Treatment of hypovolemia (dehydration) in children

Author
Michael J Somers, 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: Mar 2015. | This topic last updated: Feb 24, 2015.

INTRODUCTION — Fluid therapy maintains the normal volume and composition of

body fluids and, if needed, corrects any existing abnormalities. In children, the most
common abnormality requiring fluid therapy is hypovolemia or dehydration, often
related to vomiting and diarrhea from gastroenteritis. Clinically, it is useful to divide
fluid therapy into repletion therapy and maintenance therapy.

●Repletion therapy replaces any current existing water and electrolyte deficits, replaces
any ongoing abnormal losses, and returns the patient to a normal volume and electrolyte
status.

●Maintenance therapy replaces the expected ongoing losses of water and electrolytes
from normal physiologic processes and maintains normal volume and electrolyte status
(calculator 1). (See "Maintenance fluid therapy in children".)

Volume depletion reduces the effective arterial blood volume (also called effective
circulating volume [ECV]), which refers to that part of the arterial volume that perfuses
the tissues. If severe hypovolemia is not corrected in a timely fashion, ischemic end-
organ damage may occur and, with profound or persistent hypovolemia, shock and
death may ensue.

The treatment of hypovolemia in children will be reviewed here. The clinical

assessment and diagnosis of hypovolemia, and the treatment of hemorrhagic and
nonhemorrhagic hypovolemic shock are discussed separately. (See "Clinical assessment
and diagnosis of hypovolemia (dehydration) in children" and "Hypovolemic shock in
children: Initial evaluation and management".)

GENERAL PRINCIPLES — Repletion therapy in hypovolemic children is based on

two steps:

●The first step involves emergent correction of moderate to severe hypovolemia,

ensuring a return of adequate intravascular volume and avoiding tissue damage. This is
primarily provided with intravenous fluids in developed countries, although successful
emergent oral rehydration therapy (ORT) has also been documented.

●The second step finishes repletion of fluids and electrolyte losses in children initially
treated with emergent intravenous fluid therapy, and is the only fluid therapy required in
patients with mild to moderate hypovolemia. The second step can be completed either
intravenously or by ORT.
When repleting a hypovolemic child, several questions must be answered:

●Does the child require emergent therapy?

●By what route (oral or intravenous) should the fluid be delivered?

●What kind of fluid should be given?

●What fluid volume should be given initially and then in follow-up?

●How quickly should the fluid in each step be given?

EMERGENT FLUID PHASE — Rapid volume repletion is required in children with

severe hypovolemia. Clinical assessment of hypovolemia is based upon physical signs
that reflect the status of the effective arterial blood volume and include pulse, blood
pressure, and skin turgor (table 1). If known, changes in weight and urine output from
baseline values are also helpful in assessing the degree of volume depletion.

Severe hypovolemia presents with decreased peripheral perfusion with a capillary refill
of greater than three seconds, cool and mottled extremities, lethargy, and, in its worst
manifestation, with hypotension or even frank shock. (See "Clinical assessment and
diagnosis of hypovolemia (dehydration) in children".)

With severe hypovolemia with actual or evolving circulatory compromise, emergent

intravenous fluid therapy should begin with rapid infusion of 20 mL/kg of isotonic
saline. The child should be reassessed during and after the saline bolus, and similar
isotonic fluid infusions should be repeated as needed until adequate perfusion is
restored [1].

In patients with more moderate forms of dehydration, it remains uncertain how rapidly
intravenous rehydration should be given. In a Canadian trial of 226 children with
hypovolemia due to gastroenteritis, there was no difference in the status of hydration
two hours after initial intervention between patients who were rapidly rehydrated (60
mL/kg) versus those who were treated with the standard 20 mL/kg over one hour [2].
Both groups received 0.9 percent saline. However, a major limitation of this study was
the inconsistent and imprecise assessment of hydration [3]. As a result, patients with
mild hypovolemia who may not even require intravenous rehydration may have been
included, which may have lead to a biased outcome. In addition, oral rehydration
therapy may be sufficient to correct moderate dehydration. (See 'Oral rehydration
therapy' below.)

