Fluid Management for the Pediatric Surgical Patient

Fluid management of the pediatric surgical patient represents an important aspect of medical care, particularly for initial treatment of the ill child. ^[1] An understanding of the physiology of fluid requirements is essential for care of these children. Infants and children are sensitive to small degrees of dehydration, and commonly used protocols for pediatric fluid therapy do not consider the rapidly changing perioperative physiology in this patient population. Standard formulas for fluid therapy can be modified to account for these rapid changes in physiology.

For patient education resources, see the Children's Health Center, as well as Dehydration in Children.

Body-fluid composition

The total body water content of a term gestation newborn is 75-80%. After birth, efflux of fluid from the intracellular fluid (ICF) compartment to the extracellular fluid (ECF) compartment floods the neonatal kidney, resulting in a saltwater diuresis by 48-72 hours of life. This is reflected in loss of as much as 10% of body weight in the first week. By the age of 1 year, total body water slowly decreases to adult levels (60%). Extracellular water content falls in parallel with total body water content, from 45% at term to 20-25% of adult levels at 1 year.

For a premature neonate, both total body water and ECF vary inversely with gestational age, whereas ICF increases with gestational age. A premature neonate's extracellular water content at 28-32 weeks' gestation is approximately half of the body weight. By the age of 1 week, the loss of extracellular water can lead to a weight loss of as much as 15%; in 1 week of life, a neonate unloads what would have taken 8 weeks in utero.

Changes in body-fluid compartments progress in an orderly fashion in utero, but they are interrupted if a neonate is born prematurely. This reduction in ECF volume is important in the normal transition from fetal to postnatal life. Preterm infants with excess fluid intake have an increased incidence of patent ductus arteriosus, left ventricular failure, respiratory distress, and necrotizing enterocolitis.

Renal electrolyte and fluid physiology

The postnatal shift in body fluids is principally mediated through the kidneys' regulation of water and sodium excretion. Renal handling of water is related to glomerular filtration and tubular function. A term newborn's glomerular filtration rate (GFR) is 25% of an adult's. The newborn's GFR rapidly rises during the first week of life, then slowly increases to adult levels by age 2 years.

Despite this low GFR, term-gestation infants can handle large water loads because the positive effect of the low concentrating capacity of the newborn kidney counteracts the negative effect of the low GFR. However, premature infants have limited compensatory mechanisms and may not tolerate large water loads or hypovolemia without severe clinical complications. Fluid overload can be associated with increased neonatal morbidity and mortality. ^{[2, 3]}

Kidneys in the neonate have a limited capacity to excrete both concentrated and dilute urine. The concentrating capacity of an infant's kidneys is less than that of an adult's. The physiologic range of urine osmolality in neonates can range from a lower limit of 50 mOsm/kg to a maximum of 600-800 mOsm/kg in response to water deprivation. In contrast, maximum urine osmolality in an adult is 1200 mOsm/kg. ^[4]

Variations in the release of vasopressin or antidiuretic hormone (ADH) regulate the osmolality of ECF. Although dehydrated newborns cannot concentrate urine as efficiently as adults can, free water clearance is greater in infants than in adults. After a free water load, infants can excrete a markedly diluted urine of as much as 50 mOsm/kg; in contrast, the maximally dilute urine in adults is 70-100 mOsm/kg.

Clinical states that can increase basal fluid requirements in the infant include hyperthermia, increased evaporative losses from mechanical ventilation, and altered transepithelial losses from premature gestational age. Simple maneuvers to control these alterations of fluid balance include increasing basal fluid replacement in infants with hyperthermia or in those placed under bilirubin heating lamps and ensuring that all ventilator tubing is humidified.

The patient's state of hydration, renal function, and osmolar load determine his or her urine output and concentration. Osmolar load consists of endogenous and exogenous solutes that the kidney must clear to maintain homeostasis. The volume of renal water must be sufficient for the kidney to clear the osmolar load given its concentrating capacity.

Fluid management for the pediatric surgical patient is divided into the following three phases:

• Deficit therapy
• Maintenance therapy
• Replacement therapy

Deficit therapy

Deficit therapy is defined as the management of fluid and electrolyte losses that occur before the patient's presentation. Such management is based on the following three components:

• Estimation of the severity of dehydration
• Determination of the type of fluid deficit
• Restoration of the deficit

The severity of dehydration is estimated from the patient's history and physical condition. In children with mild dehydration (ie, loss of 1-5% of body fluid volume), findings are largely based on the history (eg, vomiting or diarrhea), with minimal findings during physical examination.

