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CHAPTER 14 Fluid and Electrolyte Management
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419
BOX
14.1
DATA COLLECTION
Clinical Evaluation of Fluid and Electrolyte Status
• Serial weight (sometimes two to three times per day)
• Heart rate
• Blood pressure
• Skin perfusion
• Urine output
• Other drainage (ostomies, gastric, chest tubes)
BOX
14.2
DATA COLLECTION
Laboratory Evaluation of Fluid and Electrolyte Status
Essential values are included in this box. Other measurements are routinely made but are less valuable in the rapid determination of fluid
status and complications of imbalances.
• Sodium (most sensitive indicator of water loss in excess of electrolytes, as is insensible water loss)
• Potassium (may rise with decreased kidney perfusion and acidosis)
• Hematocrit (will rise with extracellular fluid contraction)
• Blood urea nitrogen (relatively insensitive indicator of dehydration in
neonate)
• Creatinine (will rise slowly with renal failure)
• Total CO2 (low level indicates acidosis, either because of bicarbonate
loss or metabolic acidosis from poor tissue perfusion and anaerobic
metabolism)
adequate. Weight is the most sensitive index of
IWL and must be accurately determined at least
every 24 hours. Accurate daily weights in VLBW
infants require special nursing efforts and may be
facilitated with electronic bed scales.
Urine output should be 2 to 5 mL/kg/hr
with a specific gravity of 1.005 to 1.012.24 Blood
pressure and peripheral perfusion may be used to
reflect changes in vascular volume and cardiac output. Normal capillary refill is typically less than
3 seconds and is more reliable when tested on
the forehead or sternum. However, its sensitivity
and specificity have been questioned in infants
and should be interpreted with caution as a sign
of adequate hydration. Blood pressure and heart
rate should be evaluated in conjunction with
capillary refill time.
Loss of skin turgor is a late and variable sign
and usually is not helpful in assessing therapy,
but vital signs (heart rate, respiratory rate, and
temperature) provide useful signs about metabolic rate and stress. However, temperature may
be affected by many external factors. Drainage
volume and content from ostomies, chest tubes,
nasogastric tubes, and other sites should be quantitated accurately. Fluid samples can be submitted for
laboratory analysis to improve the accuracy of the
replacement fluids. The amounts of drainage represent maintenance requirements that must be added
to the calculation of baseline daily maintenance
needs (abnormal + normal = total maintenance).
Laboratory Data
Tests for concentrations of electrolytes (Na+,
K+, Cl−, Ca2+), red blood cells (hematocrit),
glucose, blood urea nitrogen (BUN) or creatinine, and acid-base status should be performed
serially (see Box 14.2). Occasionally, serum osmo-
lality and protein concentrations are helpful in
assessing the neonate’s condition. The anion gap
may be calculated from the difference of the positive
and negative ions, sodium, chloride, and bicarbonate: [Na]+ − ([Cl−] + [HCO
Urine volume must be recorded with every
void. Measuring urine osmolality and glucose
and electrolyte concentrations helps clarify fluid
and electrolyte balance when amounts of glucose,
protein, or other solutes appear in the urine. In a
preterm infant, especially a VLBW infant, an elevated urine pH may signal bicarbonate loss due to
renal function immaturity.
All drainage must be collected and measured,
with the concentration of solutes determined
(see Box 14.2). Accumulations over 4 to 6 hours
are preferable to a single “spot” collection, which
may be misleading. Occasionally, determining the
trace electrolyte elements, hematocrit, and protein
content of urine or drainage can be crucial to management. However, there are no “normal” values for
urine electrolyte concentrations because they must
be interpreted with respect to the infant’s clinical diagnosis, medications, and serum electrolyte
concentrations.
Electronic health records allow for real-time
evaluation of fluid balance. Data can be downloaded directly from IV pumps or entered manually on an hourly basis. The practitioner can review
−
]).
3
56
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actual intake and output (see Fig. 14.3), evaluate
total fluid balance, and quickly make adjustments,
if needed, to ensure optimal fluid balance in the
neonate. Graphs are also available to provide further
detail and trend changes over time.
TREATMENT
Techniques of IV Therapy
In modern neonatal intensive care, peripherally
inserted central venous catheters (PICCs) have
become an invaluable tool. Placement permits
long-term administration of IV fluids, avoiding multiple painful procedures for peripheral IV placement
and the need for surgical placement of a long-term
central catheter. This is particularly valuable for
ELBW infants for whom the time to establish
full enteral feedings may be prolonged. This
technique is also helpful for long-term parenteral
nutrition. Complications of long-term indwelling
central catheters include infection, thrombosis,
phlebitis, infiltration, effusion, occlusion, and
catheter breakage.73 Some reports suggest that
the risk for infection significantly increases after the
PICC has been in place for longer than 2 weeks;39
therefore, these catheters should be discontinued as
soon as enteral nutrition is adequately established.
