Clinical Manifestations

The first step in caring for the child with dehydration is to assess the degree of dehydration (Table 54-1), which dictates both the urgency of the situation and the volume of fluid needed for rehydration. The infant with mild dehydration (3-5% of body weight dehydrated) has few clinical signs or symptoms. The infant may be thirsty; the alert parent may notice a decline in urine output. The history is most helpful. The infant with moderate dehydration has clear physical signs and symptoms. Intravascular space depletion is evident from an increased heart rate and reduced urine output. This patient needs fairly prompt intervention. The infant with severe dehydration is gravely ill. The decrease in blood pressure indicates that vital organs may be receiving inadequate perfusion. Immediate and aggressive intervention is necessary. If possible, the child with severe dehydration should initially receive intravenous therapy. For older children and adults, mild, moderate, or severe dehydration represents a lower percentage of body weight lost. This difference occurs because water accounts for a higher percentage of body weight in infants (Chapter 52).

Clinical assessment of dehydration is only an estimate; thus, the patient must be continually reevaluated during therapy. The degree of dehydration is underestimated in hypernatremic dehydration because the movement of water from the intracellular space to the extracellular space helps preserve the intravascular volume.

The history usually suggests the etiology of the dehydration and may predict whether the patient will have a normal sodium concentration (isotonic dehydration), hyponatremic dehydration, or hypernatremic dehydration. The neonate with dehydration due to poor intake of breast milk often has hypernatremic dehydration. Hypernatremic dehydration is likely in any child with losses of hypotonic fluid and poor water intake, such as may occur with diarrhea, and poor oral intake due to anorexia or emesis. Hyponatremic dehydration occurs in the child with diarrhea who is taking in large quantities of low-salt fluid, such as water or diluted formula.

Some children with dehydration are appropriately thirsty, but in others, the lack of intake is part of the pathophysiology of the dehydration. Even though decreased urine output is present in most children with dehydration, good urine output may be deceptively present if a child has an underlying renal defect, such as diabetes insipidus or a salt-wasting nephropathy, or in infants with hypernatremic dehydration.

Physical examination findings are usually proportional to the degree of dehydration. Parents may be helpful in assessment of the child for the presence of sunken eyes, because this finding may be subtle. Pinching and gently twisting the skin of the abdominal or thoracic wall detects tenting of the skin (turgor, elasticity). Tented skin remains in a pinched position rather than springing quickly back to normal. It is difficult to properly assess tenting of the skin in premature infants or severely malnourished children. Activation of the sympathetic nervous system causes tachycardia in children with intravascular volume depletion; diaphoresis may also be present. Postural changes in blood pressure are often helpful for evaluating and assessing the response to therapy in children with dehydration. Tachypnea in children with dehydration may be present secondary to a metabolic acidosis from stool losses of bicarbonate or due to lactic acidosis from shock (Chapter 64).

Laboratory Findings

Several laboratory findings are useful for evaluating the child with dehydration. The serum sodium concentration determines the type of dehydration. Metabolic acidosis may be due to stool bicarbonate losses in children with diarrhea, secondary renal insufficiency, or lactic acidosis from shock. The anion gap is useful for differentiating among the various causes of a metabolic acidosis (Chapter 52). Emesis or nasogastric losses usually cause a metabolic alkalosis. The serum potassium concentration may be low as a result of diarrheal losses. In children with dehydration due to emesis, gastric potassium losses, metabolic alkalosis, and urinary potassium losses all contribute to hypokalemia. Metabolic acidosis, which causes a shift of potassium out of cells, and renal insufficiency may lead to hyperkalemia. A combination of mechanisms may be present; thus, it may be difficult to predict the child’s acid-base status or serum potassium level from the history alone.

The blood urea nitrogen (BUN) value and serum creatinine concentration are useful in assessing the child with dehydration. Volume depletion without parenchymal renal injury may cause a disproportionate increase in the BUN with little or no change in the creatinine concentration. This condition is secondary to increased passive resorption of urea in the proximal tubule due to appropriate renal conservation of sodium and water. The increase in the BUN with moderate or severe dehydration may be absent or blunted in the child with poor protein intake, because urea production depends on protein degradation. The BUN may be disproportionately increased in the child with increased urea production, as occurs with a gastrointestinal bleed or with the use of glucocorticoids, which increase catabolism. A significant elevation of the creatinine concentration suggests renal insufficiency, although a small, transient increase can occur with dehydration. Acute tubular necrosis (Chapter 529) due to volume depletion is the most common etiology of renal insufficiency in a child with volume depletion, but occasionally the child may have previously undetected chronic renal insufficiency or an alternative explanation for the acute renal failure. Renal vein thrombosis is a well-described sequela of severe dehydration in infants; possible findings include thrombocytopenia and hematuria (Chapter 513.7).

