20/03/2018 Clinical assessment and diagnosis of hypovolemia (dehydration) in children - UpToDate

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Author: Michael J Somers, MD

Section Editor: Tej K Mattoo, MD, DCH, FRCP
Deputy Editor: Melanie S Kim, MD

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All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2018. | This topic last updated: Oct 24, 2017.

INTRODUCTION — Fluid therapy is intended to maintain the normal volume and composition of body
fluids, and, if needed, to correct any existing abnormalities. In children, the most common abnormality is
hypovolemia.

Volume depletion reduces the effective circulating volume (ECV), compromising tissue and organ perfusion.
If severe hypovolemia is not corrected in a timely fashion, ischemic end-organ damage occurs leading to
serious morbidity, and, in patients in shock, death. (See "Hypovolemic shock in children: Initial evaluation
and management".)

The clinical assessment and diagnosis of hypovolemia will be reviewed here. Repletion therapy for
hypovolemia is discussed elsewhere. (See "Treatment of hypovolemia (dehydration) in children".)

ETIOLOGY — Volume depletion occurs when fluid is lost from the extracellular space at a rate that exceeds
intake. The most common sites for extracellular fluid loss are:

● Gastrointestinal tract (eg, diarrhea, vomiting, bleeding)

● Skin (eg, fever, burns)

● Urine (eg, glucosuria, diuretic therapy, diabetes insipidus)

In addition, hypovolemia can result from prolonged inadequate intake without excessive losses.

Intravascular hypovolemia can also result from intravascular fluid movement into a third space that is not in
equilibrium with the extracellular fluid. Third-space fluid sequestration occurs in children with edema due to
renal disease, liver failure, malnutrition, heart failure, or those with increased vascular permeability from
systemic inflammation; those with bleeding into a third-space (eg, retroperitoneal bleed); or patients with
ascites due to intestinal obstruction or pancreatitis. (See "Pathophysiology and etiology of edema in
children", section on 'Etiology'.)

Risk factors — Children are at increased risk for hypovolemia for the following reasons:

● There is a higher frequency of gastroenteritis (diarrhea and vomiting) in children compared with adults.

● Children, especially young children, have a higher surface area-to-volume ratio with proportionally
higher insensible losses that are accentuated in disease states (eg, fever or burns).

● Young children are unable to communicate their need for fluids or cannot independently access fluids to
replenish volume losses.

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Underlying medical conditions that may predispose affected children to hypovolemia include cystic fibrosis,
uncontrolled diabetes mellitus, and urinary concentrating defect.

VOLUME DEPLETION VERSUS DEHYDRATION — The terms volume depletion (hypovolemia) and
dehydration are often used interchangeably. However, these terms differentiate physiologic conditions
resulting from different types of fluid loss [1]. (See "General principles of disorders of water balance
(hyponatremia and hypernatremia) and sodium balance (hypovolemia and edema)".)

● Volume depletion (hypovolemia) refers to any condition in which the effective circulating volume is
reduced. It can be produced by salt and water loss (as with vomiting, diarrhea, diuretics, bleeding, or
third space sequestration) or by water loss alone (as with insensible water losses or diabetes
insipidus).

● Dehydration refers to water loss alone. The clinical manifestation of dehydration is often
hypernatremia. The elevation in serum sodium concentration, and therefore serum osmolality, pulls
water out of the cells into the extracellular fluid. (See 'Type of fluid lost' below.)

However, much of the pediatric clinical literature does not differentiate between the two terms and uses
them interchangeably [2]. Thus, we will follow this convention and use the terms hypovolemia, volume
depletion, and dehydration interchangeably as referring to all types of fluid deficits.

CLINICAL ASSESSMENT — When assessing a child with hypovolemia, the clinician needs to address two
issues:

● The degree of extracellular fluid volume depletion

● The type of fluid lost (extracellular fluid or both intracellular and extracellular fluid)

Degree of hypovolemia — Fluid repletion guidelines for children with gastroenteritis by the American
Academy of Pediatrics, Centers for Disease Control, and the World Health Organization (WHO) are based
upon the degree of volume depletion. As a result, it is important to be as accurate as possible when
assessing the degree of hypovolemia [3,4]. Severe hypovolemia requires rapid isotonic fluid resuscitation,
although oral rehydration may be sufficient for mild to moderate hypovolemia. (See "Treatment of
hypovolemia (dehydration) in children" and "Acute viral gastroenteritis in children in resource-rich countries:
Management and prevention".)