Thrombosis is more likely to occur when the
flow rate of IV fluids is extremely low (less than
1 mL/hr). Although the use of heparin in PICC-line
fluids has been shown to prolong patency of the line,
it does not decrease the incidence of thrombosis.54
Infiltration usually occurs at the site of the catheter tip. This includes infiltration into the medias-
tinum, pleural space, or pericardium, depending on
the location of the tip of the catheter (see Chapter 7).
Peripheral insertion of central venous catheters can be accomplished readily but requires
clinical training and experience. Insertion sites
include the saphenous, antecubital, axillary,
basilic, cephalic, popliteal, posterior auricular,
and external jugular veins.55 Avoidance of upper
extremity PICCs in infants with single-ventricle
cardiac anatomy is recommended to prevent thrombosis or occlusion of upper extremity veins required
in the eventual Fontan procedure.2 The catheter is
advanced so that the tip is in the superior or inferior vena cava; suboptimal positioning is associated with increased risk of complications.
14,33
The position of the catheter tip must be confirmed radiographically. Confirmation by lat-
eral radiograph is recommended with saphenous
insertion due to a risk of inadvertent placement in
spinal vessels.58 Cannulation of the subclavian vein
of VLBW infants requires insertion by a pediatric
surgeon. Venesection or cutdown of peripheral or
central vessels can be performed with appropriate
training.
Midline catheters can be used for infants who
will require more than a few days of IV fluid
administration. Midline catheters are longer than
peripheral IVs and are inserted deeper into the vein,
where blood flow is greater, but remain outside of
central vessels. Because of their placement, midline
catheters can only be used to provide fluids
appropriate for peripheral access. The length
of duration is an advantage of midlines compared
with peripheral IV lines; catheters can last 1 to 2
weeks, with some reports of midlines lasting up to
3 months.
38
Peripheral venous access continues to be a
valuable approach to IV therapy when shortterm vascular access is needed. The advent of
extremely small catheter and introducer sets has
permitted prolonged use of a single peripheral
infusion site. “Butterfly” infusion sets are rarely used
for IV access.
A rubber band is an effective tourniquet for the
extremity of a small infant. Attention must be paid
to antiseptic technique when acquiring venous
access. Before puncturing the skin, prepare materials
for placement. It is important to recognize the
significant risk for infiltration and skin necrosis
with a peripherally inserted IV line. Calciumcontaining solutions in parenteral nutrition
present an additional risk, particularly for skin
damage. Prevention of such extravasation injuries
is paramount because few treatment options are
available. Although the needle or catheter must be
taped in place, the tape should allow for adequate
visualization of the site. The fluid administered
should be recorded at least every hour, and the
site should be observed for signs of infiltration.
Although traditionally, splints/padded boards have
been used to decrease movement and increase
catheter duration, there are no studies to support
the practice in neonates.16 If splints/padded boards
are used to stabilize an IV line, it should be taped
in a manner that allows visual inspection of the
insertion site. The most common complication of
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IV therapy is infiltration, with rates as high as 70%.74
If extravasation occurs, the infusion should
be stopped immediately and the IV catheter
removed. The affected extremity should then be
elevated to limit swelling.20 Hyaluronidase is an
enzyme that degrades hyaluronic acid, a constituent
of the normal interstitial barrier, which increases
the distribution and absorption of locally injected
substances.9 By facilitating more rapid absorption
of potentially damaging fluid, tissue necrosis may be
lessened. A plastic surgery consultation should be
considered when tissue necrosis is anticipated.
Umbilical vessel catheterization should be
limited to several days’ duration until a central
catheter can be placed (see Chapter 7).
It is important to provide pain relief during
the placement of peripheral IVs, midlines, and/
or PICC lines. Methods that have been shown
to decrease pain during venipuncture in infants
include oral sucrose,61 swaddling, nonnutritive
sucking, breastfeeding, kangaroo care, and topical
anesthetics.4 The use of sucrose has been found
to be superior compared with topical lidocaine in
infants64 (see Chapter 12).
The combination of pharmacologic and non-
pharmacologic pain management modalities is
recommended, but additional research is needed.
When undergoing venipuncture, the use of topical
lidocaine and sucrose was found to be superior
compared with sucrose alone in preterm infants11
but not in term infants.64 IV morphine and the
combination of morphine and topical tetracaine
reduces the pain associated with peripheral central
line placement in ventilated neonates; however, the
use of morphine also increases the need for respiratory support,63 so it should be used with caution. At
a minimum, nonpharmacologic pain treatments
should be used for all venipuncture procedures
in neonates.
Common Problems
In NICUs, virtually all patients initially receive IV
fluid therapy. Therefore, conventional rules of pediatric fluid therapy that estimate losses and project
deficit replacement may not be appropriate. Weight,
urine output and concentration, and the concentration of various solutes in serum and other body fluids are usually known. The correct diagnosis usually
rests on clinical and laboratory measurements (not
estimates). Attempts should be made to identify the
etiology of the deficit or excess while these conditions are being corrected.