Children with moderate dehydration (ie, 6-10% loss) have histories of fluid losses plus physical findings that include tenting of the skin, weight loss, sunken eyes and fontanel, slight lethargy, and dry mucous membranes. Most patients with severe dehydration (ie, 11-15% loss) have cardiovascular instability (eg, skin mottling, tachycardia, hypotension) and neurologic involvement (eg, irritability, coma).

The type of fluid deficit can be determined from the patient's history, physical findings, electrolyte values, and serum tonicity. The following are the three categories of deficit:

• Isotonic (ie, serum osmolarity of 270-300 mOsm/L, serum Na ⁺ concentration of 130-150 mEq/L)
• Hypotonic (ie, serum osmolarity < 270 mOsm/L, serum Na ⁺ concentration < 130 mEq/L)
• Hypertonic (ie, serum osmolarity >310 mOsm/L, serum Na ⁺ concentration >150 mEq/L) - Patients with hypertonic dehydration require special attention because complications, such as cerebral edema, may occur during rehydration ^[5]

Restoration of cardiovascular function, central nervous system (CNS) function, and renal perfusion are the primary concerns in correction of a fluid deficit. Therapy should be initiated with an isotonic fluid volume expander. Total fluid-deficit restoration may require considerable time. In particular, potassium losses cannot be quickly replaced. After the child is producing urine, a small amount of potassium (< 40 mEq/L) should be added to the fluid. Deficit therapy is carefully monitored by frequently assessing the patient's clinical condition, urine output, and urine specific gravity.

Colloids vs crystalloids

Both colloid and crystalloid solutions are widely used in the fluid resuscitation of critically ill children. Several choices of colloid are available, including albumin, hydroxyethyl starch (HES; eg, Hetastarch), and dextran. Crystalloids include normal saline and lactated Ringer (LR) solution.

There has been considerable debate about the relative effectiveness of colloids and crystalloids. In a 2004 Cochrane review, investigators examined a series of randomized and quasirandomized trials of colloids compared with crystalloids in patients who required volume replacement. ^[6] However, trials in neonates were excluded. No evidence suggested that resuscitation with colloids reduced the risk of death compared with resuscitation with crystalloids in patients with trauma or burns or in those who underwent surgery.

In a 2018 update of this Cochrane review, which similarly excluded trials in neonates, the authors concluded that the use of starches, dextrans, albumin, fresh frozen plasma (FFP), or gelatins as opposed to crystalloids probably has little if any effect on mortality. ^[7]  They found that starches probably increase the need for blood transfusion and renal replacement therapy (RRT) slightly and that albumin or FFP may make little or no difference to the need for RRT. Evidence for adverse events was uncertain.

Small randomized and nonrandomized studies in term and preterm neonates showed some benefit with the use of albumin vs crystalloids or HES. Specifically, these studies reported decreased edema, negative fluid balance, and less weight gain; however, no differences in length of intensive care unit (ICU) stay, ventilation days, or mortality were noted. ^{[8, 9]}

A study of pediatric patients with severe sepsis or septic shock who were treated with crystalloids found that higher doses (median 3-day cumulative amount, >193 mL/kg) were associated with worse outcomes (higher pediatric ICU [PICU] mortality, longer PICU stays, and more ventilator days) than lower doses (< 193 mL/kg). ^[10]

There are several reasons to avoid the use of colloids for resuscitation. Colloids are not associated with improved survival. The use of colloids (eg, HES) is associated with an increased need for RRT in critically ill adult patients, and they are more expensive than crystalloids. ^{[6, 11]}

Maintenance therapy

Maintenance therapy aims to replace water and electrolytes lost under ordinary conditions. In the perioperative period, maintenance fluid administration may not sufficiently account for the increased fluid requirements caused by third-space losses into the interstitium and gut. Specific recommendations vary with the patient, the procedure, and the type and amount of fluid administered during the operation. The fluid for maintenance therapy replaces deficits arising primarily from insensible losses and urinary or gastrointestinal (GI) losses.

