Fluid management is an important part of the care of hospitalized children.
As much as 70% of lean body mass in infants is water.
Children, in general, have approximately 60% of lean body mass as water and an overall higher concentration of extracellular fluid than adults.
Daily maintenance fluids for healthy children include fluid for physiologic needs, daily output, and insensible losses.
Dehydration is a concern for morbidity and mortality in children <5 years of age.
Gastroenteritis is responsible for 200,000 hospitalizations per year for children with resulting dehydration.
There is a known, although not thoroughly precise, relationship between caloric expenditure, fluid requirements, and body weight.
H2O is generated in the process of metabolism.
Heat regulation requires H2O.
Solute excretion requires H2O.
Metabolic rate is related to body surface area (BSA) and to weight.
Metabolic rate (kcals/day) approximates fluid requirement (mL/day).
The Holliday-Segar method is commonly used to calculate maintenance fluid requirements for a 24-hour period in children.
4-2-1 Method: An additional method of calculating maintenance fluid requirements. This provides the hourly calculated rate rather than a volume for a 24-hour period.
Use a nomogram to find BSA in meters squared (m2). The patient’s height and weight are needed for nomogram.
Or, to calculate the BSA using height and weight:
Hydration refers to the proper balance between water and electrolytes.
Fluid and electrolyte therapies require careful calculation with careful attention to detail.
Dehydration can be estimated based on clinical status. In children, usually 3%, 6%, or 9%. In infants, observed as 5%, 10%, or 15%. Other evaluation methods describe dehydration as mild, moderate, or severe based on physical assessment.
Moderate to severe dehydration can lead to hypovolemic shock. Treating hypovolemia and maintaining euvolemia are critical.
Fluid and electrolytes are involved in the dehydration and rehydration process.
Shifts from intracellular to extracellular spaces can explain changing laboratory values in many cases.
Clinical features can assist in determining the level of dehydration or overhydration.
Aldosterone is released in response to the renin-angiotensin-aldosterone release in cases of extracellular volume depletion.
Antidiuretic hormone (ADH) is released in response to volume depletion, which results in decreased urine output and increased absorption of water by the kidneys.
It is most important to evaluate the child’s history to determine and treat the etiology of fluid loss as early as possible.
There are characteristic findings associated with both dehydration and overhydration.
Dehydration is more common in young children and has classic components on physical examination, which are assessed based on percentage of hydration: mild, moderate, or severe.
Assessment of dehydration includes parameters of mental status, heart rate, presence of tears, skin condition, capillary refill, blood pressure, and urine output.
Hydration can be classified based on serum sodium levels (Table 8.1).
TABLE 8.1 Classification of Dehydration
Restore circulating volume to prevent or treat shock using fluid boluses 20 mL/kg of crystalloid fluid until improvement in circulation, urine output, and capillary refill time.
Some underlying medical conditions (e.g., kidney disease, cardiac disease) require exquisite care and evaluation during fluid resuscitation to prevent fluid overload and subsequent decompensation.
Restore intracellular and extracellular water and electrolyte deficits within 24 hours in hyponatremic and isonatremic dehydration; restore over 48 hours in hypernatremic dehydration.
Replace ongoing losses, as appropriate.
Correct acid-base imbalances; may be achieved solely through treating the underlying cause.
Children can experience overhydration or water intoxication through processes that correct hyponatremia too quickly or by administering intravenous (IV) fluids including plain D5W or other hypotonic solutions.
Infants can develop hyponatremia from incorrect mixing of formula with too much water.
Overhydration can occur as a result of other pathologic problems, including nephrotic syndrome and syndrome of inappropriate antidiuretic hormone (SIADH).
Children are vulnerable to cerebral edema through correcting hyponatremia too quickly.
Methods of calculating fluid deficit.
Determine clinical/physical features that represent % dehydration.
Current weight × 1,000 × % dehydration = volume of fluid to replace.
The most precise method of determining fluid deficit is weight loss, but it is not typical to have recent pre-illness weight results.
TABLE 8.2 Oral Rehydration Fluids
Maintenance fluid calculation is addressed in the previous section.