HYPOCALCEMIA (INFANTS WITH TOTAL
SERUM CALCIUM LESS THAN 7 mg/dL)
Hypocalcemia is a common finding in critically
ill babies. Clinical findings may correlate poorly
with biochemical data (total or ionized calcium).
Jitteriness, irritability, and twitching are common, but nonspecific, initial signs. Both serum
calcium and glucose should be measured.
Hypocalcemia is often a clinical concern in infants
of diabetic mothers and in infants with asphyxia,
prematurity, and delayed nutrition. The risk for
“early” hypocalcemia within 72 hours of birth
is minimized by supplementing IV fluids with
35 or more mg/kg/day of elemental calcium or
initiating parenteral nutrition with 60 or more
mg/kg/day for preterm infants.32 Alternatively,
early neonatal hypocalcemia may be prevented with
oral calcium supplementation of 80 mg/kg/day of
elemental calcium gluconate32 (100 mg of calcium
gluconate = 9.3 mg of elemental calcium).
The normal physiologic neonatal calcium
nadir occurs at around 48 hours of neonatal
life.29 At birth, when the infant is disconnected
from the maternal calcium supply, calcium levels
begin to fall, and parathyroid hormone secretion
is stimulated. The parathyroid gland’s response is
somewhat insufficient, leading to a calcium nadir
within the first 2 days of life. During this nadir,
ionized calcium typically remains within the normal adult range but undergoes a substantial decline
from fetal levels.29 Early administration of calcium
to the neonate may interfere with the anticipated natural history of calcium homeostasis.
Treatment during this physiologic nadir, in term
infants, is often not necessary unless the infant has a
confirmed low level of ionized calcium. This would
typically be associated with other medical concerns,
such as hypoxic-ischemic encephalopathy or in
infants of diabetic mothers.
Confirmation of low serum calcium values
with an ionized calcium level is necessary
because the albumin level, acid-base balance, and
other factors could affect serum calcium levels.
Attempts to rapidly correct hypocalcemia,
using bolus infusions and slow infusions over
2 to 3 minutes, are not as successful and may
induce dysrhythmias, compared with more
gradual attempts to correct hypocalcemia.
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Either repeated slow infusions every 6 hours or
a continuous infusion is best. Additional calcium
should be given intravenously as 100 to 200 mg/
kg/dose of calcium gluconate over 4 to 6 hours
if seizures or biochemical abnormality persists.
“Late” hypocalcemia, occurring at more than
7 days of age, usually has a specific cause, such
as malabsorption, hypomagnesemia, hypoparathyroidism, long-term diuretic therapy, or rickets, and
should be evaluated in detail.
32
Care should be taken when administering IV calcium: (1) the infant should receive
cardiac monitoring to detect bradycardia; (2)
calcium administration should be discontinued
immediately if bradycardia occurs; and (3) the
peripheral IV site should be checked for patency
before and during administration because of
the potential for skin necrosis, sloughing, and
dystrophic calcification caused by infiltrated
calcium.
HYPERCALCEMIA (INFANTS WITH
SERUM CALCIUM MORE THAN 11 mg/dL)
Hypercalcemia is typically asymptomatic but may
present with nonspecific symptoms in the infant.
Symptoms can include poor feeding, emesis,
lethargy, irritability, polyuria, and constipation.
Both serum and ionized calcium should be measured,
along with phosphate and alkaline phosphatase. The
most common presentation of hypercalcemia is iatrogenic in the setting of excessive vitamin D or calcium supplementation or in response to inadequate
phosphorus supplementation during the administration of parenteral nutrition. Hypercalcemia may also
be seen secondary to maternal hypoparathyroidism
or increased maternal vitamin D intake. Neonatal
disease such as hyperparathyroidism, hyperthyroidism, Williams syndrome, and hypophosphatasia can
also present with hypercalcemia. Hypercalcemia
has been reported due to subcutaneous fat necrosis
and as drug-induced hypercalcemia with thiazide
diuretics.
13,51
Initial management is often directed at
adjusting the calcium-to-phosphorus ratio in
parenteral nutrition solutions. Hypercalcemia in
the setting of inadequate phosphorus supplementation results from increased bone reabsorption of
calcium, and therefore treatment should be aimed at
providing appropriate phosphorus supplementation
as opposed to decreasing calcium. If hypercalcemia is severe, furosemide can be given to facilitate
calcium excretion in the urine. Electrolytes must
be monitored carefully, as well as the infant’s volume status, with careful avoidance of dehydration.
Normal saline can be given if there is concern
for dehydration. Hydrocortisone can also be used
to decrease intestinal calcium absorption. If the
etiology of hypercalcemia is not apparent, further
evaluation with additional laboratory studies, such
as parathyroid hormone, 1,25-dihydroxy-vitamin D,
25-OH-vitamin D, urine calcium, and urine phosphate, should be considered.
