Clinical Chemistry 43: 205-210, 1997;
(Clinical Chemistry. 1997;43:205-210.)
© 1997 American Association for Clinical Chemistry, Inc.
Assessing fluid and electrolyte status in the newborn
John M. Lorenza
Department of Pediatrics and Human Development, Michigan State University, East Lansing, MI and Sparrow Regional Children's Center, Sparrow Hospital, Lansing, MI.
a Address correspondence to: Sparrow Hospital, P.O. Box 30480, Lansing, MI 48909-7980. Fax 517-483-3994; e-mail lorenzj{at}pilot.msu.edu
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Abstract
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Fluid and electrolyte assessment during the first week of life is
complicated by rapid changes in fluid and electrolyte balance during
the transition from fetal to neonatal life and by the newborn's small
size. A physiologic decrease in extracellular water volume, as well as
a transient increase in serum potassium and transient decreases in
plasma glucose and total plasma ionized calcium concentrations must be
taken into account. In general, the more immature the newborn, the
greater the changes that can be expected. The use of plasma creatinine
as an indicator of glomerular filtration rate is limited because it is
a function of maternal renal function at birth and because of
non-steady-state conditions in the immediate postnatal period.
Guidelines for monitoring schedules are provided on the basis of these
physiologic considerations and the author's experience. Method of
blood sampling and time to separation of serum are important
considerations in interpreting results. Minimization of sample volume
is critical to minimize blood transfusion requirements. Clinicians
should be aware of the analytical error associated with these
measurements in their own institutions. Reference ranges are
provided.
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Background
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The importance and difficulty of assessment and management of
fluid and electrolyte status during the first week of life in the
newborn can be as great as is ever encountered in medicine. One reason
is that the transition from fetal to newborn life is associated with
major changes in water and electrolyte homeostatic control. Before
birth, the fetus has a constant supply of water and electrolytes from
the mother across the placenta; fetal water and electrolyte homeostasis
is largely a function of placental and maternal homeostatic mechanisms.
After birth, the newborn must rapidly assume responsibility for its own
fluid and electrolyte homeostasis in an environment in which fluid and
electrolyte availability and losses fluctuate much more widely than in
utero. Moreover, for reasons that are not understood, the transition
from fetal to neonatal life is associated with what have come to be
accepted as normal changes in fluid and electrolyte balance. Thus, the
goal is not to maintain fluid and electrolyte status after
birth, but rather to allow these changes to occur
appropriately. Finally, because of the newborn's small size,
relatively small absolute changes in body water and electrolyte
quantity represent large proportionate changes for a neonate.
Fluid and electrolyte assessment during the first week of life
generally focuses on body water; serum sodium, potassium, glucose, and
calcium concentrations; and renal function. The changes in these
analytes in the first few days of life will be briefly reviewed. By the
end of the first week of life, fluid and electrolyte assessment becomes
part of a more comprehensive assessment of nutrition and growth that is
beyond the scope of this section.
Body water and sodium.
A weight loss of 5–10% in term
(1) infants and 10–20% in preterm
(2)(3) infants is common during the first week
of life. This loss of body weight appears to result largely from
physiologic contraction of the extracellular space after birth
(4)(5). Thus, net water and sodium loss is
accepted as appropriate after birth. Assessment of the degree and
appropriateness of this water loss is complicated by a relatively large
and highly variable insensible water loss (6)(7)(8). The more
immature the infant, the more pronounced the contraction of the
extracellular space and the higher the insensible water loss. Both of
these factors predispose to hypernatremia in the first few days of
life.
Potassium.
Serum potassium concentrations rise in the
first 24 to 72 h after birth in moderately to markedly premature
infants, even in the absence of exogenous potassium intake and in the
absence of renal dysfunction (9)(10)(11). This increase seems
to be the result of a shift of potassium from the intracellular to
extracellular space. The magnitude of this shift roughly correlates
with the degree of immaturity (11). In markedly premature
infants, this shift can result in life-threatening hyperkalemia. Serum
potassium subsequently falls as this internal potassium "load" is
excreted by the kidneys (10).
Glucose.
Before birth, fetal glucose concentration is
slightly higher than that of the mother (12). With cord
clamping, neonatal plasma glucose concentration plummets over the first
60–90 min of life (12)(13). Changes in
counterregulatory hormones and insulin result in mobilization of
glucose and fat and stimulate gluconeogenesis (14). These
changes increase endogenous glucose production, and plasma glucose
concentration rises and subsequently stabilizes. Premature infants and
growth-retarded infants are at risk for hypoglycemia because their
hepatic glycogen stores are limited (15). Perinatal stress
is associated with neonatal hypoglycemia in part because of
catecholamine-stimulated mobilization and depletion of glycogen stores.