If intravenous access is not readily obtainable, intraosseous rehydration is an effective

alternative [4].

A more detailed discussion of the treatment of hypovolemic shock can be found

elsewhere. (See "Hypovolemic shock in children: Initial evaluation and management".)

Type of fluid — Isotonic crystalloid is the only crystalloid solution recommended for
emergent volume resuscitation in pediatric patients [1]. Isotonic saline (0.9 percent
saline solution or normal saline) is the isotonic solution of choice because it is most
effective in restoring the circulatory volume. Rapid administration of hypotonic or
hypertonic crystalloid solutions for emergent volume expansion can result in serious
complications, including dysnatremias, cerebral edema, and, in children with marked
hyponatremia, cerebral demyelination [5,6]. (See 'Therapy according to serum sodium'
below.)

The use of hypotonic or hypertonic crystalloid solutions for the purpose of emergent
volume resuscitation is never recommended in pediatric patients.

Dextrose is generally not added to normal saline solution. In a clinical trial of 188
children (age range six months to six years), the administration of 5 percent dextrose
added to normal saline solution did not lower the rate of hospitalization compared with
the standard use of normal saline solution without dextrose [7]. Children who received
the dextrose-containing solution had a greater reduction in serum ketone levels, though
these levels were still markedly abnormal and there was no difference between the two
groups in degree of metabolic acidosis. Until further studies show that the addition of
dextrose provides a significant clinical benefit without adverse effect, normal saline
without dextrose is the recommended solution for emergent volume resuscitation.

Crystalloid versus colloid — Both isotonic saline-based crystalloid solutions and

colloid-containing solutions have been used historically to replace extracellular fluid
deficits. Some clinicians have advocated the administration of a colloid-containing
solution (such as 5 percent albumin or hydroxyethyl starch [hetastarch]) because of two
theoretical advantages over crystalloid repletion [8]:

●Plasma volume expansion is achieved more rapidly because more of the colloid
solution remains in the vascular space, as opposed to saline, two-thirds of which
equilibrates into the interstitium.

●Risk of pulmonary edema is decreased because diminished intravascular oncotic

pressure from dilutional hypoalbuminemia will not occur.

However, numerous controlled trials and systematic meta-analyses have failed to

demonstrate either of these theoretical benefits in adults. Although no such data are
available in children other than high-risk neonates, the same principles probably apply
throughout childhood [9-11]. As a result, an isotonic saline solution is the treatment of
choice in treating extracellular fluid losses in all age groups. Possible mechanisms for
lack of benefit are discussed elsewhere. (See "Treatment of severe hypovolemia or
hypovolemic shock in adults", section on 'Colloid versus crystalloid'.)

In children with decreased effective arterial blood volume related to low intravascular
oncotic pressure, as in nephrotic syndrome or severe sepsis, it may be useful to use
colloid-containing solution (such as albumin) to restore perfusion. In these specific
settings, salt-poor albumin is administered at a dose between 0.5 and 1 g/kg, and is
discussed separately. (See "Symptomatic management of nephrotic syndrome in
children", section on 'Furosemide and albumin' and "Evaluation and management of
edema in children", section on 'Intravenous albumin infusion'.)
SECOND FLUID PHASE — After severe volume depletion has been corrected with
intravenous fluid, fluid repletion can continue with either continued intravenous fluid or
oral rehydration therapy (ORT).

Intravenous rehydration therapy — Indications for continued intravenous therapy

include:

●Inability of the child to take ORT (eg, alteration in mental status, ileus, or anatomic
anomaly)

●Inability of the caretaker to provide ORT

●Failure of ORT to provide adequate rehydration (eg, persistent vomiting)

●Severe electrolyte problems in clinical setting where ORT cannot be closely monitored
or electrolytes frequently assessed

The type of intravenous repletion fluid that is given in this second step of fluid therapy
varies with the serum sodium concentration. During the second fluid phase, in addition
to completing repletion, fluid and electrolytes to replace any abnormal ongoing losses as
well as maintenance fluids and electrolytes must be given (table 2) (calculator 1). (See
"Maintenance fluid therapy in children".)

