Energy requirements (per kilogram body weight) and metabolic rate are higher in infancy and childhood (for further information, see Chapter 14). The ratio of BSA to volume is significantly higher in infants and children than in adults. As a result, pediatric evaporative fluid losses and fluid requirements per kilogram body weight are higher than those of adults.

Insensible water loss (IWL) is fluid lost through the skin, via evaporation and sweat, and through the respiratory tract. Normal IWL is approximately 300 to 400 mL/m² BSA per day (for more detailed information, see Evolve Table 12-2 in the Chapter 12 Supplement on the Evolve Website). Fever increases IWL by approximately 0.42 mL/kg per hour for each degree Celsius increase above 37° C. Increased IWL can occur with increased air movement across the skin, and with tachypnea, unless inspired air is humidified. IWL decreases when ambient and inspired air are humidified.

Table 12-2 Formulas for Estimating Daily Maintenance Fluid and Electrolyte Requirements for Children

	Daily Requirements	Hourly Requirements
Fluid Requirements Estimated from Weight*
Newborn (up to 72 hr after birth)	60-100 mL/kg (newborns are born with excess body water)	–
Up to 10 kg	100 mL/kg (can increase up to 150 mL/kg to provide caloric requirements if renal and cardiac function are adequate)	4 mL/kg
11-20 kg	1000 mL for the first 10 kg + 50 mL/kg for each kg over 10 kg	40 mL for first 10 kg + 2 mL/kg for each kg over 10 kg
21-30 kg	1500 mL for the first 20 kg + 25 mL/kg for each kg over 20 kg	60 mL for first 20 kg + 1 mL/kg for each kg over 20 kg
Fluid Requirements Estimated from Body Surface Area (BSA)
Maintenance	1500 mL/m² BSA	–
Insensible losses	300-400 mL/m² BSA	–
Electrolytes
Sodium (Na)	2-4 mEq/kg	–
Potassium (K)	1-2 mEq/kg	–
Chloride (Cl)	2-3 mEq/kg	–
Calcium (Ca)	0.5-3 mEq/kg	–
Phosphorous (Phos)	0.5-2 mmol/kg	–
Magnesium (Mg)	0.4-0.9 mEq/kg	–

* The “maintenance” fluids calculated by these formulas must only be used as a starting point to determine the fluid requirements of an individual patient. If intravascular volume is adequate, children with cardiac, pulmonary, or renal failure or increased intracranial pressure should generally receive less than these calculated “maintenance” fluids. The formula utilizing body weight generally results in a generous “maintenance” fluid total.

Fluid and electrolyte requirements will vary with age and clinical condition. Normal baseline fluid and electrolyte requirements are listed in Table 12-2. Critical care practitioners use estimated maintenance fluid requirements as a baseline and individualize administered fluid and electrolytes to meet patient needs.

Fluid, Electrolyte, and Glucose Balance

Serum Glucose in Critically Ill or Injured Children

Although a serum glucose concentration of 60 to 180 mg/dL is normally maintained over a wide range of conditions, critically ill or injured children often develop hypoglycemia or hyperglycemia. Infants have high glucose needs and low glycogen stores, so they can rapidly become hypoglycemic during critical illness or injury.²⁴ Providers should monitor serum glucose concentration with point-of-care testing, if possible, and treat hypoglycemia as needed. Treatment of hypoglycemia should avoid frequent, intermittent bolus administration of large quantities of glucose; provision of a continuous source of glucose is preferable.

Hyperglycemia can result from steroid administration, stress response, relative hypoinsulinemia, or insulin resistance and has been associated with increased mortality in critically ill children in some studies. A prospective, randomized study of tight control of serum glucose concentration in critically ill children (targeted to age-adjusted normal fasting glucose concentration) reduced critical care unit mortality,³⁷ but was associated with episodes of hypoglycemia. In general, an insulin infusion (0.5-1 unit regular insulin/kg per hour) is often titrated during the first 18 to 24 hours of critical care therapy to maintain the serum glucose concentration less than 150 mg/dL (range will vary; use your unit protocol). Careful monitoring is required to avoid and treat episodes of hypoglycemia. The ultimate value versus risk of this approach is still under investigation.

Electrolyte homeostasis and common imbalances

Table 12-3 presents a summary of electrolyte imbalances and associated clinical manifestations in critically ill infants and children. In the following sections, approximate ranges for normal and abnormal serum electrolyte concentrations are listed, but providers should use normal ranges referenced by the clinical laboratory in their practice settings.

