basics
ops acutely, the brain may not be able
to respond quickly enough to pre-
serve cell volume. The resultant cel-
lular contraction can lead to struc-
tural changes, tearing of the
membrane-bound blood vessels, and
development of intracranial hemor-
rhage. This combination of changes
helps explain the relatively high inci-
dence of permanent neurologic dam-
age associated with hypernatremic
dehydration. The brain’s production
of idiogenic osmoles increases its in-
tracellular osmolality and re-expands
brain cell volume. In experimental
rat studies, when hypernatremia was
maintained for 1 week, the brain was
able to regain approximately 98% of
its water content. Once idiogenic os-
moles are present, they dissipate
slowly. Therefore, the treatment of
hyperosmolality must proceed cau-
tiously. If ECW osmolality is cor-
rected too rapidly, the presence of
the idiogenic osmols within the brain
can lead to cerebral swelling during
the recovery phase.
Sodium and Water
Homeostasis
Salt Metabolism
As noted previously, sodium is the
major extracellular osmole and, in
large part, regulates the volume of
the ECW. Given the importance of
sodium in the control of both body
fluid volume and osmolality, the hu-
man body has developed complex
mechanisms to regulate both serum
sodium concentration and total body
salt content. Of particular impor-
tance to children is that sodium also
is required for growth, and any in-
crease in body size requires a positive
sodium balance. This need is partic-
ularly apparent during the first post-
natal year, when growth is rapid.
During the first 6 months after birth,
infants gain approximately 4 kg (or
2.6 L of water). To maintain their
serum sodium concentrations at
184 Pediatrics in Review Vol.27 No.5 May 2006
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140 mEq/L (140 mmol/L), infants
also must retain approximately 360
mEq (360 mmol) of sodium or
2 mEq/d (2 mmol/d). During this
time, breastfed infants ingest about 1
mEq (1 mmol)/100 kcal per day,
and formula-fed infants consume
1 to 3 mEq (1 to 3 mmol)/100 kcal
per day, so they are easily able to
achieve adequate sodium intake. For
infants and children requiring intra-
venous therapy, 2 to 3 mEq (2 to
3 mmol)/100 kcal per day is appro-
priate. One exception to this rule is
that preterm infants may require two
to three times this amount due to the
immaturity of their renal function
and initial rapid growth. Once a child
begins to eat table foods, sodium in-
take greatly exceeds recommended
amounts, with the largest contribu-
tion of ingested sodium coming from
the salt added during processing and
manufacturing. For healthy infants
and children of any age, 1 to 3 mEq
(1 to 3 mmol)/100 kcal of sodium is
sufficient.
The human body is very effective
at keeping total body sodium con-
tent constant, and with allowances
for growth, salt intake is balanced
exquisitely by salt excretion. The kid-
ney performs this function through
the filtration and reabsorption of
large amounts of glomerular filtrate.
Each day, the kidney filters a volume
approximately three times as large as
the individual’s total body water; the
tubules reabsorb 99% of the filtered
sodium and equivalent amounts of
water. Throughout the nephron, a
variety of local factors and hormones
control and modulate salt and water
reabsorption, with the most impor-
tant hormones being angiotensin II,
aldosterone (sodium), and antidi-
uretic hormone (water). Although
other hormones are important, a full
discussion of their roles is beyond the
scope of this article.
Water Metabolism
The excretion of free water (ie, water
unaccompanied by solute) is under
the control of the posterior pituitary
hormone, antidiuretic hormone
(ADH). The release of ADH is regu-
lated primarily by highly sensitive os-
moreceptors within the hypothal-
amus. Experimental studies have
demonstrated that these osmorecep-
tors can respond to changes in osmo-
lality as small as 1% to 2%. At plasma
osmolalities below 280 mosm/kg
H2O, the secretion of ADH is sup-
pressed; above this level, ADH con-
centration rises sharply. An increase
in osmolality also stimulates osmolar
thirst receptors within the brain. The
release of ADH is not equally sensi-
tive to all solutes. For example, the
release mechanism is maximally sen-
sitive to sodium, but minimally sen-
sitive to urea and glucose. ADH se-
cretion also is regulated by a less
sensitive volume receptor system.
Animal studies have shown that a loss
of approximately 5% of body water is
necessary to stimulate the release of
ADH.
The sensitivity of the osmorecep-
tor system underlies the importance
that the body places on maintaining
normal serum osmolality. For exam-
ple, in situations where excess so-
dium is retained, serum osmolality
increases transiently, causing in-
creased thirst and ADH secretion.
Water is conserved to restore serum
sodium concentration (and osmolal-
ity) to normal. Until the excess so-
dium is excreted, affected individuals
have a normal serum sodium concen-
tration and an expanded extracellular
fluid volume. Conversely, until the
patient loses approximately 5% of to-
tal body weight, losses in serum so-
dium are accompanied by propor-
tional losses in water to preserve
serum sodium concentration. Al-
though less sensitive, the volume
regulation system is more powerful