Therapy according to serum sodium — The sodium content of fluid and the rate of
correction are dependent upon the serum sodium concentration defined as:

●Hyponatremia − serum sodium less than 130 mEq/L

●Isonatremia − serum sodium between 130 and 150 mEq/L

●Hypernatremia − serum sodium greater than 150 mEq/L

The factors that contribute to the final serum sodium at presentation (the composition of
the fluid that was lost, the type of fluid intake, and the ability to excrete water during the
illness) are discussed separately. (See "Clinical assessment and diagnosis of
hypovolemia (dehydration) in children", section on 'Serum sodium'.)

The majority of cases of hypovolemia caused by gastroenteritis are isonatremic, and

fluid repletion can be performed in a few hours in the pediatrician's office or emergency
department [12-14]. However, when hypovolemia is associated with significant
hyponatremia or hypernatremia, or when hypovolemia and associated alterations in
serum sodium have evolved slowly, attention also must be paid to the rate of correction
of the serum sodium concentration to avoid excessive shifts of water out of
(hyponatremia) or into (hypernatremia) the brain that can lead to serious neurologic
complications [15]. (See "Manifestations of hyponatremia and hypernatremia".)

Volume repletion is based upon calculation and replacement of water and sodium
losses. The water deficit is best estimated from the fall in body weight from baseline,
which is usually not exactly known. The sodium deficit is equal to the deficit per liter in
serum sodium (SNa) multiplied by the volume of distribution of the osmotic effect of
sodium, which is the total body water (TBW):

●Na deficit = [TBW(n) x 140 mEq/L] - [TBW(c) x SNa]

where TBW(n) is the normal TBW and TBW(c) is the estimated current TBW.

The TBW in most children is approximately 60 percent of body weight. However, the
proportion of body weight is higher in smaller children and infants, especially low birth
weight premature infants whose TBW is approximately 80 percent of the total mass
(figure 1). (See "General principles of disorders of water balance (hyponatremia and
hypernatremia) and sodium balance (hypovolemia and edema)", section on 'Total body
water' and "Clinical assessment and diagnosis of hypovolemia (dehydration) in
children".)

Isonatremia — In patients with isonatremic hypovolemia, the above calculation can be

simplified because the serum sodium concentration is close to 140 mEq/L for both the
normal and current states. In addition, the difference between the two TBW states is the
fluid deficit.

●Na deficit = [TBW(n) - TBW(c)] x 140 mEq/L

Intravenous therapy would consist of replacement of the fluid deficit with isotonic
saline. The serum sodium concentration should not change substantially with repletion
therapy, as sodium and water are given in proportion.

Hyponatremia — Hyponatremia in hypovolemic children is usually caused by the intake

of hypotonic solutions. Some or most of the free water in these solutions cannot be
excreted because hypovolemia also enhances the secretion of antidiuretic hormone
(ADH), thereby increasing renal water reabsorption. In addition, ADH secretion due to
other nonosmotic stimuli including pain, nausea and vomiting, stress, and hypoglycemia
can be seen in children with hyponatremia and gastroenteritis [16]. (See "Hyponatremia
in children", section on 'Etiology'.)

Most affected children have mild to moderate hyponatremia and can be treated with
isotonic saline alone, similar to therapy for isonatremia. Isotonic saline will correct the
volume depletion and raise the serum sodium at the same time. The increase in serum
sodium will occur in two stages:

●The serum sodium will rise because the sodium concentration in the infused isotonic
saline (154 mEq/L) is higher than that in the extracellular fluid.

●This will be followed by a further increase in serum sodium, as volume repletion will
remove the hypovolemic stimulus to the secretion of ADH, thereby allowing urinary
excretion of the excess water.