There has been growing recognition of the increased risk of hyponatremia in hospitalized children in intensive care and postoperative settings who receive hypotonic maintenance fluids. ^{[12, 13, 14]}  Several studies, including a randomized controlled trial and a Cochrane analysis, found that the use of isotonic fluids is associated with fewer electrolyte derangements and concluded that isotonic maintenance fluids are preferable to hypotonic solutions in hospitalized children. ^{[1, 14, 15, 16, 17]}  Adding 1-2.5% glucose to isotonic maintenance fluid can help prevent the development of hypoglycemia. ^[1]

Evaporative losses consist of solute-free water losses through the skin and respiratory tract. Insensible water loss tends to be higher in preterm infants. Evaporative loss through the skin makes up about 70% of insensible water loss, whereas the remainder is lost from the respiratory tract. Ambient humidity and temperature affect insensible losses. Patients receiving humidified air have less insensible loss than those not receiving humidified air. Patients with hyperthermia or tachypnea similarly have exaggerated insensible losses.

Although the replacement of increased insensible water loss is important, the emphasis of therapy is on the prevention of excessive insensible water loss rather than on replacement alone.

In a euvolemic state, urinary losses are 280-300 mOsm/kg H₂O, with a specific gravity of 1.008-1.015. In some circumstances (eg, diabetes insipidus or prematurity), production of dilute urine is obligatory, and maintenance fluid volume must be increased. In others (eg, excessive antidiuretic hormone [ADH] secretion or physiologic stress), a patient may be unable to decrease urine osmolality to 300 mOsm/kg H₂O, and maintenance fluid volume must be decreased. In euvolemia, urinary losses account for two thirds of total maintenance fluids.

Total requirements for maintenance fluid (see Table 2 below ^[4] ) can be estimated from common formulas (see below). The patient's condition should be assessed frequently during maintenance therapy. If the estimate is correct, the patient's electrolyte levels should remain stable, and the patient should remain clinically euvolemic. Abnormal electrolyte levels or clinical signs of hypervolemia or hypovolemia indicate a need to reassess each component of the patient's maintenance therapy.

Table 2. Daily Fluid Requirements During First Week of Life (Open Table in a new window)

A guide for maintenance fluid therapy for children is as follows:

• 0-10 kg - 100 mL/kg/day (4 mL/kg/hr)
• 10-20 kg - 1000 mL/day + 50 mL/kg/day (40 mL/hr + 2 mL/kg/hr)
• >20 kg - 1500 mL/day + 25 mL/kg/day (60 mL/hr + 1 mL/kg/hr)

Replacement therapy

Replacement fluid therapy is designed to replace ongoing abnormal fluid and electrolyte losses. Because the constituents of these losses often substantially differ from the composition of maintenance fluids, simply increasing the volume of maintenance fluids to compensate for these losses may be hazardous. The authors generally replace large-volume stoma or other fluid losses with a physiologic equivalent fluid (see Table 3 below).

Table 3. Typical Electrolyte Composition of Body Fluids for Child with Abnormal Fluid and Electrolyte Losses and of Common IV Fluids (Open Table in a new window)

As an alternative, measuring the electrolyte content of these losses and replacing them milliequivalent for milliequivalent or milliliter for milliliter may be preferred in select circumstances. For patients who are under severe physiologic stress or are undergoing extensive surgery, third-space losses into the interstitium should be calculated and replacement therapy adjusted accordingly.

Pyloric stenosis

Hypertrophic pyloric stenosis often causes progressive nonbilious emesis in infants. This diagnosis can usually be confirmed by finding an enlarged pyloric olive during careful physical examination. Obtain further diagnostic studies (typically ultrasonography [US]) for infants whose histories indicate pyloric stenosis but who have no palpable pyloric mass.

The morbidity of pyloric stenosis closely relates to the degree of dehydration. The dehydration of a child with pyloric stenosis results from both fluid and electrolyte losses, with losses of H⁺ and Cl^– from gastric secretions. After progressive fluid losses, a hypokalemic-hypochloremic metabolic alkalosis develops.

Reports have suggested that a substantial number of children with pyloric stenosis may have hyperkalemia, rather than hypokalemia. ^[18] No obvious physiologic rationale for hyperkalemia in this setting is described, and the clinical importance of this finding in the management of this condition is unclear.