HYPERNATREMIA (INFANTS WITH
SERUM SODIUM MORE THAN 150 mEq/L)
13
Clinical signs of hypernatremia are rare, except
for late-occurring seizures. The most common
causes of hypernatremia are (1) dehydration, usually
caused by too little “free water” administration; (2)
injudicious use of sodium-containing solution, such as
sodium bicarbonate bolus infusion and sodium-containing medications; and (3) congenital or acquired
reduction in antidiuretic hormone resulting in excess
loss of “free water,” diabetes insipidus. Intracranial
bleeding correlates strongly with hypernatremia.40
Management should be directed toward prevention, and infants with hypernatremia should have
serum sodium reduced slowly to prevent seizures.
Infants who experience hypernatremic dehydration
often appear better hydrated than they are because
hypernatremia shifts fluid into the intravascular space.
HYPONATREMIA (INFANTS WITH SERUM
SODIUM LESS THAN 130 mEq/L)
Hyponatremia is usually asymptomatic because it
develops chronically rather than as an acute imbalance; however, a late clinical sign is seizure. The
most common causes include (1) excess hydration
as a result of administration of electrolyte-free solutions; (2) renal loss of sodium in neonates receiving
diuretic therapy, especially in VLBW infants; and (3)
the syndrome of inappropriate antidiuretic hor-
mone secretion (SIADH) that is suspected when
decreased serum sodium and decreased urine
output occur. This syndrome is associated with
central nervous system and lung pathologic conditions. Clinical criteria include (1) low serum sodium,
(2) continued inappropriately high urine sodium
loss, (3) urine osmolality greater than plasma, and
(4) normal adrenal and renal function. Management
is by volume restriction until diuresis follows, and
treatment is directed toward resolving the etiology.
CHAPTER 14 Fluid and Electrolyte Management
Necessary sodium = (Sodium desired − Sodium observed) ×
0.6 × Weight (in kilograms)
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423
TABLE
14.4
CLINICAL SIGNS ELECTROCARDIOGRAM CHANGES
Muscular weakness Short QT interval
Cardiac dysrhythmias Widening QRS
Ileus Sine wave QRS/T
HYPERKALEMIA (INFANTS WITH MORE
THAN 7 mEq/L SERUM POTASSIUM)
In the case of sodium deficit as the primary etiology, one can compute the amount of sodium required
to correct a deficit using the following formula:
The target goal amount and the replacement rate
given are a matter of clinical judgment based on
underlying diagnosis and treatments for individual
patient situations. In practice, the clinician often prescribes a percentage of the calculated deficit, repeats
the serum measurement, and modifies the IV solution.
HYPERKALEMIA (INFANTS WITH SERUM
POTASSIUM MORE THAN 7 mEq/L)
Causes of hyperkalemia include (1) acidosis with or
without tissue destruction, (2) renal failure (water
overload may limit management), (3) adrenal insufficiency (relatively uncommon), and (4) iatrogenic
secondary to inappropriate potassium administration. Nonoliguric hyperkalemia may be seen in
ELBW infants; even in the absence of potassium intake, it tends to occur more frequently
in infants at a younger gestational age who did
not receive antenatal steroids. Other electrolyte
imbalances, such as elevated phosphate, can also predispose ELBW infants to nonoliguric hyperkalemia.
If potassium levels are low at birth, the infant is less
likely to develop nonoliguric hyperkalemia. Careful
monitoring for electrolyte disturbances must occur
in this population.
37,68
Table 14.4 outlines clinical signs and electro-
cardiogram (ECG) changes that may be seen in
hyperkalemia. Management is directed toward
resolving the causes and nonspecific treatment,
depending on the severity of the hyperkalemia and
the associated clinical signs:
• Stop all potassium administration.
• Evaluate total and ionized calcium.
• If hypocalcemia is present, infuse 100 to 200
mg/kg of calcium gluconate to lower the cell
membrane threshold. This is transient therapy
but may be lifesaving.
• Infuse sodium bicarbonate 1 to 2 mEq/kg,
slowly over 30 minutes or longer. This is also a
transient therapy designed to promote intracellular sodium and hydrogen exchange for potassium.
It is particularly useful when the hyperkalemia
is associated with acidosis. However, if hyperkalemia is associated with acute renal failure, the
relatively large volume of fluid required to deliver
the sodium bicarbonate may be concerning.
• Administer 1 g/kg cation exchange resin
(sodium polystyrene sulfonate [Kayexalate]) as
an oral or rectal solution. Little experience has
been reported in neonates, and technical problems of retention can be substantial. Furthermore,
this may not be an option if the infant is on
nothing-by-mouth status or has an injured gastrointestinal tract. When this resin is used, sodium
in the resin is exchanged for serum potassium,
which may result in hypernatremia. Therefore,
careful attention must be paid to serum electrolyte concentrations. Necrotizing enterocolitis has
also been reported with this therapy.
