treatment of hypovolemia (dehydration) in children
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Página 1Treatment of hypovolemia (dehydration) in children
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Official reprint from UpToDate® www.uptodate.com
©2012 UpToDate®
Author
Michael J Somers, MD
Section Editor
Tej K Mattoo, MD, DCH, FRCP
Deputy Editor
Melanie S Kim, MD
Treatment of hypovolemia (dehydration) in children
Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Fev 2012. | This topic last updated: Fev 2, 2012.
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
or is the only fluid therapy required in patients with mild to moderate hypovolemia. The second step can be either intravenous 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 moderate to 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 in 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.
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 pediatrics [1,5,6].
Isotonic saline (0.9 percent saline solution or normal saline) is the isotonic solution of choice. Rapid administration of hypotonic or
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hypertonic crystalloid solutions for emergent volume expansion can result in serious complications, including dysnatremias, cerebral
edema, and, in children with marked hyponatremia, cerebral demyelination [7,8]. (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.
Crystalloid versus colloid — Both isotonic saline-based crystalloid solutions and colloid-containing solutions have been used
historically to replace extracellular fluid deficits. Some physicians 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 [9]:
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 [10-12]. 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.
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 care taker 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. In
addition to completing repletion during the second fluid phase, 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 [13-15]. 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 [16]. (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)
times 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. (See "Physiologic
regulation of effective arterial blood volume and plasma osmolality", 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),
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thereby increasing renal water reabsorption. In addition, ADH secretion due to other non-osmotic stimuli including pain, nausea and
vomiting, stress, and hypoglycemia can be seen in children with hyponatremia and gastroenteritis [17]. (See "Causes of hyponatremia".)
Most affected children have mild to moderate hyponatremia and can be treated with isotonic saline alone, similar to therapy with
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", section on 'Effect of potassium'.)
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 "Manifestations of hyponatremia and hypernatremia".)
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 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 [18-21].
The general recommendation in any child or adult with marked hyponatremia is that the serum sodium concentration should not be raised
by more than 12 mEq/L in the first 24 hours (an average of 0.5 mEq/L per h) [21]. (See "Overview of the treatment of hyponatremia",
section on '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 [18-20]. 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 to 154 mEq/L or 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 [21]. 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 gastroenteritis. These deficits must be accompanied by inadequate fluid
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intake that prevents repair of the free water deficit. (See "Clinical assessment and diagnosis of hypovolemia (dehydration) in children",
section on 'Serum sodium' and "Causes of hypernatremia".)
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) [16].
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 "Manifestations of hyponatremia and hypernatremia".)
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 [22,23]. This adverse response to therapy primarily occurs when the hypernatremia is corrected at a rate
exceeding 0.7 mEq/L per h [23]. In comparison, no neurologic sequelae appear to occur if the plasma sodium concentration is lowered at
a rate of ≤0.5 mEq/L per h [24].
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
"Treatment of hypernatremia".)
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 [25]. 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 [26,27]. Such hyponatremia occurs when hypotonic fluid is administered in the presence of ADH,
which is released in response to non-osmotic stimuli such as significant hypovolemia, pain, or anxiety [17]. 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 one study of children admitted with hypovolemia caused by gastroenteritis, patients were assigned randomly to receive either
hypotonic or isotonic intravenous fluid [28]. 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 those with other significant electrolyte abnormalities [29].
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" [30]. In a meta-
analysis that compared ORT to 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 [31].
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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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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 moderate or 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
those who may be hyponatremic because of the release of antidiuretic hormone by non-osmotic stimuli. (See 'Therapy according to
serum sodium' above and 'Therapy based on isotonic saline infusion' above.)
ACKNOWLEDGMENT — The editorial staff at UpToDate, Inc. would like to acknowledge Dr. Erin Endom, who contributed to an earlier
version of this topic review.
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