Table 12-3 Electrolyte Imbalances in Critically Ill Infants and Children

Sodium Homeostasis

Sodium (Na⁺), the primary extracellular cation, plays an important role in the regulation of action potentials in skeletal muscles, nerves, and the myocardium; maintenance of acid-base balance; and maintenance of ECF balance. The normal serum sodium concentration is approximately 135 to 145 mEq/L.

Alterations in sodium and fluid balance often occur concurrently and can alter serum osmolality. An abnormal serum sodium concentration often results from fluid volume deficit or excess. GFR and aldosterone secretion both affect sodium balance.

Sodium Imbalance: Hyponatremia

Etiology

Hyponatremia is a low serum sodium concentration, typically less than 130 to 135 mEq/L. It often develops as a complication of disease or therapy. The critically ill infant or child can develop hyponatremia from excessive water intake relative to sodium, excess water retention, increased sodium loss, or a combination of these factors.¹⁰

Hyponatremia can occur in conjunction with hypervolemia, euvolemia, or hypovolemia. Hypervolemic hyponatremia is associated with water intoxication, nephrotic syndrome, cardiac failure, renal failure, and the syndrome of inappropriate antidiuretic hormone (SIADH). Hypovolemic hyponatremia can occur with renal losses (e.g., osmotic diuresis, renal tubular acidosis) or extrarenal losses (e.g., diarrhea, vomiting, burns).¹⁰ Other potential causes include adrenal insufficiency, excessive use of diuretics, and cerebral salt-wasting syndrome.

A laboratory report of a low serum sodium concentration can be misleading. These pseudohyponatremic states are associated with hyperlipidemia, hyperproteinemia, or hyperglycemia. In hyperlipidemia or hyperproteinemia, the lipid or protein displaces fluid from serum, decreasing the relative volume of water and electrolytes. As a result, the reported serum sodium concentration will be low. The total body sodium actually may be normal, although its concentration (in milliequivalents per liter of plasma, or mEq/L) is reduced. Hyperlipidemia of this degree usually produces a milky white plasma.

Because the serum osmolality is determined by the combined effects of particles (solutes) in the serum—especially the sodium, glucose, and blood urea nitrogen—the serum osmolality can be normal if a fall in the concentration of one solute is accompanied by a commensurate (in osmotic effect) increase in the concentration of another solute. With significant hyperglycemia, the high glucose concentration increases serum osmolality, drawing fluid into the vascular space; this may artificially reduce the serum sodium concentration. The significance of this dilutional effect is debatable—the serum sodium concentration may still influence osmotic changes to which the cells are exposed. To estimate the potential effect of severe hyperglycemia on the serum sodium concentration, for every 100 mg/dL rise in serum glucose above normal, the serum sodium concentration is likely to be depressed approximately 1.6 mEq/L below 135 mEq/L.

Pathophysiology and Clinical Signs and Symptoms

An isolated decrease in serum sodium concentration (i.e., without a rise in glucose or blood urea nitrogen) reduces serum osmolality; an acute fall in serum osmolality produces a shift of water from the extracellular compartment (including vascular space) to the intracellular compartment. This fluid shift can cause swelling of cells (edema). Because there is limited capacity for volume expansion within the skull, swelling of brain cells (cerebral edema) can have catastrophic consequences, such as brain herniation and death.

The volume of water shift and the severity of clinical manifestations with hyponatremia are directly related to the acuity and the magnitude of the fall in serum sodium and osmolality. Infants and children who develop hyponatremia that gradually worsens over several days or weeks (e.g., with adrenocortical insufficiency) typically have milder clinical manifestations and may be asymptomatic until the serum sodium is very low.²⁶

Acute hyponatremia that develops within hours or days (i.e., <48 hours) is more likely to produce cerebral edema.²⁶ Seizures and coma are associated with a serum sodium concentration less than 120 mEq/L.

Management

If the child is at risk for hyponatremia, providers should closely monitor the child’s serum sodium concentration to detect and promptly treat hyponatremia before it becomes severe. Frequent neurologic assessments are indicated. Notify an on-call provider immediately if the child develops altered level of consciousness, seizures, or signs of increased intracranial pressure.