than the osmoregulatory system. In
the face of significant dehydration,
ADH secretion increases, free water
is retained, and the serum sodium
concentration decreases. In essence,
the body chooses to maintain blood
volume and tissue perfusion over se-
rum sodium concentration.
Disorders of Salt Metabolism
Salt-losing States
In the middle of the summer, you are
called to the emergency department to
examine a previously healthy 6-year-
old boy who has hypotonic dehydration.
He has no history of vomiting or diar-
rhea, and his mother notes that he al-
ways has been drawn to salty foods and
uses the saltshaker liberally. Examina-
tion of an old chart reveals that this is
the child’s second episode of hypotonic
dehydration in the past 2 years, the
previous one being last summer. His
urinary sodium concentration is less
than 5 mEq/L (5 mmol/L). Because
there is no history of gastrointestinal
losses, you suspect that sodium loss may
be occurring through his skin. After
rehydration, you refer him for genetic
testing, which reveals a mild variant
of cystic fibrosis.
The most common salt-losing
states in children are associated with
vomiting and diarrhea. Other causes
include cystic fibrosis, diuretic use,
salt-losing renal disease, and the
common forms of congenital adrenal
hyperplasia. Salt-losing states always
are associated with a loss of ECW,
and affected children present with
evidence of volume depletion and
weight loss. Individuals who have
chronic forms of volume depletion,
such as with chronic diuretic use,
may be reasonably well adapted to
their volume-depleted states and may
not show overt signs of volume
depletion.
When salt loss occurs, the body
has two coordinated response path-
ways: a protective response to main-
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back to basics
Figure 3. The protective and restorative responses to volume loss. When the kidney
senses a decrease in the ECW, it secretes renin, which initiates a cascade of responses
that ultimately leads to increased systemic vasoconstriction and the maintenance or
restoration of blood pressure. At the same time, volume loss (particularly if associated
with increased osmolality) leads to increased thirst and ADH secretion. Increasing ADH
levels are associated with increased water reabsorption, while ADH, along with
angiotensin II and aldosterone, increases sodium and water reabsorption. In the
absence of continuing losses, these responses lead to the restoration of the ECW
volume.
tain blood pressure and a restorative response that replaces the salt and
response to replenish the ECW vol- water losses. In addition to produc-
ume (Fig. 3). As mentioned, salt loss ing arteriolar constriction, Ang II
always is associated with ECW loss. stimulates salt reabsorption by two
Acutely, the kidneys sense this salt mechanisms. First, it acts directly in
loss as a lowered perfusion pressure the proximal tubule to induce so-
and respond by secreting renin. Once dium reabsorption. Ang II also stim-
in the bloodstream, renin cleaves the ulates the release of the potent min-
protein angiotensinogen into angio- eralocorticoid aldosterone from the
tensin I. Angiotensin I is biologically adrenal cortex. Aldosterone acts on
inactive and must be cleaved by the cortical collecting tubules of the
angiotensin-converting enzyme into kidney to increase sodium reabsorp-
angiotensin II (Ang II). Ang II is one tion. As renal sodium reabsorption is
of the most potent vasoconstrictors increased, water reabsorption fol-
known, acting directly on vascular lows, and as long as the inciting event
smooth muscle to produce arteriolar ceases, ECW volume is restored to its
constriction and increase systemic baseline state.
blood pressure. Ang II also facilitates
the release of norepinephrine, an- Salt-retaining States
other potent vasoconstrictor. During A 2-year-old boy presents with a 2-week
this cascade, ADH is stimulated, history of eyelid swelling and weight
which conserves water by concen- gain. He was seen 1 week ago, believed
trating the urine. to have an allergic reaction, and
Although the acute response pre- treated with an over-the-counter anti-
serves blood pressure and perfusion histamine. Physical examination to-
to vital organs, it is the restorative day demonstrates a weight gain of 3
Pediatrics in Review Vol.27 No.5 May 2006 185
back to basics
kg, normal vital signs, bilateral eyelid
edema, a nontender abdomen with ob-
vious ascites, and pitting edema from
his ankles to his knees. Nephrotic syn-
drome is confirmed by laboratory stud-
ies, which reveal a urine specific grav-
ity of 1.030, no blood, no glucose, and
4⫹ protein. Serum electrolytes, BUN,
and creatinine levels are normal, but
the albumin concentration is 1.7 g/dL
(17 g/L). The measured urine sodium
concentration is only 5 mEq/L
(5 mmol/L). In spite of the normal
blood pressure and pulse, this child’s
kidneys are avidly retaining sodium