Children with severe dehydration have accelerated renal K⁺ and H⁺ losses due to an attempt to retain fluid and Na⁺ ions. As the kidneys attempt to retain Na⁺, an initial compensatory excretion of K⁺ occurs. Then, as K⁺ deficit develops, the kidney attempts to retain both Na⁺ and K⁺; thus, it excretes H⁺ instead of K⁺, and paradoxic aciduria then occurs. This cycle can be broken only by adequately replacing fluids and electrolytes.

In cases of clinical dehydration, children with pyloric stenosis require rehydration with IV fluid therapy before surgery. Administer 5% dextrose in water (D5W) with 0.45% NaCl IV at 1.5 times the maintenance rate. Severely dehydrated children should receive initial deficit fluid therapy with 0.9% NaCl.

When urine output is demonstrated, KCl 10-20 mEq/L can be added to the fluids. Defer surgery for pyloric stenosis until the child is adequately rehydrated. The severity of dehydration can be estimated by physical examination and by measuring serum Cl^– and HCO₃^– levels. The degree of dehydration and the clinical response to fluid replacement therapy guide the duration of preoperative preparation in a child with pyloric stenosis.

Optimal resuscitation is determined by normal skin turgor, by moist mucous membranes, and, most important, by urine output greater than 1 mL/kg/hr and a serum HCO₃^– level lower than 30 mEq/dL with a Cl^– level higher than 100 mEq/dL. ^[19]

Enteral feeds can usually be started within 2 hours after uncomplicated pyloromyotomy, and full feeds can be given within 12-24 hours. Postoperative electrolyte abnormalities are rare and should not be routinely checked.

Gastroschisis

Gastroschisis is a defect of the anterior abdominal wall just lateral to the umbilicus. In contrast to an omphalocele, no peritoneal sac is present; thus, evisceration of the bowel occurs through the defect during intrauterine life. The irritating effect of amniotic fluid on the exposed bowel wall results in a chemical form of peritonitis characterized by a thick, edematous, occasionally exudative membrane. Fluid management for an infant with gastroschisis can be complex and requires strict attention to the rapidly changing needs of the neonate, who may be critically ill.

After birth, neonates with gastroschisis are subject to tremendously increased insensible fluid losses related to exposure of the eviscerated bowel. Hypothermia, hypovolemia, and sepsis are the major problems to prevent. To limit fluid and heat losses, the eviscerated bowel is covered in moist nonadherent sponges, and the lower half of the baby, including the eviscerated bowel, is covered in plastic bag or a bowel bag.

Fluid requirements in a neonate with gastroschisis can range up to 2.5 times those of a healthy newborn in the first 24 hours of life. As a general rule, the more matted and inflamed the exposed viscera appear, the greater the fluid requirements of the infant.

Initial resuscitation of an infant with gastroschisis is generally begun with a 10- to 20-kg bolus of 0.9% NaCl or LR solution in addition to maintenance fluids. Additional isotonic fluid is administered until urine output is established. The infant's ongoing fluid needs are tailored to his or her specific hemodynamics, but volumes are generally 120-175 mL/kg/day of D5W with 0.45% NaCl with added potassium.

The patient's acid-base balance should be closely monitored because metabolic acidosis is common as a result of poor perfusion related to hypovolemia. The infant is kept in a thermoneutral environment, and an orogastric tube is placed in the stomach to prevent the patient from swallowing air and aspirating intestinal contents because infants with gastroschisis tend to have a prolonged, adynamic ileus.

Omphalocele

Patients with omphalocele also have an abdominal-wall defect, though it is typically covered and protrudes directly through the umbilicus. The development is felt to be due to the failure of the lateral embryonic folds to fuse in the midline. ^[20] Because omphalocele occurs early in gestation, other associated anomalies of midline structures are frequently present, most commonly in the heart. ^[21] Pulmonary hypoplasia is also a serious associated problem and is related to the compression of the developing lungs.

Because the defect is covered, fluid resuscitation is typically not as vigorous as it is in patients with gastroschisis. However, Aizenfisz et al demonstrated an increased fluid requirement for patients presenting with ruptured omphalocele. ^[22] Patients with ruptured omphalocele had a larger fluid requirement than those with gastroschisis or an intact omphalocele sac.