Hemoconcentration due to dehydration causes increases in hematocrit, hemoglobin, and serum proteins. These values normalize with rehydration. A normal hemoglobin concentration during acute dehydration may mask an underlying anemia. A decreased albumin level in a dehydrated patient suggests a chronic disease, such as malnutrition, nephrotic syndrome, or liver disease, or an acute process, such as capillary leak. An acute or chronic protein-losing enteropathy may also cause a low serum albumin concentration.

Calculation of the Fluid Deficit

Determining the fluid deficit necessitates clinical determination of the percentage of dehydration and multiplication of this percentage by the patient’s weight; a child who weighs 10 kg and is 10% dehydrated has a fluid deficit of 1 L.

Approach to Dehydration

The child with dehydration needs acute intervention to ensure that there is adequate tissue perfusion. This resuscitation phase requires rapid restoration of the circulating intravascular volume and treatment of shock with an isotonic solution, such as normal saline (NS) or Ringer lactate (LR) (Chapter 64). The child is given a fluid bolus, usually 20 mL/kg of the isotonic fluid, over approximately 20 min. The child with severe dehydration may require multiple fluid boluses and may need to receive the boluses as fast as possible. In a child with a known or probable metabolic alkalosis (the child with isolated vomiting), LR should not be used because the lactate would worsen the alkalosis.

Colloids, such as blood, 5% albumin, and plasma, are rarely needed for fluid boluses. A crystalloid solution (NS or LR) is satisfactory, with both less infectious risk and lower cost. Blood is obviously indicated in the child with significant anemia or acute blood loss. Plasma is useful for children with a coagulopathy. The child with hypoalbuminemia may benefit from 5% albumin, although there is evidence that albumin infusions increase mortality in adults. The volume and the infusion rate for colloids are generally modified compared with crystalloids (Chapters 464 and 467).

The initial resuscitation and rehydration phase is complete when the child has an adequate intravascular volume. Typically, the child shows clinical improvement, including a lower heart rate, normalization of blood pressure, improved perfusion, better urine output, and a more alert affect.

With adequate intravascular volume, it is appropriate to plan the fluid therapy for the next 24 hr. A general approach is outlined in Table 54-2, with the caveat that there are many different approaches to correcting dehydration. In isonatremic or hyponatremic dehydration, the entire fluid deficit is corrected over 24 hr; a slower approach is used for hypernatremic dehydration (discussed later). To assure that the intravascular volume is restored, the patient receives an additional 20-mL/kg bolus of an isotonic fluid over 2 hr. The child’s total fluid needs are added together (maintenance + deficit). The volume of isotonic fluids that the patient has received is subtracted from this total. The remaining fluid volume is then administered over 24 hr. The potassium concentration may need to be decreased or, less commonly, increased, depending on the clinical situation. Potassium is not usually included in the intravenous fluids until the patient voids. Children with significant ongoing losses need to receive an appropriate replacement solution (Chapter 53).

Monitoring and Adjusting Therapy

The formulation of a plan for correcting a child’s dehydration is only the beginning of management. All calculations in fluid therapy are only approximations. This statement is especially true for the assessment of percentage dehydration. It is equally important to monitor the patient during treatment and to modify therapy on the basis of the clinical situation. The cornerstones of patient monitoring are listed in Table 54-3. The patient’s vital signs are useful indicators of intravascular volume status. The child with decreased blood pressure and an increased heart rate will probably benefit from a fluid bolus. Central venous pressure is an excellent indicator of fluid status in the critically ill child with shock.

The patient’s intake and output are critically important in the dehydrated child. The child who, after 8 hr of therapy, has more output than input because of continuing diarrhea needs to be started on a replacement solution. See the guidelines in Chapter 53 for selecting an appropriate replacement solution. Urine output is useful for evaluating the success of therapy. Good urine output indicates that rehydration has been successful.

Signs of dehydration on physical examination suggest the need for continued rehydration. Signs of fluid overload, such as edema and pulmonary congestion, are present in the child who is overhydrated. An accurate daily weight measurement is critical for the management of the dehydrated child. There should be a gain in weight during successful therapy.