17
• An insulin infusion given simultaneously with
a dextrose infusion can help shift potassium
to the intracellular space. There are several
challenges to this form of therapy. First, the
actual dose of insulin administered to the patient
varies unpredictably because the insulin adsorbs
to plastic IV tubing. Second, significant hypoglycemia and seizures may occur. The serum glucose
concentration must be monitored frequently and
the glucose infusion adjusted accordingly.
• Administer albuterol.
17,57
Albuterol inhalation
may be useful in rapidly lowering serum potassium. Albuterol and other beta-adrenergic agents
induce the intracellular movement of potassium.
• Administer furosemide. The administration of
furosemide, a loop diuretic, will result in renal
excretion of potassium. This may be useful in
patients who are not experiencing renal failure,
although the amount of potassium excretion is
not predictable.
17
• Perform peritoneal dialysis. With neonatal
hyperkalemic peritoneal dialysis, sodium bicarbonate frequently must be added to dialysate to
prevent acidosis. Peritoneal dialysis is a complicated procedure in neonates, involving catheter
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placement and dialysis monitoring. It may be
technically impossible in VLBW babies and difficult or impossible when there is injured bowel,
as with NEC.
HYPOKALEMIA (INFANTS WITH SERUM
POTASSIUM LESS THAN 3.5 mEq/L)
About 90% of the body’s total potassium is
intracellular. Low serum potassium always implies
significant intracellular depletion; most potassium is
intracellular, and total body potassium can be low
even with normal serum levels. Management is
directed toward the cause. The most common causes
of hypokalemia are (1) increased gastrointestinal
losses from an ostomy or nasogastric tube and (2)
renal losses from diuretic therapy. Diuretic-induced
hypokalemia can be treated with supplemental
potassium chloride. Caution is needed, particularly
if sending the patient home on this medication,
because incorrect dosing can have serious consequences. Caution must also be used in providing
supplementation if the patient is treated with potassium-sparing medications such as spironolactone or
captopril.
Clinical signs of hypokalemia are related to
muscular weakness and cardiac dysrhythmias.
Ileus may also occur. Electrocardiographic changes
include decreased T waves and ST depression.
Common Clinical Syndromes
RESPIRATORY DISTRESS SYNDROME
Before the widespread use of surfactant, pulmonary
function in RDS tended to improve following a
period of brisk diuresis on the third or fourth day
of life. It was hypothesized that increased endogenous surfactant production led to improved pulmonary capillary integrity and lymphatic drainage.
As a result, hypotonic interstitial lung fluid was
reabsorbed back into circulation, and a delayed
physiologic diuresis occurred. Although antenatal
corticosteroids and routine use of exogenous
surfactant have altered the natural history of
RDS, the preterm infant remains at risk for
a more severe course should excessive fluid
overload occur. Daily fluid intake should be
monitored closely and restricted to allow for the
natural contraction of extracellular volume to occur.
Because of the observation of improved lung
function associated with diuresis, furosemide and
other diuretics have been suggested for the treatment
of RDS. Although short-lived improvements in lung
function were seen, no long-term effects on morbidity or mortality rates were shown.23 The use of
diuretics shortly after birth could also lead to hypotension and compromised peripheral perfusion, as
well as electrolyte disturbances. Aggressive use of
diuretics is not indicated in the setting of RDS.
PATENT DUCTUS ARTERIOSUS
Excessive fluid overload can increase the risk of
PDA in premature infants. Treatment of a PDA
with nonsteroidal antiinflammatory drugs can lead
to renal vasoconstriction, with a resultant decrease in
renal blood flow and the glomerular filtration rate.
Therefore, it is not uncommon to see an increase in
serum creatinine, oliguria, and hyponatremia during
PDA treatment. Nonsteroidal antiinflammatory
drugs should be given in the lowest effective dose,
and concomitant administration of other nephrotoxic drugs should be minimized. Once the drug
effect diminishes, accumulated free water should be
excreted rapidly, especially if the ductus has closed
and cardiovascular status has improved. Fluid status
and electrolytes must be monitored closely before,
during, and after PDA treatment.
BRONCHOPULMONARY DYSPLASIA
Infants with BPD typically have increased metabolic
needs and require higher caloric intake. However,
volume overload can potentiate the worsening
of pulmonary disease.21 It becomes a delicate
balance to provide adequate nutrition while
avoiding excess volume. Diuretics are often used
in this population, creating an additional set of complications, as discussed previously. Electrolytes must
be monitored closely, and diuretic dose and duration
should be minimized.
CONGENITAL HEART DISEASE
Knowledge of the underlying physiology associated
with the infant’s specific heart lesion will ultimately
guide the infant’s fluid needs and management.
Fluid restriction is typically indicated in lesions
with left-to-right shunting to manage pulmonary overcirculation. Diuretics are also commonly
used in this population. Lesions with outflow tract
obstructions will typically respond well to liberal
fluid volumes.
