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Fluid Management for the Pediatric Surgical Patient-emedicine
Fluid Management for the Pediatric Surgical Patient-emedicine
Body-fluid composition
The total body water content of a term gestation newborn is 75-80%. Total body
water decreases by 4-5% during the first week of life and is reflected in weight
loss. By 1 year of age, total body water slowly decreases to the adult levels of
60%. Extracellular water content decreases in parallel with total body water
content from 45% at term to 20-25% of adult levels by 1 year of age.
For a premature neonate, both total body water and extracellular fluid (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 1 week of life, the proportion of extracellular water decreases 12%;
neonate unloads in 1 week of life what would have taken 8 weeks in utero.
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. A newborn's GFR rapidly rises during the first
week of life and then slowly increases to adult levels by the age of 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.
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.
Section 4 of 7
PARADIGM FOR FLUID MANAGEMENT
Author Information Introduction Renal Physiology Paradigm For Fluid Management Specific Clinical Scenarios
Summary Bibliography
Deficit therapy
Deficit therapy is the management of fluid and electrolyte losses that occur before
the patient's presentation. Deficit therapy has 3 components: estimation of the
severity of dehydration, determination of the type of fluid deficit, and 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 their history (eg, of vomiting/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 estimated from the patient's history, physical
findings, electrolyte values, and serum tonicity. Types of dehydration are isotonic
(ie, serum osmolarity of 270-300 mOsm/L, serum Na+ concentration of 130-150
mEq/L), hypotonic (ie, serum osmolarity of <270 mOsm/L, serum Na+
concentration of <130 mEq/L), or hypertonic (ie, serum osmolarity of >310
mOsm/L, serum Na+ concentration of >150 mEq/L). Patients with hypertonic
dehydration require special attention because complications, such as cerebral
edema, may occur during rehydration.
Restoration of cardiovascular function, 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 replaced quickly. After the child is
producing urine, add a small amount of potassium (<40 mEq/L) to the fluid.
Continually monitor the adequacy of deficit therapy by assessing the patient's
clinical condition, urine output, and urine specific gravity.
Rapid rehydration therapy
Both colloid and crystalloid solutions are widely used in the fluid resuscitation of
critically ill children. Several choices of colloid are available: albumin, hydroxyethyl
starch (Hetastarch), and dextran.
Debate about the relative effectiveness of colloids compared with crystalloid fluids
(eg, Ringer lactate solution, normal saline) is ongoing. In a recent Cochrane
Database Review, investigators examined a series of randomized and
quasirandomized trials of colloids compared with crystalloids in patients requiring
volume replacement (Roberts, 2005). 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.
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 (Roberts,
2005).
Maintenance therapy
The aim of maintenance therapy is to replace water and electrolytes lost under
ordinary conditions. In the perioperative patient, maintenance fluid administration
often does not sufficiently account for the increased fluid requirements caused by
third-space losses into the interstitium and gut. Table 1 outlines a plan for
perioperative maintenance fluid therapy.
The fluid for maintenance therapy replaces losses from 2 processes: evaporative
(ie, insensible) losses and urinary losses. Evaporative losses consisted of solute-
free water losses through the skin and lungs. Under ordinary conditions,
insensible losses account for approximately 30-35% of total maintenance volume,
and this free water represents approximately a third of the total requirement for
maintenance fluid. 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.
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,
prematurity), the production of dilute urine is obligatory, and the volume of
maintenance fluids must be increased appropriately. In other circumstances (eg,
excessive ADH secretion, physiologic stress), a patient may be unable to
decrease urine osmolality to 300 mOsm/kg of water, and the volume of
maintenance fluids must be decreased. Under euvolemic conditions, urinary
losses account for two thirds of total maintenance fluids.
A guide for maintenance fluid therapy for term infants and older children is as
follows:
Newborn
o Day 1 - 50-60 mL/kg/d D10 in water
o Day 2 - 100 mL/kg/d 10% dextrose D10 in 1/4 NS
o After day 7 - 100-150 mL/kg/d D5-10 in 1/4 NS
Child
o 0-10 kg - 100 mL/kg/d (4 mL/kg/h)
o 10-20 kg - 1000 mL/d + 50 mL/kg/d (40 mL/h + 2 mL/kg/h)
o >20 kg - 1500 mL/d + 25 mL/kg/d (60 mL/h + 1 mL/kg/h)
Replacement therapy
Table 2. Typical Electrolyte Composition of Body Fluids for a Child with Abnormal Fluid
and Electrolyte Losses and of Common IV Fluids
Electrolytes (mEq/L)
Body or IV Fluid
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
RL solution 130 4 109 28
Isotonic NS (0.9% NaCl) 154 0 154 0
1/2 Isotonic NS (0.45% NaCl) 77 0 77 0
Pyloric stenosis
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.
Of interest, reports have suggested that the a substantial number of children with
pyloric stenosis may have hyperkalemia, rather than hypokalemia (Schwartz, 2003).
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 paradoxical aciduria, as 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+, so it excretes H+ instead of
K+, and paradoxical aciduria then occurs. This cycle can be broken only by
adequately replacing fluids and electrolytes.
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, urine output of more than 1 mL/kg/h, serum HCO3- level
less than 28 mEq/dL, and Cl- level of more than 100 mEq/dL. Enteral feeds can
usually be started soon after uncomplicated pyloromyotomy, and full feeds can be
given within 24-48 hours. Postoperative electrolyte abnormalities are rare.
Gastroschisis
Gastroschisis is a defect of the anterior abdominal wall just lateral to the umbilicus.
Unlike an omphalocele, no peritoneal sac is present in cases of gastroschisis;
therefore, evisceration of the bowel occurs through the defect during intrauterine
life. The irritating effect of amniotic fluid (pH 7) on the exposed bowel wall results in
a chemical form of peritonitis characterized by a thick, edematous membrane that is
occasionally exudative. 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.
Fluid requirements in a neonate with gastroschisis can range up to 2.5 times that 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.
Patient Education:
BIBLIOGRAPHY Section 7 of 7
Author Information Introduction Renal Physiology Paradigm For Fluid Management Specific Clinical Scenarios Summary
Bibliography