Infants of diabetic mothers are at risk for hypoglycemia in spite of
increased glycogen and fat stores as the result of hyperinsulinism
(16).
Catecholamine-mediated mobilization of glycogen stores can result in
marked hyperglycemia in association with stress (17).
Premature infants are at risk for hyperglycemia with exogenous glucose
infusion because they secrete insulin sluggishly in response to rising
serum glucose concentrations (18).
Calcium.
Total calcium concentration in cord plasma
increases with increasing gestational age and is significantly higher
than paired maternal values (19)(20). With the
abrupt termination of calcium transport across the placenta at
delivery, plasma calcium falls, reaching a nadir at age 24–48 h
(20). Serum parathyroid hormone (PTH) increases
postnatally in response to this fall in plasma calcium concentration.
This increase in PTH mobilizes calcium from bone, and plasma calcium
concentration rises and subsequently stabilizes even in the absence of
exogenous calcium intake. Clinically significant hypocalcemia occurs in
premature infants (20), asphyxiated newborns
(21), and infants of diabetic mothers (22).
The etiology in all these circumstances is a sluggish response in PTH
secretion to the postnatal fall in plasma calcium concentration.
Approximately 50% of total plasma calcium is bound (predominantly to
albumin) and 50% is ionized. Plasma ionized calcium is the best
indicator of physiologic blood calcium activity. Changes in plasma
ionized calcium concentration parallel those described above for total
plasma calcium concentration (20)(23). Lower
serum albumin concentrations and acidosis, not uncommonly found in
premature infants, result in a lower total plasma calcium concentration
for a given plasma ionized calcium concentration. In practice, however,
because changes in ionized plasma calcium mirror those in total plasma
calcium concentration and because of the larger sample volume required
in many labs for determination of the former, calcium status is
routinely monitored with total plasma calcium concentration. However,
correlation is poor in individual infants (23)(24)(25) and the
electrocardiogram lacks sensitivity in detecting hypocalcemia
(26), so that determination of plasma ionized calcium is
necessary if calcium status is critical.
Renal function.
Plasma creatinine concentration is of
limited value in assessing renal function in the first week of life
(27). First, plasma creatinine concentration in cord blood
is a function of maternal renal function and is almost identical to the
maternal concentration (28)(29). Second,
abrupt changes in extracellular volume (4)(5)
and glomerular filtration rate (GFR) (30)(31)(32) after birth
result in non-steady-state conditions in the first few days of life.
In general, plasma creatinine concentration decreases exponentially
during the first few days of life in normal term infants
(27). However, GFR increases with increasing gestational
age (33)(34)(35). Therefore, with
increasing prematurity, the postnatal fall in creatinine concentration
is more protracted (36). Thus, in the extremely premature
newborn, plasma creatinine concentration may not change significantly
over the first 5 days of life (27). However, the relation
between the rate of change in plasma creatinine in the first week of
life and gestational age has not been accurately quantified. Thus,
change in plasma creatinine concentration over a period of days in the
first week of life can be only a rough, qualitative indication of GFR.
The blood urea nitrogen is a function of metabolic state, protein load,
changes in extracellular volume, and GFR. Therefore, it adds little to
plasma sodium or creatinine concentration in the assessment of
extracellular volume or GFR (37).
The marked changes in body water, sodium, and potassium balance and the
associated abrupt changes in renal function (as well as the marked
variability in the magnitude and timing of these changes
(30)(31)(32)) limits the usefulness of measurement of urine
osmolality, urine sodium and potassium concentration or excretion
rates, and fractional excretion of sodium in the first few days of
life. Reference ranges that are appropriate for gestational age and
postnatal age are not available.
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Routine Monitoring Schedules (Table 1
)
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As discussed above, the likelihood and magnitude of perturbations
in fluid and electrolyte status varies with the degree of prematurity
and associated conditions. The schedules recommended in Table 1
reflect
this variability. These schedules are provided as guidelines on the
basis of the author's experience.
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Preanalytic Considerations
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The route by which the blood specimen is obtained and the time
from sampling to separation of serum can have clinically significant
effects on serum electrolyte and glucose concentrations. Blood samples
are obtained in neonates by finger or heel puncture capillary samples,
by peripheral vessel, and from indwelling (usually arterial) catheters.
Route of sampling.
