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.
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.
●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 systemic perfusion in children", section on 'Capillary refill time'.)
Although the degree of hypovolemia is a continuum, hypovolemia is divided into three clinical categories primarily for management decisions 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].
It has been proposed that combinations of signs and symptoms would 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 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 [6,9]. 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 [9,10]. (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 [11-13], 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.
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 "Diabetic ketoacidosis in children: Clinical features and diagnosis".)
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 less 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 [2,14]. 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 [2,14].
●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 [11,15]. 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 [12,16], 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 [11]. This entity is referred to as hypernatremic dehydration [17,18].
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.
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 [19]. 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 [20]. This effect of pH does not appear to be as important with lactic acidosis or ketoacidosis [21]. 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 [2,14]. 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 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 — 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 '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 — 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, 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.)
