2. Sodium Homeostasis
Serum Na+ values should be kept between 135-145
mEq/L.
In general, as long as the infant’s fluid balance is
stable, maintenance Na+ requirements do not exceed 3-
4 mEq/kg/day, and providing this amount usually
ensures the positive Na+ balance necessary for
adequate growth.
Some of the most immature infants may have Na+
requirements of as much as 6-8 mEq/kg/day because of
the decreased capacity of their kidneys to retain Na+.
3. Hyponatremia
Hyponatremia (serum Na+ <130 mEq/L)
may be caused by either total body Na+
deficit or free water excess.
In both situations, total body water may
be (hyponatremia with volume
contraction), normal, or (hyponatremia
with volume expansion).
4. Hyponatremia
To initiate effective treatment, it is
important to attempt to determine the
primary cause of the hyponatremia
and whether there is associated
volume expansion or contraction.
5. Hyponatremia
The most common cause of
hyponatremia in the sick neonate is
excessive administration or retention of
free water.
In these situations the total body Na+
content is normal, and the appropriate
treatment is restriction of free water
intake and not administration of Na+.
6. Hyponatremia
In situations of true Na+ deficit, the
deficits can be estimated by assuming
70% of total body weight as the
distribution space of Na+.
The formula for calculating Na+ deficit is:
Na+ deficit (or excess) (mEq) =
0.7 × kg × [ (Na+) desired − [ (Na+) actual]
7. Hyponatremia
In most situations of depletional
hyponatremia, the Na+ deficit should be
replaced on a schedule that provides two
thirds replacement in the first 24 hours and
the remainder in the next 24 hours.
Frequent measurements of serum
electrolytes are needed to ensure that the
correction is occurring appropriately.
8. Hyponatremia
If the serum Na+ concentration is <120
mEq/L, regardless of whether the hyponatremia is due
to free water overload or total body Na+ deficit, then
correction of the serum Na+ concentration up to 120
mEq/L is recommended with administration of 3% saline
solution.
This correction should be done over 4-6 hrs, depending
on the severity of hyponatremia and using the previous
formula.
Rapid IV bolus administration of 4-6 mL/kg of 3% saline
9. Hyponatremia
Additional therapy should be directed
at fluid restriction if the hyponatremia
is dilutional or Na+ repletion if the
hyponatremia is depletional.
More stable infants with chronic Na+
losses can also be corrected with
enteral NaCl.
10. Hypernatremia
Hypernatremia (serum Na+ >145 mEq/L)
reflects a deficiency of water relative to
total body Na+ and is most often a
disorder of water rather than Na+
homeostasis.
Hypernatremia does not reflect the total
body Na+ content, which can be
high, normal, or low depending on the
cause of the condition.
11. Hypernatremia
The hypernatremia-induced hypertonicity causes
water to shift from the intracellular to the
extracellular compartment, resulting in
intracellular dehydration and the relative
preservation of the extracellular compartment.
This shift is the main reason that neonates with
chronic hypernatremic dehydration often do not
demonstrate overt clinical signs of intravascular
depletion and dehydration until late in the course
of the condition.
12. Hypernatremia
The CNS has a unique adaptive capacity to respond to
the hypernatremia-induced hypertonicity, leading to a
relative preservation of neuronal cell volume.
The shrinkage of the brain stimulates the uptake of
electrolytes (immediate effect) as well as the synthesis
of osmoprotective amino acids and organic solutes
(delayed response).
These idiogenic osmols aid in maintaining normal brain
cell volume during longer periods of hyperosmolar
stress.
13. Hypernatremia
As long as hypernatremia develops rapidly (within
hours), as in accidental Na+ loading, a relatively rapid
correction of the condition improves the prognosis
without raising the risk of cerebral edema formation.
Intracellular fluid accumulation does not occur because
the accumulated electrolytes are rapidly extruded from
the brain cells, and cerebral edema is unlikely.