Hyponatremia associated with neurologic symptoms is a neurologic emergency. Urgent treatment includes administration of 2 to 4 mL/kg of 3% saline (513 mEq sodium/L, or 0.513 mEq/mL); this will typically raise the child’s serum sodium concentration approximately 1 to 2 mEq/L and raise serum osmolality sufficiently to slow the intracellular water shift. If the SIADH produces seizures or other severe symptoms, hyponatremia and water intoxication can be treated acutely by administration of hypertonic saline (2-4 mL/kg of 3% saline) and furosemide (1-2 mg/kg). These medications will increase the serum sodium concentration and eliminate excess free water (see section, Specific Diseases, Syndrome of Inappropriate Antidiuretic Hormone).

Management of hyponatremia includes restoration of appropriate intravascular volume, replacement of the sodium deficit, and identification and treatment of the underlying cause. Symptomatic hypovolemia is treated with boluses of normal saline or lactated Ringer’s solution. Management of hypervolemic hyponatremia may include fluid restriction and administration of loop diuretics.

Once the child’s neurologic status is stable and perfusion is adequate, plans are made to replace the sodium deficit. The following formula ³⁶ is used to calculate the sodium deficit:

During treatment of hyponatremia, providers must closely monitor the serum sodium concentration and the rate of rise in the concentration. If the serum sodium and osmolality are raised too rapidly, the resulting water shifts from the cellular to the extracellular (including intravascular) compartments can produce neurologic complications including intracranial bleeding (Box 12-1). In general, the serum sodium should be raised no faster than approximately 0.5-1.0 mEq/L per hour.³⁵ Additional important assessments include strict monitoring of intake and output, urine specific gravity, serum electrolytes, serum osmolality, and daily weights.

Box 12-1 Advanced Concepts: Potential Central Nervous System Complications of Rapid Changes in Serum Sodium and Osmolality

The brain does not tolerate rapid or significant water shifts into and out of the cells. A shift of water into brain cells—such as that occurring with an acute fall in serum sodium concentration and serum osmolality—is likely to produce cerebral edema. A rapid shift of water from cells, including brain cells, can cause the cells to shrink and can result in cerebral dysfunction. Cells in the gray matter and tissue in the white matter in the brain swell and shrink at different rates when water shifts occur. As a result, significant water shifts between intracellular and extracellular compartments in the brain can cause tearing of cerebral bridging veins and intracranial bleeding.

Rapid correction of hyponatremia has been shown to result in cerebral dysfunction, linked with damage to the myelin sheath of neurons. This myelinolysis is called central pontine myelinolysis if it occurs in the pons (brainstem) and osmotic demyelinization syndrome if it occurs elsewhere in the brain. Signs of brain dysfunction can include decreased level of consciousness, lack of coordination, paralysis, and dysphagia. Because there is no known treatment for such cerebral dysfunction, and it can cause permanent disability, prevention is critical. In general, unless neurologic symptoms indicate the need for more aggressive treatment, providers should aim to correct hyponatremia or hypernatremia no faster than approximately 0.5 mEq/L per hour (or 10-12 mEq/L per day). For more information, consult the National Institutes of Health Web site: http://www.ninds.nih.gov/disorders/central_pontine/central_pontine_myelinolysis.htm.

Sodium Imbalances: Hypernatremia

Etiology

Hypernatremia (serum Na⁺ >145-150 mEq/L) occurs less frequently than hyponatremia. One of the body’s major defenses against hypernatremia is thirst. Infants, small children, and any children with significant developmental delay, decreased level of consciousness, or critical illness have an increased risk of hypernatremia during episodes of fluid loss, because they may not be able to signal caregivers of thirst or drink additional fluids.

Hypernatremia is most likely to result from a water deficit (e.g., dehydration, diuretic use, diabetes insipidus, DI). Less commonly, hypernatremia can result from excessive sodium intake, such as if powder for infant formula is incorrectly diluted. The child with hypernatremia may be hypovolemic, euvolemic, or hypervolemic; therefore, it is important to assess the child’s fluid volume status when determining the cause of the hypernatremia.

Pathophysiology and Clinical Signs and Symptoms

Hypernatremia typically increases the serum osmolality. The rise in osmolality stimulates the posterior pituitary to release ADH, which increases renal water reabsorption until the osmolality returns to normal. The increased osmolality associated with hypernatremia also leads to a shift in water from the intracellular to the extracellular compartment, including into the vascular space. This water movement from the cells can cause cellular dehydration and central nervous system dysfunction. Complications including subdural, subarachnoid, and intracerebral bleeding and sinus vein thrombosis can develop with acute and severe increases in serum sodium concentration and the resulting water shift (see Box 12-1). Permanent central nervous system dysfunction can result when the serum sodium concentration is extremely high (e.g., >165-170 mEq/L).¹² When serum osmolality is chronically elevated, brain cells will generate idiogenic osmoles to maintain cell volume (Box 12-2).