and water. The amount of salt re-
tained over the past 2 weeks can be
calculated, noting that the child has
gained 3 kg of weight or about 3 L of
water. Because his serum sodium con-
centration remains normal, his kid-
neys have had to retain 140 mEq
(140 mmol) of sodium for each liter of
water retained, for a total of 420 mEq
(420 mmol) of sodium or about 3 tsp of
salt. Retaining 3 tsp of salt, therefore,
led to his 3-kg weight gain.
When total body sodium concen-
trations are low, salt retention is the
appropriate response. There are nu-
merous conditions, however, in
which salt is retained in the face of
normal or increased total body so-
dium content. When plasma oncotic
pressure is low (as in liver disease,
cirrhosis, or severe malnutrition) or
when tissue is damaged and mem-
brane permeability is increased, ex-
amination of the Starling forces pre-
dicts the movement of fluid from the
intravascular to the extravascular
compartment. Such movement of
fluid out of the intravascular com-
partment is termed “third spacing.”
The kidney senses this situation as a
reduction in perfusion pressure and
acts to increase salt and water reten-
tion, even though there is no net loss
of salt or water from the body.
Another situation in which salt is
retained is congestive heart failure.
186 Pediatrics in Review Vol.27 No.5 May 2006
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Clinically, affected patients present
with increased body weight (due to
retained water) and a relatively nor-
mal serum sodium concentration.
Depending on the degree of sodium
retention, edema commonly is
present. The primary abnormality is
abnormal salt retention, with water
being conserved to maintain serum
osmolality within the normal range.
A third category of disorders, pri-
mary salt retention, is relatively un-
common in pediatrics. In these situ-
ations, salt is retained due to primary
mineralocorticoid excess (Cushing
syndrome, primary hyperaldosteron-
ism, the less common forms of con-
genital adrenal hyperplasia), adminis-
tration of exogenous steroids, or rare
genetic syndromes of increased renal
salt retention. Affected patients also
present with increased body weight
and a serum sodium concentration
within the normal range. A clinical
distinction is the frequent prominent
physical finding of hypertension and
rarity of edema.
As discussed previously, changes
in total body salt content are associ-
ated with concomitant changes in to-
tal body water, with salt-retaining
states leading to weight gain and salt-
losing states associated with weight
loss. In both of these situations, se-
rum sodium concentrations gener-
ally are maintained within the normal
range, which leads to the somewhat
counterintuitive statement that “dis-
orders of sodium metabolism present as
changes in total body weight (body wa-
ter).”
Disorders of Water
Metabolism
In addition to the movement of wa-
ter and sodium within the kidney, in
a number of conditions, water loss or
retention occurs independently of
sodium movement. When water is
lost in excess of sodium, the result is
volume depletion and hypernatre-
mia. Conversely, the retention of wa-
ter in excess of sodium intake leads to
hyponatremia. Because these state-
ments refer to sodium and water rel-
ative to each other, hyper- and hypo-
natremia can be present with a total
body water content that is decreased,
normal, or even increased and leads
to another seemingly counterintui-
tive statement that “disorders of water
metabolism present as changes in se-
rum sodium concentration.” These
changes are most obvious when
caused by primary disorders of water
metabolism (diabetes insipidus, syn-
drome of inappropriate secretion of
antidiuretic hormone [SIADH]).
A full discussion of these complex
disorders is beyond the scope of this
article.
Hypernatremia
A 6-month-old infant presents with his
second episode of diarrhea and hyper-
natremic dehydration (serum sodium
173 mEq/L [173 mmol/L]). His
mother notes that he is always hungry
and that she feeds him at least 32 oz/d
of a commercially prepared ready-to-
feed formula. He has at least 15
“soaked” diapers each day and except
for the two episodes of diarrhea, he gen-
erally is constipated. Family history re-
veals that the mother had a brother
who died in infancy of unknown
causes. Intravenous rehydration is dif-
ficult and requires large amounts of
fluid over several days before the serum
electrolyte values return to normal.
Throughout this period, the infant has
copious urine output, and the urine
specific gravity is always less than
1.005. Because recurrent hypernatre-
mic dehydration is uncommon, you
search for a possible underlying cause.
The infant’s BUN, creatinine, and
renal ultrasonography findings are
normal, ruling out chronic kidney dis-
ease. Given the presence of normal re-
nal function and the suspicious family
history, you suspect that the infant is