Volume depletion is most objectively measured as a change in weight from baseline. Acute loss of body
weight reflects the loss of fluid, not lean body mass; thus, a 2 kg weight loss should reflect the loss of two
liters of fluid.

However, a recent pre-illness weight is often not available. As a result, a number of findings on physical
examination coupled with the pertinent clinical history are used to help assess the severity of hypovolemia.
These findings include:

● History of increased thirst, decreased urine output, lethargy, or irritability.

● Pulse and respiratory rate – Pulse and respiratory rates increase with increasing volume depletion
(table 1).

● Blood pressure – Low blood pressure is seen in children with severe hypovolemia and in some cases
of moderate hypovolemia (table 2 and table 3).

● Skin turgor – If the skin on the thigh, calf, or forearm is pinched in normal subjects, it will immediately
return to its normally flat state when the pinch is released. This elastic property, called turgor, is partially
dependent upon the interstitial volume of the skin and subcutaneous tissue. Interstitial fluid loss leads
to diminished skin turgor, and the skin flattens more slowly after the pinch is released.

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● Decreased peripheral perfusion, including delay in capillary refill – When using a standardized method
of moderate pressure on the finger for five seconds at an ambient temperature of 20 to 25°C, a
capillary refill time greater than three seconds is considered abnormal [5]. (See "Assessment of
perfusion in pediatric resuscitation", section on 'Skin examination and capillary refill'.)

The degree of hypovolemia is divided into three categories based on the above findings (table 4):

● Mild hypovolemia (3 to 5 percent volume loss) – A history of fluid losses may be the sole finding, as
clinical signs may be absent or minimal. Such patients may have a reduction in urine output, but this
may not be appreciated.

● Moderate hypovolemia (6 to 9 percent volume loss) – Signs and symptoms are now apparent and can
include the following: tachycardia, orthostatic falls in blood pressure, decreased skin turgor, dry mucous
membranes, irritability, decreased peripheral perfusion with a delay in capillary refill between two and
three seconds, and deep respirations with or without an increase in respiratory rate. There may be a
history of reduction in urine output and decreased tearing, and, in infants, an open fontanelle will be
sunken on physical examination.

● Severe hypovolemia (≥10 percent volume loss) – Such children typically have a near-shock
presentation as manifested by hypotension, decreased peripheral perfusion with a capillary refill of
greater than three seconds, cool and mottled extremities, lethargy, and deep respirations with an
increase in rate. Severe hypovolemia requires immediate aggressive isotonic fluid resuscitation to
restore the effective circulating volume (ECV) and prevent ischemic tissue injury.

In a systematic review of the literature, the most useful clinical signs that predicted 5 percent hypovolemia in
children were delayed capillary refill time, reduced skin turgor, and deep respirations with or without an
increase in absolute respiratory rate [2].

However, a combination of signs and symptoms appear to be better than an individual finding at predicting
hypovolemia [2,6]. Clinical scales have been developed in the hopes of improving the assessment of
dehydration, such as the four-item Clinical Dehydration and Gorelick scales [7,8]. In a systematic review of
the literature, the use of clinical scales appeared to improve the diagnostic accuracy of determining
moderate dehydration (>6 percent volume loss) [6]. In resource limited areas, assessment tools (eg, WHO
guidelines (table 5)) using a combination of signs and symptoms are used to evaluate the degree of
hydration for children with acute diarrhea. However, a small prospective study that included children with no
or mild dehydration reported that these clinical scales are of limited diagnostic value in determining the
severity of dehydration [9]. (See "Approach to the child with acute diarrhea in resource-limited countries",
section on 'Hydration status'.)

Accordingly, the ability to identify children both with and without dehydration using clinical signs and
symptoms remains suboptimal [6].

Type of fluid lost — The clinical assessment for volume depletion outlined above is most pertinent to
states of extracellular fluid losses as seen with gastroenteritis. In children with gastrointestinal illness, the
fluid loss usually is isosmotic and is mostly from the extracellular space. The diarrheal isotonic fluid typically
has a sodium plus potassium concentration between 40 and 120 mEq/L [10-12], and organic solutes, such
as urea and fermentation products, make up the remaining osmoles.

In contrast to diarrheal fluid loss, insensible fluid losses and losses in states of urinary concentrating defects
(diabetes insipidus) represent water loss alone and, as noted above, result in hypernatremia. The
associated increase in serum osmolality from the hypernatremia pulls water out of the cells, which initially
minimizes the degree of extracellular fluid volume loss. This also minimizes some of the physical findings
that are associated with isotonic extracellular fluid loss.