Box 12-2 Advanced Concepts: The Role of Idiogenic Osmoles in Brain Cells

When extracellular (including serum) osmolality rises, water shifts from the intracellular to the extracellular compartment, and cells typically shrink. When the serum osmolality is chronically elevated, brain cells generate idiogenic osmoles (e.g., glycine and taurine) to help brain cells maintain normal cell volume despite a water shift to the extracellular space. These idiogenic osmoles, however, may contribute to cerebral edema if a high serum osmolality is lowered too rapidly.

Patients who are unable to produce and/or respond to ADH (e.g., patients with DI) are at risk for development of significant hypernatremia and hypovolemia. These patients must be closely monitored to detect and treat these complications before they become severe.

Management

If the patient with hypernatremia has signs of inadequate tissue perfusion (i.e., shock), administer isotonic crystalloid by bolus (20 mL/kg) until perfusion is adequate. Avoid excessive bolus fluid administration (i.e., beyond that needed to treat shock), because it can contribute to a rapid fall in serum sodium and osmolality resulting in cerebral edema and other neurologic complications (see Box 12-2).

Once shock is corrected, estimate the fluid deficit and plan to replace the deficit over 48 to 72 hours, while providing for maintenance fluid requirements as well as for replacement of any ongoing additional fluid losses (e.g., persistent diarrhea). The type of IV fluids administered will vary depending on the rate at which the serum sodium is falling during therapy. Generally, the serum sodium should decrease at a rate no faster than 0.5 to 1.0 mEq/L per hour.

Monitor patients for the clinical manifestations of cerebral edema throughout the course of their treatment. Management of the child with hypervolemic hypernatremia will typically involve loop diuretics and decreased sodium administration.

Potassium Homeostasis

Potassium is the primary intracellular cation (i.e., a positively charged ion). The magnitude of the transmembrane (i.e., between intracellular and extracellular) potassium gradient determines the excitability of nerve and muscle cells (including skeletal and heart muscle) and the rate of conduction of nerve impulses. Potassium also plays a significant role in the maintenance of acid-base balance.

The normal serum potassium (K⁺) concentration is 3.0 to 5.0 mEq/L. The intracellular potassium concentration is much higher, approximately 150 mEq/L.²⁸ Small alterations in serum potassium concentration can significantly affect the transmembrane gradient and therefore neuromuscular and cardiac function. The serum K+ concentration is affected by potassium intake and excretion, renal regulation, and serum pH. Because the intravascular (serum) potassium concentration represents only a small proportion of the total body potassium, accurate interpretation of the child’s potassium balance requires consideration of the child’s clinical status and acid-base balance.

Potassium ions normally shift between the intra- and extracellular compartments with changes in the serum pH (see Evolve Fig. 12-2 in the Chapter 12 Supplement on the Evolve Website). When the serum hydrogen ion concentration increases (i.e., with acidosis or a fall in pH), hydrogen moves from the extracellular to the intracellular compartment, where it is buffered. To maintain a balance of cation movement across cell membranes, the intracellular movement of hydrogen ions is associated with an extracellular shift of potassium. Thus, acidosis or a fall in pH (e.g., with correction of alkalosis) is associated with a rise in serum potassium concentration. In contrast, alkalosis or a rise in serum pH (e.g., with treatment of acidosis) is associated with a fall in serum potassium, because hydrogen ion shifts out of cells and is replaced by potassium.

The change in serum potassium concentration associated with changes in serum pH will always be in the direction opposite the change in pH. That is, if the pH falls (as in acidosis) the serum potassium usually rises; as acidosis is corrected (the pH rises) the serum potassium should fall. Hypokalemia with acidosis is particularly dangerous: as acidosis is treated and the serum pH rises, the serum potassium concentration will fall further. Thus, correction of acidosis in the child with hypokalemia and acidosis may result in a dangerously low serum potassium concentration. The potassium concentration should always be evaluated in light of the patient’s present acid-base status, and likely changes in potassium concentration should be anticipated in response to changes in acid-base status that will result from planned therapy.

The kidneys play a critical role in potassium homeostasis. Renal failure limits the kidney’s ability to excrete potassium and may result in hyperkalemia (see Chapter 13).