Careful attention must be paid to meeting the
nutritional needs of infants with congenital heart
disease. Surgical outcomes can be improved by
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providing optimal nutrition, but this can be difficult to achieve in the face of increased metabolic
demands, poor mesenteric perfusion, and delayed
enteral feeding.
PERSISTENT PULMONARY
HYPERTENSION
70
Fluid management in the infant with persistent
pulmonary hypertension is crucial because hypovolemia can exaggerate right-to-left shunting,
leading to worsening disease. Once euvolemia is
achieved, there is no additional benefit to repeated
volume boluses. Hypoglycemia and hypocalcemia
should be avoided because these states can also
exacerbate pulmonary hypertension.
NECROTIZING ENTEROCOLITIS
60
Necrotizing enterocolitis often results in a shocklike state in the infant. Capillary integrity and
lymphatic drainage are often compromised, leading to fluid accumulation in the interstitium
and diffuse bowel or other tissue edema (the
“third space”). As effective circulating volume is
diminished, antidiuretic hormone is released, and
the renin-angiotensin-aldosterone system is activated, leading to sodium and free water retention.
Management is aimed at maintaining adequate
intravascular volume and perfusion with the
use of volume expanders, vasopressors, and/
or inotropes. Corticosteroids may also be useful to
mitigate the effects of capillary leak. Discontinue all
potassium-containing fluids because the combination
of oliguria and bowel necrosis can quickly result in
hyperkalemia.
If an oral-gastric tube is placed to facilitate intestinal decompression, monitor output closely, and
consider partially replacing this volume every 8 to
12 hours. Gastric fluid is typically sodium rich, so
the sodium loss should be replaced as well. Strictly
monitor fluid intake and output, and attempt to
maintain adequate urine output.
CONGENITAL ADRENAL HYPERPLASIA
The most common form of congenital adrenal
hyperplasia is caused by the absence of 21-hydroxylase, which is required to produce aldosterone.
Whereas affected females typically present at birth
with ambiguous genitalia, males classically present in crisis at 1 to 3 weeks of life with profound
hyponatremia, hyperkalemia, and metabolic acidosis.
Treatment is initially guided at correcting electrolyte
abnormalities. Sodium bicarbonate administration
at 1 to 2 mEq/kg may be most useful in correcting hyperkalemia, hyponatremia, and acidosis.
Additional treatment strategies for hyponatremia and
hyperkalemia are discussed earlier in this chapter.
Long-term treatment is aimed at appropriate replacement of mineralocorticoids and glucocorticoids.
RENAL DYSFUNCTION/RENAL DISEASE
Acute renal failure is most often caused by
(1) extrinsic factors such as perinatal asphyxia,
shock, and heart failure; (2) intrinsic factors
such as congenital or acquired lesions; and (3)
obstructive uropathy, including urethral obstruction or extra-genitourinary mass. Oliguria or
anuria usually occurs initially.
During initial oliguria, electrolyte-free glucose
infusion should be limited to IWL and urine
output. Frequently, this entails providing total
fluids of 50 to 80 mL/kg/day. Recovery is usually
associated with natriuresis (excessive urinary sodium
loss) and osmotic diuresis. This may develop rapidly
with sodium losses as high as 20 mEq/kg/day. Body
weight and fluid losses must be carefully and
frequently measured, at least every 12 hours.
Nonrenal losses, such as gastrointestinal drainage,
must also be measured. Ideally, fluid and electro-
lyte therapy is directed toward maintaining the
current weight or a weight loss of 1% per day
until recovery is nearly complete. This may be
accomplished initially by ordering replacement of
IWL as a basal fluid order and replacing a percentage
of additional fluid losses on a per-volume basis. The
choice of fluid used for replacement depends on the
electrolyte content of the fluid lost. Thus, it may be
helpful to measure urinary sodium and potassium
loss concentrations and urine volume, recognizing
that any “spot check” of these electrolytes will not
fully reflect the loss over a 24-hour period.
Serial determination of serum electrolytes will
help refine the fluid orders. As the patient recov-
ers and renal function normalizes, the transition to
more standard fluids and electrolytes should occur.
The renal ability of the patient to concentrate urine
must be evaluated serially. If the patient remains
in high-output renal failure and fluids are
restricted, dehydration may occur. Dehydration
will result in weight loss, increased serum electrolyte
concentration, and hypernatremia with dilute urine.
Weight change during renal failure demands a
careful reevaluation of the fluid plan.
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ASPHYXIA
Perinatal depression can result in renal insult
and acute tubular necrosis, leading to decreased
urine output. SIADH may also occur following perinatal asphyxia, further reducing urine
output. Fluids must be restricted to avoid fluid
overload. The use of therapeutic hypothermia for
the treatment of hypoxic-ischemic encephalopathy
may further worsen fluid retention and the risk of
hyponatremia.49 Fluid restriction to as low as 30
to 40 mL/kg/day may be required because this
amount should replace only insensible losses.