Measurement of serum electrolyte levels at least daily is appropriate for any child who is receiving intravenous rehydration. Such a child is at risk for sodium, potassium, and acid-base disorders. It is always important to look at trends. For instance, a sodium value of 144 mEq/L is normal; but if the sodium concentration was 136 mEq/L 12 hr earlier, then there is a distinct risk that the child will be hypernatremic in 12 or 24 hr. It is advisable to be proactive in adjusting fluid therapy.

Both hypokalemia and hyperkalemia are potentially serious (Chapter 52). Because dehydration can be associated with acute renal failure and hyperkalemia, potassium is withheld from intravenous fluids until the patient has voided. The potassium concentration in the patient’s intravenous fluids is not rigidly prescribed. Rather, the patient’s serum potassium level and underlying renal function are used to modify potassium delivery. The patient with an elevated creatinine value and a potassium level of 5 mEq/L does not receive any potassium until the serum potassium level decreases. Conversely, the patient with a potassium level of 2.5 mEq/L may require additional potassium.

Metabolic acidosis can be quite severe in dehydrated children. Although normal kidneys eventually correct this problem, a child with renal dysfunction may be unable to correct a metabolic acidosis, and a portion of the patient’s intravenous sodium chloride may have to be replaced with sodium bicarbonate or sodium acetate.

The serum potassium level is modified by the patient’s acid-base status. Acidosis increases serum potassium by causing intracellular potassium to move into the extracellular space. Thus, as acidosis is corrected, the potassium concentration decreases. Again, it is best to anticipate this problem and to monitor the serum potassium concentration and adjust potassium administration appropriately.

Hyponatremic Dehydration

The pathogenesis of hyponatremic dehydration usually involves a combination of sodium and water loss and water retention to compensate for the volume depletion. The patient has a pathologic increase in fluid loss, and the lost fluid contains sodium. Most fluid that is lost has a lower sodium concentration, so patients with only fluid loss would have hypernatremia. Diarrhea has, on average, a sodium concentration of 50 mEq/L. Replacing diarrheal fluid with water, which has almost no sodium, causes a reduction in the serum sodium concentration. The volume depletion stimulates synthesis of antidiuretic hormone, resulting in reduced renal water excretion. Hence, the body’s usual mechanism for preventing hyponatremia, renal water excretion, is blocked. The risk of hyponatremia is further increased if the volume depletion is due to loss of fluid with a higher sodium concentration, as may occur with renal salt wasting, third space losses, or diarrhea with high sodium content (cholera).

The initial goal in treating hyponatremia is correction of intravascular volume depletion with isotonic fluid (NS or LR). An overly rapid (>12 mEq/L over the first 24 hr) or overcorrection in the serum sodium concentration (>135 mEq/L) is associated with an increased risk of central pontine myelinolysis (Chapter 52). Most patients with hyponatremic dehydration do well with the same basic strategy that is outlined in Table 54-2. Again, potassium delivery is adjusted according to the initial serum potassium level and the patient’s renal function. Potassium is not given until the patient voids.

The patient’s sodium concentration is monitored closely to ensure appropriate correction, and the sodium concentration of the fluid is adjusted accordingly. Patients with ongoing losses require an appropriate replacement solution (Chapter 53). Patients with neurologic symptoms (seizures) as a result of hyponatremia need to receive an acute infusion of hypertonic (3%) saline to increase the serum sodium concentration rapidly (Chapter 52).

Hypernatremic Dehydration

Hypernatremic dehydration is the most dangerous form of dehydration due to complications of hypernatremia and of therapy. Hypernatremia can cause serious neurologic damage, including central nervous system hemorrhages and thrombosis. This damage appears to be secondary to the movement of water from the brain cells into the hypertonic extracellular fluid, causing brain cell shrinkage and tearing blood vessels within the brain (Chapter 52).

The movement of water from the intracellular space to the extracellular space during hypernatremic dehydration partially protects the intravascular volume. Unfortunately, because the initial manifestations are milder, children with hypernatremic dehydration are often brought for medical attention with more profound dehydration.

Children with hypernatremic dehydration are often lethargic, and they may be irritable when touched. Hypernatremia may cause fever, hypertonicity, and hyperreflexia. More severe neurologic symptoms may develop if cerebral bleeding or thrombosis occurs.

