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Clinical assessment of hypovolemia (dehydration) in children

Clinical assessment of hypovolemia (dehydration) in children
Literature review current through: Jan 2024.
This topic last updated: Feb 13, 2023.

INTRODUCTION — 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 in resource-abundant settings: Initial evaluation and management".)

The clinical assessment of hypovolemia in pediatric patients will be reviewed here. Treatment of hypovolemia is discussed elsewhere. (See "Treatment of hypovolemia (dehydration) in children in resource-abundant settings" and "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management".)

ETIOLOGY — Hypovolemia can occur from any of the following mechanisms; some patients may have a combination of these:

Excessive fluid loss – Common causes include:

Losses from the gastrointestinal tract (eg, diarrhea, vomiting)

Insensible losses from the skin (eg, fever, burns)

Major bleeding

Urinary losses (eg, glucosuria, diuretic therapy, diabetes insipidus)

Inadequate fluid intake.

Third-spacing – 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 can occur in children with the following conditions:

Edema due to kidney disease, heart failure, or critical illness

Liver failure

Malnutrition

Increased vascular permeability from systemic inflammation

Bleeding into a third-space (eg, retroperitoneal bleed)

Ascites due to acute intraabdominal pathology

INCREASED VULNERABILITY TO HYPOVOLEMIA — Compared with adults, pediatric patients 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.

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 volume depletion

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

Estimating degree of hypovolemia

Preferred method (change in weight) — 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, an acute 2 kg weight loss generally reflects the loss of two liters of fluid.

Other methods — If the pre-illness weight is not known, the degree of volume loss can be estimated based upon a physical examination findings and the clinical history (table 1).

Factors to assess – The following should be assessed and taken into account when estimating the degree of volume loss:

History of decreased urine output, lethargy, or irritability.

Pulse and respiratory rate – Significant tachycardia and/or an abnormal breathing pattern (deep respirations, tachypnea) suggest moderate to severe volume depletion. Normal respiratory and heart rates according to age are summarized in the table (table 2).

Blood pressure – Blood pressure is generally preserved in children with hypovolemia. Normal blood pressure ranges according to age are summarized in the tables for males (table 3) and females (table 4). Hypotension indicates severe hypovolemia and/or a secondary pathology (eg, distributive shock due to sepsis). (See "Septic shock in children in resource-abundant settings: Rapid recognition and initial resuscitation (first hour)".)

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.

Peripheral perfusion and capillary refill – A capillary refill time greater than three seconds is considered abnormal [3]. (See "Assessment of systemic perfusion in children", section on 'Capillary refill time'.)

Categorizing the degree of hypovolemia – Based on the above findings, the degree of hypovolemia can be categorized as mild, moderate, or severe (table 1):

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 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 abnormal respiratory pattern (deep respirations and/or tachypnea). 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) – Signs of severe hypovolemia include decreased peripheral perfusion with delayed capillary refill, cool and mottled extremities, lethargy, abnormal respiratory pattern, tachycardia, and even hypotension in the most severe cases. Severe hypovolemia requires immediate aggressive isotonic fluid resuscitation to restore the effective circulating volume (ECV) and prevent cardiovascular collapse. (See "Treatment of hypovolemia (dehydration) in children in resource-abundant settings", section on 'Intravenous rehydration therapy'.)

In a systematic review of the literature, the most useful clinical signs that identified children with clinically significant hypovolemia (ie, >5 percent) were delayed capillary refill time, reduced skin turgor, and abnormal respiratory pattern [2].

When estimating the degree of hypovolemia, it is generally better to asses a combination of findings rather than focusing on a single parameter [2,4]. Clinical scales have been developed for this purpose, such as the four-item Clinical Dehydration and Gorelick scales [5,6].

In systematic reviews of the literature, the use of the Clinical Dehydration scale appeared to improve the diagnostic accuracy of determining moderate dehydration (>6 percent volume loss) in developed countries [4,7]. However, in resource-limited areas, assessment tools, including the Clinical Dehydration and Gorelick scales and WHO guidelines (table 5), were of limited diagnostic value in determining the severity of dehydration [7,8]. (See "Approach to the child with acute diarrhea in resource-limited settings", section on 'Clinical assessment'.)

Type of fluid lost — The type of fluid loss differs depending on the clinical scenario. As examples:

Gastrointestinal losses – In children with gastrointestinal illness (eg, gastroenteritis), 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 [9-11]. Organic solutes, such as urea and fermentation products, make up the remaining osmoles.

Diabetic ketoacidosis (DKA) – In children with volume depletion causes by marked hyperglycemia in the setting of diabetes mellitus or DKA, the hyperosmolar state pulls water out of the cells, thereby minimizing the degree of extracellular hypovolemia. This also minimizes some of the physical findings that typically indicate hypovolemia (eg, poor skin turgor). (See "Diabetic ketoacidosis in children: Clinical features and diagnosis".)

