Fluid Management for the Pediatric Surgical Patient 

Updated: Feb 10, 2017
  • Author: Charles L Snyder, MD; Chief Editor: Robert K Minkes, MD, PhD  more...
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Background

Fluid management of the pediatric surgical patient represents an important aspect of medical care, particularly for initial treatment of the ill child. 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.

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Renal Physiology

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. [1] By age 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 increase with decreasing gestational age. For example, a premature neonate's extracellular water content at 28-32 weeks' gestation is 52% of his or her body weight. By age 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, [2] 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.

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 osmolarity in neonates can range from a lower limit of 50 mmol/L 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. [1]

Variations in the release of vasopressin [3] 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.

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Paradigm for Fluid Management

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
  • Repair 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 the 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 possible types:

  • 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 [4]

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

In a trial by Spandorfer et al that compared recombinant human hyaluronidase-facilitated subcutaneous (rHFSC) rehydration with standard IV rehydration in children with mild-to-moderate dehydration, rHFSC hydration, though inferior to IV hydration for the primary outcome measure—total fluid volume administered (emergency department [ED] plus inpatient )—was noninferior in the ED phase. [5] Thus, rHFSC hydration may br a reasonable treatment option for children with mild-to-moderate dehydration, especially when IV access is difficult.

Rapid rehydration therapy

In volume-depleted children, increasing importance is being given to the use of rapid replacement of extracellular fluid (ECF) losses as opposed to classic deficit therapy (see above). [6] For example, after severe burns, patients improve and mortality declines with rapid, generous expansion of ECF. The total amount of fluid given in the first 6-12 hours is often approximately 100 mL/kg of an ECF-type fluid (eg, normal saline or lactated Ringer [LR] solution). [7]

In describing rapid rehydration therapy, Friedman suggested that in children with moderate dehydration who cannot tolerate oral rehydration, ECF should be rapidly restored by administering LR solution at a dosage of 40 mL/kg in 1-2 hours [6] ; oral rehydration should be started after the intravenous (IV) infusion is completed.

In patients with severe dehydration, ECF should be rapidly restored with IV administration of lactated Ringer solution, 0.9% NaCl (ie, isotonic NaCl solution, normal saline), or both at a rate of 40 mL/kg over 1-2 hours. If skin turgor, alertness, and pulse rate do not return to normal by the end of the infusion, additional doses of 20-40 mL/kg should be infused over 1-2 hours.

A randomized pragmatic controlled trial by Freedman et al, which included 226 children with a diagnosis of dehydration secondary to gastroenteritis, concluded that rapid rehydration offered no relevant clinical advantages over standard IV rehydration in this setting. [8]

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 LR solution.

Debate about the relative effectiveness of colloids and crystalloids is ongoing. In a Cochrane review, investigators examined a series of randomized and quasirandomized trials of colloids compared with crystalloids in patients who required volume replacement. [9] 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.

Small randomized and nonrandomized studies in term and preterm neonates have shown some benefit with the use of albumin versus crystalloids or HESs. Specifically, these studies reported decreased edema, negative fluid balance, and less weight gain; however, no difference in length of intensive care unit (ICU) stay, ventilation days, or mortality were noted. [10, 11]

Because colloids are not associated with improved survival and because they are more expensive than crystalloids, their continued use in critically ill patients is probably not justified outside the context of randomized controlled trials. [9]

Maintenance therapy

The aim of maintenance therapy is to replace water and electrolytes lost under ordinary conditions. In the perioperative period, maintenance fluid administration often does not sufficiently account for the increased fluid requirements caused by third-space losses into the interstitium and gut. A plan for perioperative maintenance fluid therapy is outlined in Table 1 below.

Table 1. Guide for Early Postoperative and Maintenance Therapy (Open Table in a new window)

Age (mo) < 12 Hours After Surgery Maintenance Fluids
< 6 10% dextrose in water (D10W) with 0.45% NaCl at 1.5 times maintenance rate D10W with 0.2% NaCl plus KCl 10-20 mEq/L at maintenance rate
>6 5% dextrose in water (D5W) with lactated Ringer solution at 1.5 times maintenance rate D10W with 0.45% NaCl plus KCl 10-20 mEq/L at maintenance rate

The fluid for maintenance therapy replaces deficits arising from the following two processes:

  • Evaporative (ie, insensible) losses
  • Urinary and gastrointestinal (GI) losses

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

In a euvolemic state, urinary losses are 280-300 mOsm/kg of water, 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 of water, 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 [1] ) can be estimated from common formulas (see below). Frequently assess the patient's condition 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)

Birth Weight Day 1 Day 2 Day 3 Day 4 Day 5 Day 6 Day 7
<1000 g 80 100 120 130 140 150 160
1000-1500 g 80 95 110 120 130 140 150
>1500 g 60 75 90 105 120 135 150

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)

Body or IV Fluid Electrolytes (mEq/L)
Na+ K+ Cl HCO3
Gastric 70 5-15 120 0
Pancreas 140 5 50-100 100
Bile 130 5 100 40
Ileostomy 130 15-20 120 25-30
Diarrhea 50 35 40 50
Lactated Ringer solution 130 4 109 28
0.9% NaCl 154 0 154 0
0.45% NaCl 77 0 77 0

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 under severe physiologic stress or for those undergoing extensive surgery, calculate third-space losses into the interstitium, and adjust replacement therapy accordingly.

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Specific Clinical Scenarios

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) 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 the a substantial number of children with pyloric stenosis may have hyperkalemia, rather than hypokalemia. [12] No obvious physiologic rationale for hyperkalemia in this setting is described, and the clinical importance of this finding on managing 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. The urine pH of severely dehydrated children may demonstrate a paradoxic aciduria because the renal mechanisms for acid resorption are lost in an attempt to retain Na+ and K+ 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, moist mucous membranes, and most importantly by urine output of more than 1 mL/kg/hr and a serum HCO3 level less than 30 mEq/dL with a Cl level of more than 100 mEq/dL.

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 10-20/kg bolus of 0.9% NaCl or lactated Ringer (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. An orogastric tube is placed in the stomach to prevent the patient from swallowing air and aspirating intestinal contents because an infant with gastroschisis has a prolonged, adynamic ileus. The infant is given parenteral antibiotics (ampicillin and gentamicin) and kept in a thermoneutral environment.

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 failure of the lateral embryonic folds to fuse in the midline. [13] Because omphalocele occurs early in gestation, other associated anomalies of midline structures are frequently present, most commonly in the heart. [14] 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. [15] Patients with ruptured omphalocele had a larger fluid requirement than those with gastroschisis or an intact omphalocele sac.

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