Another factor that can promote correction of the hyponatremia is the administration of
potassium. Potassium is the major intracellular solute and is as osmotically active as
sodium. Thus, in a hypovolemic patient who also is hypokalemic, the addition of 40
mEq of potassium into each liter of isotonic saline creates a slightly hypertonic solution
that will raise the serum sodium more rapidly than isotonic saline alone. Potassium,
however, should not be added to intravenous fluids in patients with oliguria, anuria, or
significantly diminished renal function. Potassium can be added with the establishment
of good urinary flow, adequate renal function, and ability to closely monitor serum
potassium concentration. (See "Overview of the treatment of hyponatremia in adults".)

Symptomatic hyponatremia — Symptomatic hyponatremia manifests most commonly

with neurologic dysfunction and results more from the rate of change of sodium (rapid
alterations less well tolerated than slowly acquired disorders) than the degree of
hyponatremia. As the serum sodium falls, an osmotic gradient develops between the
intravascular space and the intracellular space, resulting in water movement from the
extracellular space into the intracellular space.

Such volume shifts are attenuated to some extent by both acute and chronic regulatory
mechanisms that exist in cells to minimize cell volume shifts. The more rapid and
extensive the degree of change, the less time is available for regulatory mechanisms to
minimize cell volume change and the less efficacious these changes will be. Because of
limited space in the skull, such rapid shifts may significantly increase brain volume and
result in cerebral edema with concomitant neurologic signs and symptoms. As the
sodium falls acutely below 125 mEq/L, patients may begin to complain of nausea and
malaise. Headache, lethargy, obtundation, and seizures may occur as the serum sodium
continues to fall below 120 mEq/L. (See "Hyponatremia in children", section on
'Clinical manifestations'.)

Because of the existence of these cell volume regulatory mechanisms, when fluid
repletion is initiated in children with severe hyponatremia, an important goal is
controlling the rate of rise of the serum sodium concentration to prevent fluid shifts
from the central nervous system (CNS) cells into the intravascular space. Data from
animal models and adults have shown that overly rapid correction of severe
hyponatremia can lead to the development of an osmotic demyelination in the CNS and
irreversible neurologic injury [17-20].

The general recommendation in any child or adult with marked hyponatremia is that the
serum sodium concentration should not be raised by more than 8 mEq/L in the first 24
hours [20]. (See "Hyponatremia in children", section on 'Rate of correction' and
"Overview of the treatment of hyponatremia in adults", section on 'The optimal rate of
correction'.)

However, the primary problem with symptomatic hyponatremia is evolving cerebral

edema, and the risk of morbidity from delayed therapy is greater than the risk of
complication from too rapid correction and osmotic demyelination. As a result, more
aggressive initial correction is indicated for the first three to four hours (or until the
symptoms resolve) at a rate not to exceed a rise in serum sodium of 2 mEq/L per hour
[17-19]. Often, an initial goal is to raise the serum sodium by 5 mEq/L over the first
several hours.

Symptomatic hyponatremia is one of the rare clinical settings in children in which

hypertonic (3 percent) saline is used (sodium concentration of 513 mEq/L compared
with 154 mEq/L in 0.9 percent in isotonic saline). Every two mL of 3 percent saline
contain 1 mEq of sodium.
Based upon the above considerations, the volume of 3 percent saline needed to raise the
serum sodium by 5 mEq/L is calculated in the following manner:

●Na dose = TBW x 5 mEq/L

●Volume of 3 percent saline = Na dose (in mEq) x 2 mL/mEq of Na

Suppose, for example, a 10 kg child (TBW is 0.6 times body weight) presents with
seizures and a serum sodium of 115 mEq/L. The quantity of 3 percent saline needed to
increase the serum Na to 120 mEq/L (such a 5 mEq/L increase is often associated with
cessation of CNS symptoms related to hyponatremia) can be calculated as follows:

●Na dose = (0.6 x 10 kg) x 5 mEq/L = 30 mEq of sodium

●Volume of 3 percent saline = 30 mEq x 2 mL/mEq = 60 mL

●Rate of delivery over three hours would be 20 mL per hour

Despite the more aggressive initial therapy in patients with symptomatic hyponatremia,
the rate of elevation in serum sodium should still not exceed 12 mEq/L over the course
of 24 hours [20]. It is important to appreciate that the TBW calculation is only an
estimate and that calculation of how much a given amount of fluid will raise the serum
sodium does not take into account ongoing losses. As a result, careful serial monitoring
of the serum sodium is required.

