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).