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These considerations also apply to children with diabetes mellitus with significant hyperglycemia, which
causes a hyperosmolar state that pulls water out of the cells, thereby minimizing the degree of extracellular
hypovolemia. (See "Clinical features and diagnosis of diabetic ketoacidosis in children and adolescents".)

LABORATORY TESTING

Overview — Laboratory testing often reveals normal electrolytes and acid base balance in children with
mild hypovolemia. As a result, measurement of serum electrolytes is typically limited to children with
moderate to severe hypovolemia who require intravenous fluid repletion. These children are more severely
volume depleted and are, therefore, at greater risk for electrolyte and acid-base abnormalities. Blood
glucose should be measured in hypovolemic children who present with lethargy as hypoglycemia can be a
concomitant finding. With ongoing volume depletion, renal salt and water avidity increase as manifested by
urine sodium concentrations greater than 25 mEq/L.

Laboratory testing is less useful for assessing the degree of volume depletion. This was illustrated in the
previously mentioned systematic review of the literature and a prospective study of children who required
intravenous fluid for volume repletion [2,13]. The following findings were noted:

● Serum bicarbonate was the most useful laboratory test to assess degree of dehydration in children. A
value below 17 mEq/L differentiated children with moderate and severe hypovolemia from those with
mild hypovolemia [2,13].

● The blood urea nitrogen (BUN) rose with increasing severity of hypovolemia, reflecting the decline in
glomerular filtration rate and increase in sodium and water reabsorption and urea recycling. The
sensitivity of BUN elevation was not sufficient to be clinically useful, however, since it may be increased
by other factors such as bleeding or catabolic tissue breakdown.

Serum sodium — The serum sodium concentration is determined by the ratio between sodium salts and
water in the extracellular fluid [10,14]. Thus, the serum sodium concentration in a child with hypovolemia
varies with the relative loss of solute to water. Changes in the serum sodium concentration play an
important role in deciding the type and speed of fluid repletion therapy, especially in children with severe
hyponatremia or hypernatremia. (See "Treatment of hypovolemia (dehydration) in children".)

● Hyponatremia – The development of hyponatremia (serum sodium less than 130 mEq/L) reflects net
solute loss in excess of water loss. This does not occur directly, as losses such as diarrhea are not
hypertonic to plasma. Rather, solute and water are lost in proportion, and water is taken in and retained
(because hypovolemia-induced secretion of antidiuretic hormone [ADH] limits water excretion),
lowering the serum sodium concentration (see 'Secretion of ADH' below).

● Isonatremia – A serum sodium between 130 and 150 mEq/L reflects isonatremia. In this setting, solute
is lost in proportion to water loss. As an example, in patients with secretory diarrhea (eg, Vibrio
cholerae gastroenteritis), the solute concentration of the diarrheal fluid is similar to the plasma solute
concentration [11,15], thus the serum sodium concentration is not affected.

● Hypernatremia – The development of hypernatremia (serum sodium greater than 150 mEq/L) reflects
water loss in excess of solute loss. In children with viral gastroenteritis (eg, rotavirus), the solute
concentration of the diarrheal fluid typically ranges between 40 and 100 mEq/L. Loss of this relatively
dilute fluid will tend to induce hypernatremia if there is no concomitant water intake [10]. This entity is
referred to as hypernatremic dehydration [16,17].

Fever or tachypnea often accompany pediatric illness associated with hypovolemia, resulting in
increased insensible water losses, especially in young children. Water is, again, lost in excess of solute,
contributing to an increase in sodium concentration. A similar effect is seen with dilute urinary losses in
children with diabetes insipidus.

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Secretion of ADH — Although the composition of the fluid that is lost is the initial factor that affects the
serum sodium, subsequent ADH release also may be important. ADH secretion promotes the retention of
free water in the distal nephron and is stimulated by hyperosmolality or moderate to severe hypovolemia
(figure 1). In children with hypernatremia and associated hyperosmolality, ADH secretion and avid water
reabsorption by the kidney decreases urinary water loss and tends to prevent a further increase in serum
sodium. In children with hypovolemia who are not hypernatremic, ADH-induced decreases in water loss can
lead to hyponatremia if water intake is maintained. (See "General principles of disorders of water balance
(hyponatremia and hypernatremia) and sodium balance (hypovolemia and edema)".)