After the resolution of symptoms, fluid management is determined by calculating the

deficits of sodium and water as noted above.

Hypernatremia — Hypernatremia in hypovolemic patients results from the loss of free

water due to increased insensible losses because of fever or sweating, urinary
concentrating defects as in diabetes insipidus, or relatively dilute diarrheal fluid (sodium
plus potassium concentration less than that in the plasma) in most cases of
gastroenteritis. These deficits must be accompanied by inadequate fluid intake that
prevents repair of the free water deficit. (See "Clinical assessment and diagnosis of
hypovolemia (dehydration) in children", section on 'Serum sodium' and "Hypernatremia
in children", section on 'Etiology'.)

Hypernatremia causes hyperosmolality that initially promotes water movement out of

brain cells into the extracellular fluid space, leading to cerebral contraction. However,
within one to three days, brain volume is largely restored because of water movement
from the cerebrospinal fluid into the brain (thereby increasing the interstitial volume)
prompted by generation of idiogenic osmoles within the brain cells (thereby pulling
water into the cells and restoring the cell volume) [15].

As occurs in severe hyponatremia, overly rapid correction of hypernatremia can have

adverse effects. Quickly lowering the serum sodium concentration once the cerebral
adaptation has occurred causes osmotic water movement into the brain, resulting in
cerebral edema, which can lead to seizures, permanent neurologic damage, or death.
(See "Hypernatremia in children", section on 'Clinical manifestations'.)
Children with a serum sodium concentration above 155 mEq/L who are corrected too
rapidly are at greatest risk of such neurologic sequelae, particularly seizures [21,22].
This adverse response to therapy primarily occurs when the hypernatremia is corrected
at a rate exceeding 0.7 mEq/L per hour [22]. In comparison, no neurologic sequelae
appear to occur if the plasma sodium concentration is lowered at a rate of ≤0.5 mEq/L
per hour [23].

Thus, the goals of therapy in children with hypovolemia and serum sodium above 155
mEq/L are correction of the volume deficit and gradual correction of the hypernatremia
at a rate of less than 12 mEq/L per day (less than 0.5 mEq/L per hour). The overall fluid
deficit in hypernatremic hypovolemia is a combination of the free water deficit that
raised the serum sodium and an isotonic fluid deficit from the abnormal volume losses
(which may be large in children with gastroenteritis and minimal in children with
diabetes insipidus who have mainly free water loss).

Estimation of the free water deficit (essentially the amount of free water that would
have to be lost to produce the observed elevation in serum sodium) is based upon the
serum sodium and the estimated current TBW:

●Free water deficit = Current TBW [(SNa/140) - 1]

(See "Treatment of hypernatremia", section on 'Derivation of the water deficit formula'.)

Suppose, for example, a 10 kg child (TBW 0.6 times body weight) has a 1 L fluid loss
and a serum 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. (See 'Emergent fluid
phase' above.)

Subsequent therapy to replace water loss would include the water deficit (686 mL), the
remainder of the isotonic fluid loss (114 mL), plus ongoing excess fluid losses (eg,
diarrhea, vomiting, or urinary losses in diabetes insipidus) and the patient's maintenance
fluid requirements. (See "Maintenance fluid therapy in children".)

The water deficit should be replaced over more than 36 hours so that the serum sodium
would be lowered at a rate below 0.5 mEq/L per hour. The serum sodium concentration
must be monitored to ensure that the actual decrease is consistent with the therapeutic
plan. (See "Hypernatremia in children", section on 'Treatment'.)