Diabetes insipidus (DI) – Fluid losses in states of urinary concentrating defects such as DI consist of water loss alone, resulting 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.

LABORATORY TESTING

Whom to test — Laboratory testing is warranted for children with moderate to severe hypovolemia and/or those who require intravenous fluid repletion. Testing is generally not necessary for children with mild volume depletion since electrolytes and acid base balance are typically normal in these patients.

Tests to perform — We suggest performing the following tests when assessing children with moderate to severe volume depletion:

Serum electrolytes

Blood glucose

Blood urea nitrogen (BUN) and creatinine

Urine osmolarity or specific gravity

Urine sodium

Additional testing may be warranted depending on the etiology of volume depletion. The suggested laboratory evaluation for some common causes of hypovolemia is provided separately:

(See "Acute viral gastroenteritis in children in resource-abundant countries: Clinical features and diagnosis", section on 'Laboratory evaluation'.)

(See "Diabetic ketoacidosis in children: Clinical features and diagnosis", section on 'Laboratory tests'.)

(See "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Laboratory studies'.)

(See "Moderate and severe thermal burns in children: Emergency management", section on 'Diagnostic studies'.)

Interpretation

Serum sodium — 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 in resource-abundant settings".)

Hyponatremia – Hyponatremia (serum sodium <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 'Factors that affect sodium' 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 [10,12], 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 [9]. This entity is referred to as hypernatremic dehydration [13,14].

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.

Factors that affect sodium

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 [15]. 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 [16]. This effect of pH does not appear to be as important with lactic acidosis or ketoacidosis [17]. 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 — A low serum bicarbonate concentration (<17 mEq/L) generally reflects at least a moderate degree of hypovolemia [2,18]. In some causes of hypovolemia, the low bicarbonate also reflects the underlying process (eg, loss of bicarbonate in the stool in children with gastroenteritis, ketoacidosis in children with DKA).

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.

Blood urea nitrogen — An elevated BUN level is consistent with hypovolemia and the level generally correlates with the severity of hypovolemia. The BUN level reflects the decline in glomerular filtration rate and increase in sodium and water reabsorption and urea recycling. However, BUN may be increased by other factors such as bleeding or catabolic tissue breakdown.

Urine sodium — A low urine sodium concentration (<25 mEq/L) is consistent with a hypovolemic state. However, the interpretation needs to be considered within the clinical context of the individual patient as higher values do not necessarily exclude hypovolemia.

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 <25 mEq/L and may actually become non-detectable. However, in the setting of both avid sodium and water resorption, both sodium excretion and urine volume are low and the urine sodium concentration may be 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".)

Urine osmolality and specific gravity

Urine osmolality – 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 arginine vasopressin deficiency (AVP-D, previously called central diabetes insipidus) or arginine vasopressin resistance (AVP-R, previously called 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.

Specific gravity – Measuring the specific gravity also can assess urinary concentration. A value >1.015 is suggestive of a concentrated urine, as is usually seen with hypovolemia. 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. Specific gravity is a poor indicator of volume status in patients with DKA 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 'Specific gravity'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Fluid and electrolyte disorders in children".)

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

Etiology – Hypovolemia can occur from any of the following mechanisms; some patients may have a combination of these (see 'Etiology' above):

Excessive fluid loss, including losses from the gastrointestinal tract (eg, diarrhea, vomiting, insensible losses from the skin (eg, fever, burns), major bleeding, or urinary losses (eg, glucosuria, diuretic therapy, diabetes insipidus).

Inadequate fluid intake.

Third-spacing.

Increased vulnerability in children – 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. In addition, young children may not be able to independently access fluids to replenish their losses. (See 'Increased vulnerability to hypovolemia' above.)

Estimating the degree of hypovolemia – Volume depletion is most objectively measured as a change in weight from baseline. If the pre-illness weight is not known, the degree of volume loss can be estimated based upon a physical examination findings and the clinical history as summarized in the table (table 1). (See 'Estimating degree of hypovolemia' above.)

Laboratory testing – Laboratory testing is warranted for children with moderate to severe hypovolemia and/or those who require intravenous fluid repletion. Testing is generally not necessary for children with mild volume depletion since electrolytes and acid base balance are typically normal in these patients.

We suggest performing the following tests when assessing children with moderate to severe volume depletion (see 'Tests to perform' above):

Serum electrolytes

Blood glucose

Blood urea nitrogen (BUN) and creatinine

Urine osmolarity or specific gravity

Urine sodium

The interpretation of these tests is reviewed in detail above. (See 'Interpretation' above.)

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