Prior fluid replacement — Prior to seeking medical treatment, replacement therapy using oral fluids
with varying concentrations of sodium may have been provided to the patient. Most often, such fluid
replacement is hypotonic and will lower sodium concentration due to the net loss of solute and ADH-
induced decreases in urinary water loss.

Serum potassium — Either hypokalemia or hyperkalemia can occur in hypovolemic patients. Hypokalemia
is more common, as children with gastroenteritis lose potassium in diarrheal stool.

However, the serum potassium concentration may be higher than expected or even elevated if a marked
acidosis is present. In this setting, excess hydrogen ions enter the cells to be buffered, and electroneutrality
is maintained in part by potassium movement from the cells into the extracellular fluid [18]. The effects of
hypovolemia upon potassium balance are reversed with correction of the acidosis, leading to a fall in the
serum potassium concentration to a degree consistent with the true potassium deficit. In children with
borderline potassium reserves, this fall can result in hypokalemic symptoms, such as muscle weakness,
intestinal ileus, flattening of the T waves and the development of U waves on electrocardiogram, and
potentially lethal arrhythmias [19]. This effect of pH does not appear to be as important with lactic acidosis
or ketoacidosis [20]. Hyperkalemia can occur in these disorders but often arises because of other factors.
(See "Potassium balance in acid-base disorders".)

Thus, clinicians managing children with significant hypovolemia must be prepared to recognize and treat
acute hypokalemia, especially if the serum potassium is borderline low or depressed in a child with acidosis.

Serum bicarbonate — As mentioned above, a low serum bicarbonate concentration (less than 17 mEq/L)
may be useful in assessing the degree of hypovolemia [2,13]. The low serum bicarbonate in hypovolemia
almost always represents metabolic acidosis. In children with gastroenteritis, the acidosis is because of the
loss of bicarbonate in the stool.

Other causes of acidosis associated with diarrheal losses include:

● Increased acid production from shock (lactic acidosis) or from enhanced fat breakdown (eg, starvation
or fasting ketosis) (see "Fasting ketosis and alcoholic ketoacidosis")

● Decreased acid excretion by the kidney caused by a reduction in renal perfusion resulting from a
reduction of effective circulatory perfusion due to hypovolemia

The acid-base status may be different in children with vomiting rather than diarrheal losses. In this setting,
the loss of hydrochloric acid in gastric secretions will lead to metabolic alkalosis and an elevated serum
bicarbonate.

Urine sodium — A low urine sodium concentration less than 25 mEq/L is a finding consistent with reduced
tissue perfusion and is usually present in hypovolemic patients. However, higher values do not necessarily
exclude the diagnosis of hypovolemia and hence its interpretation needs to be considered within the clinical
context of the individual patient

The response of the kidney to volume depletion is to conserve sodium and water to restore the effective
circulating volume (ECV). In hypovolemia, the urine sodium concentration in a random void should be less
than 25 mEq/L and may actually become non-detectable. However in the setting of both avid sodium and
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water resorption both sodium excretion and urine volume are low and the urine sodium concentration is
higher than expected (>25 mEq/L) because of the high rate of water reabsorption from the renal filtrate.

The effect of the relative differences in water reabsorption and urine concentration can be eliminated by
calculating the fractional excretion of sodium (FENa) in standard units (calculator 1) or for SI (international
units) (calculator 2). The FENa is most useful in patients with an increasing serum creatinine, decreased
urinary volume, and concern regarding an evolving acute renal failure. In that setting, a FENa <1 percent
suggests volume depletion or a "pre-renal" state that should respond to fluid resuscitation. A value greater
than 2 percent suggests intrinsic renal impairment. (See "Acute kidney injury in children: Clinical features,
etiology, evaluation, and diagnosis", section on 'Fractional excretion of sodium'.)

Use of the FENa in other clinical scenarios is fraught with potential error because the value for FENa that
defines hypovolemia varies inversely with the glomerular filtration rate. This issue is discussed in detail
separately. (See "Fractional excretion of sodium, urea, and other molecules in acute kidney injury (acute
renal failure)".)

Urine osmolality and specific gravity — In hypovolemic states, the urine should be concentrated with an
osmolality exceeding 450 mosmol/kg. However, this response may not be seen if concentrating ability is
impaired by renal disease, an osmotic diuresis, the administration of diuretics, or central or nephrogenic
diabetes insipidus. In addition, neonates are unable to form a maximally concentrated urine due to renal
immaturity. Thus, a high urine osmolality is consistent with hypovolemia, but a relatively isosmotic value
does not exclude hypovolemia.