Therapy based on isotonic saline infusion — If the hypovolemic child requires

hospitalization and intravenous therapy, an alternative method to fluid therapy
recommends the use of isotonic saline for repletion of fluid losses at an initial dose of
20 to 40 mL/kg over two to four hours [24]. Maintenance fluid rates, again using
isotonic saline, would be initiated when the patient became euvolemic.

This approach was suggested to prevent hospital-acquired hyponatremia associated with

the administration of intravenous hypotonic fluids in the setting of significant ADH
release [25,26]. Such hyponatremia occurs when hypotonic fluid is administered in the
presence of ADH, which is released in response to nonosmotic stimuli such as
significant hypovolemia, pain, or anxiety [16]. In this clinical setting, the use of isotonic
saline would prevent the development of hyponatremia. Administration of isotonic
saline also simplifies the treatment regimen by eliminating the need to calculate sodium
and water losses. (See "Causes of hyponatremia in adults".)

In one study of children admitted with hypovolemia caused by gastroenteritis, patients

were assigned randomly to receive either hypotonic or isotonic intravenous fluid [27].
The administration of hypotonic solution (0.45 percent saline) did not alter the mean
sodium level of children who were hyponatremic (from 132 to 133 mEq/L), but
decreased the mean sodium level of children who were initially normonatremic (from
137 to 135 mEq/L). The use of isotonic solution increased mean serum sodium levels of
initial hyponatremic patients (from 132 to 134 mEq/L), but there was no change in
mean sodium levels in the initial normonatremic patients (from 137 to 138 mEq/L). The
degree of hypovolemia was not assessed at the time of admission nor was a
standardized infusion protocol used, making it difficult to draw firm conclusions about
the full ramifications of this study. Moreover, the clinical significance of these small
changes in sodium in normonatremic children is unclear.

Nonetheless, the use of isotonic saline infusions as the basis for fluid therapy has been
recommended as a safe and effective option for hospitalized children with hypovolemia
from gastroenteritis. Such an approach should not be used to formulate therapy in
children with hypernatremia who need free water replacement or in those with other
significant electrolyte abnormalities [28].

Oral rehydration therapy — Oral rehydration therapy (ORT) is recommended by the

American Academy of Pediatrics (AAP) as "the preferred treatment of fluid and
electrolyte losses caused by diarrhea in children with mild to moderate dehydration"
[29]. In a meta-analysis that compared ORT with traditional intravenous (IV)
rehydration, the overall failure rate with ORT (defined as the need to revert to IV
therapy) was only 3.6 percent, without an increased incidence of iatrogenic
hyponatremia or hypernatremia [30].

Advantages of ORT include lower cost, elimination of the need for IV line placement,
and involvement of the parents in a rehydration process they can continue at home and
utilize in future illnesses.

As discussed above, the first step in treatment with ORT is to assess the degree of
hypovolemia (table 1). In most developed countries, severe hypovolemia is treated
initially with a rapid infusion of 10 to 20 mL/kg of isotonic saline. The patient should
then be reassessed and the saline bolus repeated as needed until adequate perfusion is
restored. (See 'Emergent fluid phase' above.)
ORT is started after effective arterial blood volume has been restored, or as initial
therapy in patients with mild or moderate hypovolemia. ORT involves the
administration of frequent small amounts of fluid by spoon or syringe. A full discussion
on oral rehydration therapy is found elsewhere in the program. (See "Oral rehydration
therapy".)

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materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces
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are best for patients who want in-depth information and are comfortable with some
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Here are the patient education articles that are relevant to this topic. We encourage you
to print or e-mail these topics to your patients. (You can also locate patient education
articles on a variety of subjects by searching on “patient info” and the keyword(s) of
interest.)