In these cases, reducing serum Na+ concentration by 1
mEq/L per hour (24 mEq/L per day) is appropriate.
14. Hypernatremia
However, because of the slow dissipation of idiogenic osmols
over a period of several days, in cases of chronic
hypernatremia, the hypernatremia should be corrected more
slowly, at a maximum rate of 0.5 mEq/L per hour (12 mEq/L
per day).
If correction is performed more rapidly in these cases, the
abrupt fall in the extracellular tonicity results in the movement
of water into the brain cells, which have a relatively fixed
hypertonicity because of the presence of the osmoprotective
molecules.
The result is the development of brain edema with deleterious
15. Hypernatremia
In the breastfed term neonate, hypernatremia
most commonly develops because of
dehydration caused by inadequate breast
milk intake, but may also be caused by high
Na+ levels in maternal breast milk. Reduction
in breastfeeding frequency has been shown
to be associated with a marked rise in the
Na+ concentration of breast milk.
16. Hypernatremia
The central and nephrogenic forms of diabetes
insipidus are much less commonly encountered and
result in hypernatremia because of the lack of
production of and renal responsiveness to
ADH, respectively.
Hypernatremia can also develop in response to
excessive sodium supplementation, mainly in the sick
neonate receiving repeated volume boluses for
cardiovascular support. In these cases, clinical signs of
edema, increased body weight, and the history of
volume boluses help to establish the diagnosis.
18. Conditions Causing Hypernatremia
EUVOLEMIC HYPERNATREMIA
1. Decreased Production of ADH: Central
diabetes insipidus, head trauma, CNS tumors
(craniopharyngioma), meningitis, or
encephalitis
2. Decrease or Absence of Renal
Responsiveness: Nephrogenic diabetes
insipidus, extreme immaturity, renal insult and
medications such as
amphotericin, hydantoin, aminoglycosides.
20. Treatment of Hypernatremia
Thorough analysis of the medical history and the
changes in clinical signs, laboratory findings, and
body weight usually aid in determining the major
etiologic factor in hypernatremia and thus the
appropriate treatment.
Although some cases of hypernatremia are a
result of sodium excess with normal or high
TBW, most cases in neonates are due to
hypernatremic dehydration.
21. Treatment of Hypernatremia
Treatment of this condition is generally
divided into two phases: the emergent phase
where the intravascular volume is
restored, usually by administration of 10-20
mL/kg of isotonic saline, and the rehydration
phase, where the sum of the remaining free
water deficit and usual maintenance needs
are administered evenly over at least 48
22. Treatment of Hypernatremia
The free water deficit can be calculated as:
H2O deficit (or excess) (L) =
[ 0.7 × kg ] ×
It is important to note that the amount of free
water required to decrease the serum Na+ by 1
mEq/L is 4 mL/kg with moderate
hypernatremia, but only 3 mL/kg when the
hypernatremia is as high as 195 mEq/L.
23. Treatment of Hypernatremia
Therefore the amount of free water required to
decrease serum Na+ by 12 mEq/L over a 24-hour period
when hypernatremia is moderate is calculated as:
Free water required = Current weight × 4mL/kg ×
12mEq/L or Current weight × 48 mL/kg/day
And the amount of free water required to decrease Na+
sodium by 12 mEq/L over a 24-hour period when
hypernatremia is severe is calculated as:
Free water required = Current weight × 36 mL / kg / day
24. Potassium Homeostasis
Serum potassium should be kept between
3.5-5 mEq/L.
In the early postnatal
period, neonates, especially immature
preterm infants, have higher Na+ and K+
concentrations than older persons.
In general, K+ supplementation should be
started only after urine output has been well
25. Potassium Homeostasis
Supplementation should be started at 1-2 mEq/kg/day
and increased over 1-2 days to the usual maintenance
requirement of 2-3 mEq/kg/day.