Potassium supplementation should be avoided. As
the kidney recovers from acute tubular necrosis, a
polyuric phase may ensue, with large sodium losses.
Urine output must be monitored closely, urinary sodium quantified, and fluid replacement
adjusted accordingly.
Major Surgery
Surgical trauma is superimposed on the normal
metabolic responses of the neonate. The type and
extent of surgery and the gestational and postnatal
age of the infant determine the clinical impact.
In healthy term infants, a negative balance of
water, electrolytes, nitrogen, and calories with
associated weight loss occurs during the first 3
to 5 days, followed by a transition to a positive balance and weight gain by 7 to 10 days.
Parallel transition times for preterm infants vary
enormously. Deficits may exist as a result of delayed
diagnosis, with external loss or internal loss. “Third
space” losses can be significant, with peritoneal losses being a notorious source of deficit
underestimation.
Predicting the metabolic response to surgery
is difficult, reflecting wide variation among individual patients, even patients with similar lesions.
Uncontrollable and immeasurable variables prevent a standardized postoperative physiologic
response for neonates, especially those weighing
less than 2 kg. Thermoregulation is a particular
challenge for operative procedures. The patient
is draped and shielded from radiant heat sources.
Measuring and managing the patient’s internal temperature with evaporative heat and water loss complicating the situation is difficult once the incision
is made. Transport incubators, prewarmed operating
rooms, radiant warmers, warming pads, and prewarmed solutions may help achieve thermoneutrality.
Intraoperative fluid balance is rarely precise despite
the clinicians’ best efforts. Blood loss on sponges,
drapes, and other objects should be measured, but
IWL from open body cavities is difficult to estimate.
The principles of postoperative management
are as follows:
• Monitor clinical and chemical variables fre-
quently, at least every 4 to 6 hours; evaluate fluid
balance and measure drainage.
• Recognize that insensible water losses may
include “third space losses.” These include water
lost into the lumen of the bowel or into the peritoneum secondary to peritonitis, resulting in the
loss of both water and electrolytes from the intravascular compartment. At least a proportion of the
fluids used to anticipate these losses should contain
high sodium content similar to plasma. Clinical
judgment is used to estimate the third space
losses because they cannot be measured. Serial
evaluations of blood pressure, heart rate, urine
output, and skin perfusion together may help
determine if the volume prescribed is sufficient.
• Gastric output in patients undergoing intestinal
surgery should also be closely assessed in order
to provide adequate replacement of free water and
electrolytes, particularly sodium and chloride.
• Provide parenteral nutrition early if significant
enteral feedings (less than 50 kcal/kg) cannot
be achieved by 3 to 5 days postoperatively.
Gastrointestinal motility returns rapidly in term
infants compared with adults. Almost all VLBW
infants require parenteral nutrition after surgery.
Diuretics and Electrolytes
Diuretics represent one of the most common classes
of drugs administered to sick neonates and infants.
Electrolyte disturbances are the most common
adverse effects of diuretic therapy and can lead
to a variety of consequences. Clinical indications for the use of diuretics in neonates and
infants include BPD, congenital heart disease,
and renal failure. The classes of diuretics most
commonly used in this age group include loop
diuretics, thiazides, and potassium-sparing diuretics.
A discussion of the mechanism of action, diuretic
efficacy, and common side effects follows.
LOOP DIURETICS
Loop diuretics bind to one of the chloride binding sites on the Na+/K+/2Cl– transporter, thus
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inhibiting the reabsorption of sodium and chloride
in the thick ascending limb of the loop of Henle.
Water passively follows the movement of sodium
and thus allows for diuresis.
Furosemide is the most widely studied diuretic
in neonates and is consequently the prototype loop
diuretic. It produces a 3-fold to 5-fold increase
in sodium excretion and a 10-fold increase in
urine flow.
47,75
Therefore, hyponatremia, hypo-
chloremia, and hypovolemia are common with
chronic use of furosemide. Hypokalemia is also
of significant concern with chronic use of furosemide. The mechanism of potassium loss is due
to blockage of tubular reabsorption of potassium
and increased aldosterone production in the presence of sodium losses.65 In addition to potassium
losses, furosemide also promotes urine calcium and
magnesium excretion. The reabsorption of these
cations is decreased because of furosemide’s ability
to eliminate the transepithelial potential difference.
Chronic hypercalciuria leads to hypocalcemia
and the possibility of renal calcifications and
nephrocalcinosis. Compensatory mechanisms lead
to increased parathyroid hormone secretion with
associated bone resorption, bone demineralization,
osteopenia, and possibly rickets.
Bumetanide is another loop diuretic commonly
used in neonates and infants. It is 40 times more
potent than furosemide. The side effects are the
same as those seen with furosemide.
THIAZIDES
Hydrochlorothiazide and chlorothiazide are the
most widely used thiazide diuretics in neonates
and infants. Thiazides exert their effect by blocking
the Na+-Cl– transporter at the distal convoluted
tubule, collecting tubule, and early collecting duct.