●Basics topics (see "Patient information: Dehydration (The Basics)" and "Patient
information: Rotavirus infection (The Basics)")

●Beyond the Basics topics (see "Patient information: Acute diarrhea in children
(Beyond the Basics)" and "Patient information: Nausea and vomiting in infants and
children (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Fluid therapy maintains the normal volume and composition of body fluids and, if
needed, corrects any existing abnormalities.

●In children who are hypovolemic, repletion therapy is composed of two steps. The first
is to emergently correct severe volume depletion with intravenously administered
isotonic fluids. The second step is to finish repletion of fluids and electrolytes either
with intravenous fluids or oral rehydration therapy. (See 'General principles' above and
'Emergent fluid phase' above and 'Second fluid phase' above.)

●In the second phase of repletion, if intravenous fluids are used, the choice of
intravenous fluid is dependent upon the serum sodium. Alternatively, isotonic fluids can
be used in any child who continues to be repleted by the intravenous route, especially in
those who may be hyponatremic because of the release of antidiuretic hormone by
nonosmotic stimuli. (See 'Therapy according to serum sodium' above and 'Therapy
based on isotonic saline infusion' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge

Erin E Endom, MD, who contributed to an earlier version of this topic review.

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hyponatremia in children: a physiologic approach. J Pediatr 2004; 145:584.
25. Hoorn EJ, Geary D, Robb M, et al. Acute hyponatremia related to intravenous
fluid administration in hospitalized children: an observational study. Pediatrics
2004; 113:1279.
26. Moritz ML, Ayus JC. Prevention of hospital-acquired hyponatremia: a case for
using isotonic saline. Pediatrics 2003; 111:227.
27. Neville KA, Verge CF, Rosenberg AR, et al. Isotonic is better than hypotonic
saline for intravenous rehydration of children with gastroenteritis: a prospective
randomised study. Arch Dis Child 2006; 91:226.
28. Schwartz R. Comments from another student of Gamble and Darrow on fluids.
Pediatrics 1996; 98:314.
29. Practice parameter: the management of acute gastroenteritis in young children.
American Academy of Pediatrics, Provisional Committee on Quality
Improvement, Subcommittee on Acute Gastroenteritis. Pediatrics 1996; 97:424.
30. Gavin N, Merrick N, Davidson B. Efficacy of glucose-based oral rehydration
therapy. Pediatrics 1996; 98:45.

Topic 6103 Version 20.0

GRAPHICS
Physical findings of volume depletion in infants and children
Mild(3 to 5 Moderate(6 to 9
Finding Severe(≥10 percent)
percent) percent)
Pulse Full, normal rate Rapid Rapid and weak OR absent
Systolic
Normal Normal to low Low
pressure
Deep, rate may be Deep, tachypnea OR
Respirations Normal
increased decreased to absent
Tacky or slightly
Buccal mucosa Dry Parched
dry
Anterior
Normal Sunken Markedly sunken
fontanelle
Eyes Normal Sunken Markedly sunken
Skin turgor Normal Reduced Tenting
Skin Normal Cool Cool, mottled, acrocyanosis
Normal or mildly
Urine output Markedly reduced Anuria
reduced
Listlessness,
Systemic signs Increased thirst Grunting, lethargy, coma
irritability
Graphic 76198 Version 5.0
Calculation of maintenance fluids based on body weight (Wt) in children and infants
Body Daily maintenance fluid*(mL/24 Hourly maintenance
Wt(kg) hours) fluid*(mL/hour)
1 to 10 100 x Wt (kg) 4 x Wt (kg)
>10 to 20 1000 plus 50 x Wt over 10 kg 40 plus 2 x Wt over 10 kg
>20 1500 plus 20 x Wt over 20 kg 60 plus 1 x Wt over 20 kg
* Maximum fluid per 24 hours is 2400 mL or 100 mL/hour.
Graphic 65412 Version 6.0
Total body water and its major subdivisions as a function of age

Data from: Friis-Hansen B. Body water compartments in children: changes during

growth and related changes in body composition. Pediatrics 1961; 28:169.
Graphic 56512 Version 2.0

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