Some preterm infants may need more K+
supplementation after the completion of their postnatal
volume contraction, because of their increased plasma
aldosterone concentrations, prostaglandin
excretion, and disproportionately high urine flow rates.
Most term and preterm neonates will require K+
supplementation if they are receiving diuretics.
26. Hypokalemia
Hypokalemia in the neonate is usually
defined as a serum K+ level of < 3.5 mEq/L.
Hypokalemia can occur from K+ loss due to
diuretics, diarrhea, renal dysfunction, or
nasogastric drainage from inadequate K+
intake or from intracellular movement of K+ in
the presence of alkalosis.
27. Hypokalemia
Except in patients receiving digoxin, hypokalemia is
rarely symptomatic until the serum K+ concentration is
less than 2.5 mEq/L.
ECG manifestations of hypokalemia include flattened T
waves, prolongation of the QT interval, or the
appearance of U waves.
Severe hypokalemia can result in cardiac
arrhythmias, ileus, and lethargy.
28. Treatment of Hypokalemia
Hypokalemia is treated by slowly replacing K+ either IV
or orally, usually in the daily fluids.
Rapid administration of KCl is not
recommended, because it is associated with life-
threatening cardiac dysfunction.
In extreme emergencies, K+ can be given as an infusion
over 30 to 60 minutes of not more than 0.3 mEq/kg KCl.
If hypokalemia is secondary to alkalosis, the alkalosis
should be corrected before considering increasing the
K+ intake.
29. Hyperkalemia
Hyperkalemia in the neonate is defined as a
serum K+ level > 6 mEq/L in a nonhemolyzed
specimen.
It is important to understand that most of the
body’s K+ is contained within cells; therefore
serum K+ levels do not accurately reflect total
body stores. However, a serum K+ > 6.5-7 mEq/L
can be life threatening, even if stores are normal
or low, because of its effect on cardiac rhythm.
30. Hyperkalemia
ECG manifestations of hyperkalemia include peaked T waves
(the earliest sign), a widened QRS configuration, bradycardia,
tachycardia, SVT, ventricular tachycardia and ventricular
fibrillation.
Because pH affects the distribution of K+ between the
intracellular and the extracellular space, serum K+ levels rise
during acidosis, which may occur acutely. The clinician
should be aware of the potential for life-threatening
arrhythmias to occur in infants with chronic lung disease on
diuretics and K+ supplements who develop a sudden
respiratory deterioration with acidosis.
31. Hyperkalemia
Another common cause of hyperkalemia is renal
dysfunction, of particular concern in very preterm and
asphyxiated infants.
In addition, infants who have suffered IVH or tissue
trauma and those with intravascular hemolysis often
have hyperkalemia caused by the release of K+ during
breakdown of RBCs.
Finally, hyperkalemia may be one of the earliest
manifestations of congenital adrenal hyperplasia.
33. Treatment of Hyperkalemia
1. Eliminate all sources of K+ from the diet or IVF .
2. Administer a cation exchange resin such as Kayexalate®
(sodium polystyrene sulfonate) or Sorbisterit® (calcium
polystyrene sulfonate).
3. Administer IV NaHCO3 1 mEq/kg IV over 10 to 30 min
(causes a rapid shift of K+ into cells) (used with caution; can
precipitate hypocalcemia and Na+ overload).
4. Infusion of glucose and insulin (Glucose 0.5 g/kg; insulin 0.1
U/kg IV over 30 min)
5. Beta-agonists (Salbutamol 0.4 mg (0.08 mL)/kg/dose Q2h via
nebulizer; can cause tachycardia).
34. Treatment of Hyperkalemia
6. Exchange transfusion with washed packed
cells.
7. Calcium gluconate 0.5 to 1.0 mL/kg IV over
5 to 10 min should be administrated in
presence of ECG changes (with continuous
ECG monitoring for bradycardia and
arrhythmias) to counteract the effects of
hyperkalemia on the myocardium.
8. The definitive therapy for significant