Measuring the specific gravity also can assess urinary concentration. This test, however, is less accurate
than the osmolality, as it is dependent upon the size as well as the number of solute particles in the urine.
As a result, it should be used only if the osmolality cannot be measured; a value above 1.015 is suggestive
of a concentrated urine, as is usually seen with hypovolemia. This does not apply to diabetic ketoacidosis
because glucose is larger than the main solutes in normal urine (eg, sodium, potassium, ammonium, and
urea); as a result, a glucose solution has a higher specific gravity at a given osmolality than normal urine
(figure 2). (See "Urinalysis in the diagnosis of kidney disease", section on 'Urine osmolality'.)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics"
and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have about a given
condition. These articles are best for patients who want a general overview and who prefer short, easy-to-
read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more
detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want
in-depth information and are comfortable with some medical jargon.

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 topic (see "Patient education: Dehydration in children (The Basics)")

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

SUMMARY AND RECOMMENDATIONS — Volume depletion occurs when fluid is lost from the
extracellular space at a rate that exceeds intake. Extracellular fluid losses commonly occur from the
gastrointestinal tract (eg, diarrhea, vomiting, and bleeding), skin (eg, fever and burns), and urine (eg,
diuretic therapy and diabetes insipidus).

● Children are at increased risk for hypovolemia compared with adults because they have a higher
incidence of gastroenteritis and higher insensible loss due to a greater surface area-to-volume ratio,

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and may not be able to independently access fluids to replenish their losses. (See 'Introduction' above.)

● The evaluation of a child with hypovolemia includes determining the degree of extracellular fluid
depletion and the type of fluid lost, which may affect the serum concentration of electrolytes. (See
'Clinical assessment' above.)

● Volume depletion is most objectively measured as a change in weight from baseline. However, in most
cases, a previous recent weight is not available. As a result, a number of findings on physical
examination as well as pertinent history are used to help assess the severity of hypovolemia; mild (3 to
5 percent volume loss), moderate (6 to 9 percent volume loss), and severe (≥10 percent volume loss).
These findings include the pulse, blood pressure, skin turgor, systemic signs, and changes in urine
output (table 4).

● Laboratory testing can detect associated electrolyte and acid-base abnormalities, and impaired urinary
concentration.

● Serum sodium concentration varies with the relative loss of solute to water, which is affected by the
sodium and potassium concentration of the fluid loss, secretion of antidiuretic hormone (ADH), and the
amount of sodium and potassium concentration of replacement fluid. (See 'Serum sodium' above.)

● In children with gastroenteritis, hypokalemia is common due to loss of potassium in diarrheal stool.
However, serum potassium concentration may be higher than expected because of acidosis, which
promotes intracellular potassium movement to the extracellular fluid. (See 'Serum potassium' above.)

● Serum bicarbonate levels ≤17 mEq/L differentiate children with moderate to severe hypovolemia from
those with mild hypovolemia. In children with gastroenteritis, the low serum bicarbonate represents
metabolic acidosis usually due to loss of bicarbonate in the stool. (See 'Serum bicarbonate' above.)

● In children with hypovolemia, urine sodium concentration is usually less than 25 mEq/L and urinary
osmolality greater than 450 mosmol/kg. (See 'Urine sodium' above and 'Urine osmolality and specific
gravity' above.)

REFERENCES

1. Mange K, Matsuura D, Cizman B, et al. Language guiding therapy: the case of dehydration versus
volume depletion. Ann Intern Med 1997; 127:848.
2. Steiner MJ, DeWalt DA, Byerley JS. Is this child dehydrated? JAMA 2004; 291:2746.
3. 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.
4. King CK, Glass R, Bresee JS, et al. Managing acute gastroenteritis among children: oral rehydration,
maintenance, and nutritional therapy. MMWR Recomm Rep 2003; 52:1.
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children: a systematic review. Arch Dis Child 2015; 100:239.
6. Freedman SB, Vandermeer B, Milne A, et al. Diagnosing clinically significant dehydration in children
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dehydration in children. Pediatrics 1997; 99:E6.
9. Falszewska A, Dziechciarz P, Szajewska H. Diagnostic accuracy of clinical dehydration scales in
children. Eur J Pediatr 2017; 176:1021.

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10. Rose BD. New approach to disturbances in the plasma sodium concentration. Am J Med 1986;
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