unable to concentrate his urine be-
cause of X-linked diabetes insipidus.
Hypernatremia can result from
two primary mechanisms: an increase
in sodium intake by a patient who has
no access to “free water” and the loss
of water in excess of salt. The activa-
tion of osmoreceptors within the
brain stimulates both the release of
ADH and the sensation of thirst. Be-
cause the desire to drink is so intense,
most patients who present with hy-
pernatremia are very old, very young,
or physically unable to get to water.
For example, as soon as children who
have diabetes insipidus can access wa-
ter independently, they are able to
maintain normal serum tonicity and,
in the absence of intercurrent illness,
do not develop hypernatremia.
Hyponatremia
You note that one of the hospitalized
patients you are covering, a 6-year-old
boy (status-postappendectomy) has sig-
nificant electrolyte abnormalities. His
serum sodium level is 126 mEq/L
(126 mmol/L), potassium is 3.7 mEq/
L (3.7 mmol/L), chloride is 111 mEq/
L (111 mmol/L), and bicarbonate is
25 mEq/L (25 mmol/L). His BUN is
5 mg/dL (1.8 mmol/L) and creati-
nine is 0.3 mg/dL (26.5 mcmol/L).
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He has received several doses of mor-
phine for pain. He has taken nothing
orally since the operation, receiving
D5 1⁄4 normal saline as his mainte-
nance intravenous (IV) fluid. Over
the past 11⁄2 days, he has had approxi-
mately 2 L of IV intake and has uri-
nated only 500 mL. You tentatively
diagnose SIADH due to both the pain
and morphine. Because he is asymp-
tomatic, you limit his free water intake
and put his IV on “Keep open” status.
The child recovers without incident.
Acute hyponatremia most often is
a consequence of acute dehydration,
which results from two mechanisms.
First, infants who have diarrhea fre-
quently are given hypotonic solu-
tions and second, the decreased vol-
ume stimulus for ADH release causes
the kidney to reabsorb water and
maintain blood pressure even at the
expense of hyponatremia. Other
causes of acute hyponatremia are re-
lated to the administration of water
in excess of the kidney’s ability to
excrete it. Such water excess can oc-
cur in both acute and chronic renal
failure as well as in neonates, the el-
derly, and postoperative patients
who inadvertently receive excess
fluid. Mild hyponatremia often is
present in cases in which there is a
back to basics
chronic decrease in “perceived” in-
travascular volume, most commonly
chronic diuretic use or congestive
heart failure. In both cases, the mild
hyponatremia is due to increased
ADH secretion, released appropri-
ately by the pituitary to preserve in-
travascular volume. Chronic, severe
hyponatremia is due most likely to a
hormonal disorder that affects the
kidney’s ability to excrete water. In
addition to ADH, two other hor-
mones, thyroid hormone and corti-
sol, are required for the kidney to
excrete a water load. Thus, patients
having either hypothyroidism or Ad-
dison disease may develop hypona-
tremia.
Suggested Reading
Keating JP, Schears GJ, Dodge PR. Oral
water intoxication in infants: an Ameri-
can epidemic. Am J Dis Child. 1991;
145:985–990
Shaffer SG, Bradt SK, Hall RT. Postnatal
changes in total body water and extracel-
lular volume in the preterm infant with
respiratory distress syndrome. J Pediatr.
1986;109:509 –514
Trachtman H. Cell volume regulation: a
review of cerebral adaptive mechanisms
and implications for clinical treatment of
osmolal disturbances. I. Pediatr Neph-
rol. 1991;5:743–750
Pediatrics in Review Vol.27 No.5 May 2006 187
back to basics