Calculation of fluid deficit can be accomplished in several ways:
Calculate percentage of weight loss, if known.
Estimate the percentage of fluid loss based on clinical evaluation.
Percentage of dehydration × Weight in kg × 10 = mL fluid needs.
Replacement of fluid deficit can be accomplished either through oral rehydration therapy if shock is not present, or with IV fluids.
Oral rehydration fluids should have goal of replacing deficit volume over 4 to 6 hours, then to replace ongoing losses (Table 8.2).
See Table 8.3.
Replace half of the deficit plus one-third of the maintenance over 8 hours, then the remaining half of the deficit and two-third of the maintenance over the next 16 hours, or replace the whole deficit over 8 hours, then the whole day’s maintenance over 16 hours.
Combine the total volume deficit plus the maintenance volume for 48 hours; administer this total volume divided over 48 hours. Prevents osmotic fluid shifts resulting in cerebral edema and seizures. Ensure serum sodium level is not corrected by >10 mEq/L/day.
TABLE 8.3 Intravenous Fluid Composition
Fluid losses normally occurring through the skin, respiratory tract, and gastrointestinal (GI) tract.
Losses through the kidney system are not insensible losses.
In some conditions (e.g., diabetes insipidus (DI), kidney disease), calculation of insensible fluid losses may be used to determine appropriate fluid administration (e.g., replacing insensible losses and urine output or replacing insensible losses only).
Prescription for daily electrolytes:
Sodium: 2 to 3 mEq/100 mL of fluid.
Potassium: 2 mEq/100 mL of fluid.
Chloride: 5 to 6 mEq/100 mL of fluid.
Replacement for electrolyte loss:
Sodium replacement: calculating the sodium deficit.
Only correct sodium quickly to avoid compromise such as seizures.
Na deficit = (135 – measured Na) mEq/L × 100/L
It is difficult to accurately assess potassium deficit, as potassium is mainly intracellular and shifts based on catabolism, cell injury, and acid-base balance.
It is estimated that 1 mEq/L potassium loss = 10% to 30% total body potassium loss.
Calcium is a component of multisystem body functions, including neuronal activity, muscular contraction, myocardial contraction, hemocoagulation, and bone formation.
Calcium is present in three forms in plasma.
Bound to albumin (plasma protein).
Diffusible (such as calcium citrate or calcium phosphate).
Ionized calcium is the form most important for body functions.
Calcium concentration is regulated by renal, skeletal, and GI systems.
Hypocalcemia: serum calcium <9 mg/dL; ionized calcium <1.1 mmol/L.
Hypercalcemia: serum calcium >10 mg/dL.
Binding of ionized calcium to citrate after red cell transfusion, ethylene glycol ingestion, malabsorption, hypoparathyroidism, renal failure, rhabdomyolysis, sepsis, tumor lysis syndrome, and pancreatitis.
DiGeorge syndrome, malnutrition, certain medications such as furosemide.
Electrolyte abnormalities of hyperphosphatemia and hypomagnesemia.
Excessive intake, excessive vitamins A and D intake, hyperparathyroidism, immobility, malignancy, sarcoidosis, and thiazide diuretics.
Regulation via GI, renal, and bone.
Primary regulation by parathyroid hormone (PTH).
PTH promotes calcium absorption from the bone and decreases renal excretion of calcium.
PTH mediates the process of conversion of vitamin D to active form, thus increasing intestinal absorption of calcium.
Risk of hypocalcemia in neonates is increased due to decreased calcium intake, increased fetal calcium levels leading to transient parathyroid suppression, and PTH resistance.
Can include neuromuscular irritability, Chvostek sign, confusion, irritability, laryngospasm, muscle cramps, numbness and tingling, paresthesias and weakness, seizures, tetany, and Trousseau sign.
ECG changes include sinus tachycardia, long QT interval, and AV blocks.
Evidence of myocardial irritability with severe hypocalcemia can include hypotension and bradycardia.
Can be asymptomatic.
Severe hypercalcemia is indicated by GI signs of nausea, anorexia, constipation, neurologic signs such as anxiety, depression, headache, lethargy, hypotonia, seizures, and coma. Cardiac arrhythmias include shortened QT interval, sinus bradycardia, first-degree heart block, and ventricular tachycardia.