Capillary samples are not adequate
for determination of serum potassium if abnormal values are likely or
suspected. This route of sampling is associated with hemolysis that
will spuriously increase serum potassium concentration in the sample.
Hemolysis can also occur when blood is obtained by vessel puncture, or
through a catheter, as the result of turbulent, nonlaminar flow if it
is withdrawn forcefully or injected into the sample tube forcefully.
The solution with which an indwelling line is perfused must be
considered when obtaining samples and interpreting the results of
subsequent analyses because the perfusate can contaminate the sample.
For example, sampling from catheters perfused with dextrose solutions
with no or a low concentration of sodium may lead to spurious
hyponatremia as the result of dilution of the sample by the infusate.
Most such errors can be minimized by first aseptically withdrawing 3–5
times the volume of the infusate system through which the sample is
obtained (dead space volume) to clear it of infusate (41).
The volume withdrawn to clear the catheter should be reinfused after
the sample is obtained. However, this technique is not adequate to
allow blood samples obtained for plasma glucose determinations to be
drawn from catheters infused with dextrose solutions (41).
Time to separation of serum.
Serum samples for glucose
determination should be separated from erythrocytes as soon as
possible. Whole-blood glucose values may drop 7% per hour if the
sample is allowed to stand at room temperature (42).
Sample volume.
One of the greatest "costs" of
monitoring fluid and electrolyte status in newborns, especially those
with very low birth weights, is the volume of blood required. The most
important determinant of volume of blood transfusions required is
volume of blood sampled (43). Blood transfusion in a
critically ill newborn may be required when 
10% of blood volume (80
mL/kg body weight in the full term; 100 mL/kg body weight in the
preterm) is withdrawn over <2–3 days. Thus, for a 750-g infant,
withdrawal of as little as 8 mL of blood over a short period may
necessitate blood transfusion. Considering that the smallest and
sickest infants will require the most frequent and numerous monitoring
tests, sample volumes submitted to the laboratory should be the minimum
practical. To this end, it is critical that phlebotomists, nurses, and
physicians caring for newborns be knowledgeable about the volume of
blood required for a test or combination of tests; that sample volume
in very low birth weight and critically ill newborns be monitored; and
that tests are grouped in such a way as to minimize sample volume.
Table 2
provides an example of such information that is posted in the
newborn intensive care unit at one institution. It is not recommended
that excess sample volume be routinely obtained because of the
possibility that repeat analysis might be indicated in the case of an
unusual result.
Coordination among services.
There are usually routine
morning phlebotomy rounds in the newborn intensive care unit. The
results of these analyses, although routine, will determine the
immediate treatment of these patients. It is recommended that the
laboratory and clinical staff coordinate blood drawing, availability of
laboratory instruments (to avoid delays associated with changing work
shifts), and morning patient rounds to expedite return of results in a
timely manner.
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Analytic Concerns
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As discussed previously, minimization of sample volume is required
for laboratory analyses. Therefore, micromethod assays are mandatory.
All analyses listed in Table 1
should be available 24 h a day, 7
days per week, with an intralaboratory turnaround time of 2 h. It
is reasonable to expect that results of analyses ordered stat should be
available with a median intralaboratory turnaround time of 25–30 min
and no longer than 60 min (44).
There is no information about allowable error for these analytes
specific to the newborn intensive care unit. Total analytical error is
composed of intralaboratory imprecision and interlaboratory inaccuracy.
Table 3
lists the allowable error specified for analytical equipment
performance by the 1988 CLIA requirements (45). These
limits have become maximum limits for allowable errors so that, in
practice, total allowable error must be less (46).
Precision is particularly important in the neonatal intensive care unit
because changes over time can be as important as the absolute value
measured. At a minimum, it is important that clinicians be aware of the
total error of analyte measurements in their own
institutions, so that they can appropriately interpret the
significance of differences in values over time.
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Reference Ranges (Table 4
)
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Reference ranges are usually established on the basis of the
statistical distribution of results within a sample of the population.
Values within these ranges have no adverse consequences under usual
circumstances; values outside these ranges may or may not have
pathophysiological effects. Reference ranges in newborns are
complicated by the fact that the statistical distribution of results
for these analytes in a population sample is dependent on gestational
and (or) postnatal age. Furthermore, even values that are not
statistically unusual for gestational/postnatal age may have
pathophysiologic consequences that require intervention. However, in
most cases, there is little information specific to the neonate about
the likelihood of clinically significant effects with degree of
deviation from normal.
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Acknowledgments
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I am grateful for the assistance of Anthony Koller in the
preparation of this manuscript.
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