PIR Quiz
Quiz also available online at www.pedsinreview.org.

10. Although sodium concentration is the major determinant of plasma osmolality, other compounds can
contribute to total solute load. Excessive plasma concentrations of which of the following compounds is
most likely to lead to the development of an osmotic gradient?
A. Ethanol.
B. Glucose.
C. Lactate.
D. Potassium.
E. Urea.

11. Idiogenic osmoles are organic compounds produced by cells to preserve cell volume in states of
hyperosmolality such as hypernatremia. Production of idiogenic osmoles is limited to which of the
following cell types?
A. Brain.
B. Cardiac.
C. Hepatic.
D. Muscle.
E. Renal.

12. Which of the following diseases is most likely to be associated with a disorder of water metabolism?
A. Acute glomerulonephritis.
B. Bacterial meningitis with SIADH.
C. Congestive heart failure.
D. Cushing syndrome.
E. Nephrotic syndrome.

Disorders of sodium metabolism present with changes in total body weight, and disorders of water metabolism
present as changes in serum sodium concentration. Match the following patients with the most likely findings
in body weight and sodium concentration.

13. A 4-year-old who has congestive heart failure.

14. A 7-year-old who has Cushing syndrome.

A. Increased body weight, normal serum sodium concentration.
B. Increased body weight, increased serum sodium concentration.
C. Decreased body weight, normal serum sodium concentration.
D. Decreased body weight, increased serum sodium concentration.
E. Decreased body weight, decreased serum sodium concentration.

188 Pediatrics in Review Vol.27 No.5 May 2006

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 Body Composition: Salt and Water
Jennifer L. Ruth and Steven J. Wassner
Pediatr. Rev. 2006;27;181-188
DOI: 10.1542/pir.27-5-181

Updated Information including high-resolution figures, can be found at:

& Services http://pedsinreview.aappublications.org/cgi/content/full/27/5/181

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