Hypercalcemia can result in polyuria, renal calculi, and renal tubular dysfunction.
Serum laboratory analysis should include total serum calcium, ionized calcium, and complete metabolic panel, PTH, pH, and 25-hydroxy vitamin D and 1,25-dihydroxy vitamin D.
Urine calcium, phosphate, and creatinine.
Radiographs of ankle and wrist for bone density.
Chest radiograph for evaluation of presence of thymus.
Serum laboratory analysis should include total serum calcium, ionized calcium, complete metabolic panel, PTH, pH, 25-hydroxy vitamin D and 1,25-dihydroxy vitamin D, and urine electrolytes. PTH-related protein level if suspected malignancy and fluorescence in situ hybridization probe for Williams syndrome.
Abdominal radiography (kidneys, ureters, and bladder [KUB]) or renal ultrasound to evaluate for renal calculi.
Symptomatic hypocalcemia, acute repletion:
Parenteral calcium replacement:
Calcium chloride (10-20 mg/kg/dose) given through central venous catheter only.
Calcium gluconate (100 mg/kg/dose) given through either peripheral or central venous catheter.
Chronic hypocalcemia, subacute or chronic repletion:
Enteral supplements such as calcium carbonate, citrate, calcium gluconate, glubionate, lactate, along with vitamin D supplements and 1,25-dihydroxy vitamin D for patients unable to convert vitamin D.
Identification and treatment of underlying disease.
Hydration with normal saline (NS) (often 2-3 times maintenance rate).
Hypercalcemia may cause increased urinary output, resulting in dehydration.
Increased urinary sodium excretion enhances calcium excretion.
Diuresis with loop diuretics, which aids in calcium excretion.
Avoid thiazide diuretics that reduce calcium excretion in urine.
Glucocorticoids—reduce effects and level of vitamin D.
Only calcitonin for rapid correction of calcium or if hypercalcemia is refractory to hydration and diuresis.
Bisphosphonates for rapid treatment of severe hyperphosphatemia, in consultation with endocrinologist.
If severe or refractory, hemodialysis may be indicated.
Ionized calcium should be interpreted in relation to serum pH.
Hypomagnesemia may lead to hypocalcemia.
If hypocalcemia is refractory, replace magnesium.
Correct severe hyperphosphatemia prior to correction of related hypocalcemia to avoid soft tissue calcification.
The major role of chloride is to maintain electrical neutrality by balancing cations (usually sodium) in the blood.
Functions as a regulator of acid-base balance in the body due to inverse relationship with bicarbonate.
Hypochloremia: serum chloride <97 mmol/L.
Hyperchloremia: serum chloride >108 mmol/L.
Hypochloremia is associated with:
Removal of gastric secretions by nasogastric tube.
Metabolic alkalosis contributes to hypochloremia.
Hyperchloremia: associated with:
Excessive chloride administration.
Renal tubular acidosis (RTA).
Urinary diversion into the colon or ileum.
Chloride regulation is by renal and GI mechanisms.
Indirectly affected by aldosterone, as it passively follows renal sodium reabsorption.
Passively follows sodium absorption in GI tract.
Actively absorbed in the presence of bicarbonate excretion in intestine.
Hydrochloric acid represents active secretion of chloride by stomach.
Rarely occurs as sole electrolyte abnormality.
When associated with metabolic alkalosis, may exhibit arrhythmias, decreased respiratory effort, seizures in severe states.
When associated with volume depletion or dehydration, may exhibit thirst, lethargy, tachycardia, tachypnea, and delayed capillary refill.
Hypocalcemia, due to increased binding of calcium to albumin.
Often does not result in any symptoms.
May exhibit Kussmaul respirations (especially in diabetes ketoacidosis); possible neurologic symptoms include lethargy, headache, and confusion.
Altered cardiac function and response to inotropes.
Associated with hypernatremia and hyperkalemia.
Serum electrolyte evaluation and serum pH.
Urine chloride and sodium.
Laboratory studies will be based on determining the cause of hyperchloremia and associated acidosis.