Overly rapid treatment of hypernatremic dehydration may cause significant morbidity and mortality. Idiogenic osmoles are generated within the brain during the development of hypernatremia. These idiogenic osmoles increase the osmolality within the cells of the brain, providing protection against brain cell shrinkage caused by movement of water out of the cells and into the hypertonic extracellular fluid. They dissipate slowly during the correction of hypernatremia. With overly rapid lowering of the extracellular osmolality during the correction of hypernatremia, an osmotic gradient may be created that causes water movement from the extracellular space into the cells of the brain, producing cerebral edema. Symptoms of the resultant cerebral edema can range from seizures to brain herniation and death.

To minimize the risk of cerebral edema during the correction of hypernatremic dehydration, the serum sodium concentration should not decrease by >12 mEq/L every 24 hr. The deficits in severe hypernatremic dehydration may need to be corrected over 2-4 days (Table 54-4).

The initial resuscitation of hypernatremic dehydration requires restoration of the intravascular volume with NS. LR should not be used because it is more hypotonic than NS and may cause too rapid a decrease in the serum sodium concentration, especially if multiple fluid boluses are necessary.

To avoid cerebral edema during correction of hypernatremic dehydration, the fluid deficit is corrected slowly. The rate of correction depends on the initial sodium concentration (see Table 54-4). There is no general agreement on the choice or the rate of fluid for correcting hypernatremic dehydration. The choice and the rate of fluid administration are not nearly as important as vigilant monitoring of the serum sodium concentration and adjustment of the therapy according to the result (see Table 54-4). The rate of decrease of the serum sodium concentration is roughly related to the “free water” delivery, although there is considerable variation between patients. Free water is water without sodium. NS contains no free water, half-normal saline () is 50% free water, and water is 100% free water. Smaller patients, to achieve the same decrease in the sodium concentration, tend to need higher amounts of free water delivery per kilogram because of higher insensible fluid losses. Five percent dextrose (D5) with is usually an appropriate starting solution for a patient with hypernatremic dehydration. Some patients, especially infants with ongoing high insensible water losses, may need to receive D5 0.2NS. Others require a higher sodium concentration than is present in D5 . A child with dehydration due to pure free water loss, as usually occurs with diabetes insipidus, usually needs a more hypotonic fluid than a child with depletion of both sodium and water due to diarrhea.

Adjustment in the sodium concentration of the intravenous fluid is the most common approach to modifying the rate of decrease in the serum concentration (see Table 54-4). For difficult patients with severe hypernatremia, having 2 intravenous solutions (D5 and D5 NS, both with the same concentration of potassium) at the bedside can facilitate this approach by allowing for rapid adjustments of the rates of the 2 fluids. If the serum sodium concentration decreases too rapidly, the rate of D5 NS can be increased and the rate of D5 can be decreased by the same amount. Adjustment in the total rate of fluid delivery is another approach to modifying free water delivery. For example, if the serum sodium concentration is decreasing too slowly, the rate of the intravenous fluid can be increased, thereby increasing the delivery of free water. There is limited flexibility in modifying the rate of the intravenous fluid because patients generally should receive 1.25-1.5 times the normal maintenance fluid rate. Nevertheless, in some situations, it can be a helpful adjustment.

Because increasing the rate of the intravenous fluid increases the rate of decline of the sodium concentration, signs of volume depletion are treated with additional isotonic fluid boluses. The serum potassium concentration and the level of renal function dictate the potassium concentration of the intravenous fluid; potassium is withheld until the patient voids. Patients with hypernatremic dehydration need an appropriate replacement solution if they have ongoing, excessive losses (Chapter 53).

Seizures are the most common manifestation of cerebral edema from an overly rapid decrease of the serum sodium concentration during correction of hypernatremic dehydration. Acutely, increasing the serum concentration via an infusion of 3% sodium chloride can reverse the cerebral edema. Each 1-mL/kg of 3% sodium chloride increases the serum sodium concentration by approximately 1 mEq/L. An infusion of 4 mL/kg often results in resolution of the symptoms. This strategy is similar to that used for treating symptomatic hyponatremia (Chapter 52).

In patients with severe hypernatremia, oral fluids must be used cautiously. Infant formula, because of its low sodium concentration, has a high free water content, and especially if added to intravenous therapy, it may contribute to a rapid decrease in the serum sodium concentration. Less hypotonic fluid, such as an oral rehydration solution, may be more appropriate initially (Chapter 332). If oral intake is allowed, its contribution to free water delivery must be taken into account, and adjustment in the intravenous fluid is usually appropriate. Judicious monitoring of the serum sodium concentration is critical.