Because only a small portion of sodium reabsorption occurs in the distal tubule, thiazide diuretic
efficacy is limited.
Chronic use of thiazide diuretics leads to elec-
trolyte disturbances, although they usually are less
severe than with loop diuretics. Hyponatremia and
hypokalemia are the most common side effects.
Hypokalemia is the result of greater sodium-potassium exchange that occurs secondary to a higher
concentration of sodium found in the distal tubule.
Whereas loop diuretics promote calcium
loss, thiazide diuretics can increase serum calcium concentrations by increasing renal calcium
reabsorption both proximally and distally.40 This
decrease in urinary calcium can be used to reverse
loop diuretic–induced renal calcifications.
POTASSIUM-SPARING DIURETICS
Whereas loop and thiazide diuretics directly alter
sodium reabsorption via direct inhibition of sodium
transporters, potassium-sparing diuretics such as
spironolactone competitively antagonize the
aldosterone receptor. The primary binding site is
the principal cell of the cortical collecting tubule.
Aldosterone enhances sodium reabsorption in the
collecting tubule and promotes potassium secretion. Therefore, antagonizing aldosterone results in
diminished sodium reabsorption with a consequent
increase in serum concentrations of potassium and
hydrogen. However, spironolactone inhibits the
reabsorption of less than 2% of filtered sodium
and is thus not an effective primary diuretic.
The major use is to prevent urinary potassium loss
induced by other diuretics.
Hyperkalemia is the primary electrolyte dis-
turbance to monitor with the use of spironolactone.
This side effect is usually not of great concern
because spironolactone is frequently used in conjunction with other potassium-wasting diuretics.
Spironolactone should be avoided in renal failure.
COMPLICATIONS
Excessive fluid administration has been associated with BPD and PDA and is increasingly
being shown to demonstrate a negative effect
on clinical outcomes in critically ill infants.
3,6,25
Inadequate fluid administration may also have
adverse effects, having been associated with
dehydration, decreased urine output, hypernatremia, poor tissue perfusion, and potentially,
tissue damage.
PARENT TEACHING
The need for and presence of an IV line in a
newborn may be frightening for the parents.
Clear, medically and physiologically sound explanations (in nonmedical jargon) of the need for
fluid and electrolyte support for their infant help
allay parents’ fears (Box 14.3). Scalp vein IV lines
are of particular concern because a common
misconception is that the needle is positioned
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BOX
14.3
PARENT/CAREGIVER TEACHING
Parent Teaching About Fluid and Electrolyte Management
• Most babies cannot be fed immediately and will require intravenous
(IV) fluids.
• Umbilical venous and arterial catheters must be removed in a few
days.
• IV fluids will be given through percutaneous central venous catheters,
peripheral IV lines, or surgically placed lines.
• Scalp IV lines go only into subcutaneous veins, not into the brain.
• Placing the IV line is painful, and analgesia will be provided during
the procedure, but the IV line will be painless afterward, unless
infiltrated.
• Peripheral IV lines are subject to infiltration, which may be serious if
the fluid is hyperalimentation fluid or contains calcium. IV lines are
checked every hour.
• Central venous catheters (percutaneously or surgically placed) carry
the risks of thrombosis, infection, or infiltration into body cavities
such as the pleura or pericardium.
• IV fluids will be discontinued as soon as enteral nutrition is sufficiently advanced.
in the infant’s brain. Explain to parents that scalp
vein IV lines are in the large veins of the head and
not the brain and that an IV line in the head may
stay in longer, thus decreasing the need for multiple
vein punctures, and allows the infant mobility of all
four extremities. In answer to the question “Does it
hurt?” a truthful answer is “Yes, when it is put in,
but not after it is in the vein.” Explaining the strategies used to decrease pain associated with IV line
placement may also help allay their concerns.
The concept of the use of central venous catheters should be presented to the parents early in
the hospital course if a delay in enteral nutrition
is anticipated. The advantages are fewer painful
procedures, increased mobility of the patient,
and decreased risk for infiltrate. These should
be clearly explained in lay language. Explaining the
potential complications—such as infection; thrombosis; and the specific risk for the extravasation of
fluid into body cavities, pleura, and pericardium—is
also necessary. Potential infiltration of peripheral
IV sites should be addressed prospectively with
parents. Erythema and edema are expected.
Sloughing of the skin occasionally occurs in
VLBW infants and is more common on the feet
and hands than on the scalp. Well-illustrated par-
ent education materials often are very helpful when
explaining these situations to parents.
Including parents in the care of their sick
neonate requires an explanation about the importance of measuring intake and output. Inadvertent
disposal of diapers and giving fluids that are not
recorded should be prevented, emphasizing the
importance of saving diapers for the infant’s nurse. “A
little spitting up” after feeding may be inappropriately
dismissed if parents are not instructed in the importance of telling the nurse and saving it for evaluation.
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