Clinical Chemistry 43:1
205-210 (1997)
Assessing fluid and electrolyte status in the
newborn
John M. Lorenz
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 phys-
iologic 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 creat-
inine as an indicator of glomerular filtration rate is
limited because it is a function of maternal renal func-
tion at birth and because of non-steady-state conditions
in the immediate postnatal period. Guidelines for mon-
itoring 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 re-
sults. 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.
Background
The importance and difficulty of assessment and manage-
ment of fluid and electrolyte status during the first week
of life in the newborn can be as great as is ever encoun-
tered 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
Department of Pediatrics and Human Development, Michigan State Uni-
versity, East Lansing, MI and Sparrow Regional Children’s Center, Sparrow
Hospital, Lansing, MI.
Address correspondence to: Sparrow Hospital, P.O. Box 30480, Lansing,
MI 48909-7980. Fax 517-483-3994; e-mail lorenzj@pilot.msu.edu.
Received July 30, 1996; revised October 15, 1996; accepted October 15, 1996.
205
NACB Symposium
newborn must rapidly assume responsibility for its own
fluid and electrolyte homeostasis in an environment in
which fluid and electrolyte availability and losses fluctu-
ate 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 bal-
ance. 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 – 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 –11]. This
increase seems to be the result of a shift of potassium from
the intracellular to extracellular space. The magnitude of
206 Lorenz: Assessing fluid and electrolyte status
this shift roughly correlates with the degree of immaturity
[11]. In markedly premature infants, this shift can result in
life-threatening hyperkalemia. Serum potassium subse-
quently 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 counterregula-
tory hormones and insulin result in mobilization of glu-
cose and fat and stimulate gluconeogenesis [14]. These
changes increase endogenous glucose production, and
plasma glucose concentration rises and subsequently sta-
bilizes. 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 hyper-
glycemia with exogenous glucose infusion because they
secrete insulin sluggishly in response to rising serum
glucose concentrations [18].
Calcium. Total calcium concentration in cord plasma in-
creases with increasing gestational age and is significantly
higher than paired maternal values [19, 20]. With the
abrupt termination of calcium transport across the pla-
centa 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 hypocal-
cemia occurs in premature infants [20], asphyxiated new-
borns [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 albu-
min 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 [23–25] and the electrocardio-
gram 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 lim-
ited 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 –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 [33–35]. Therefore, with increasing prema-
turity, 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 creati-
nine concentration in the assessment of extracellular vol-
ume 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 –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.
Routine Monitoring Schedules (Table 1)
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.
Preanalytic Considerations
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
 Clinical Chemistry 43, No. 1, 1997 207

Table 1. Guidelines for routine monitoring of fluid and electrolyte status in the newborn.
Gestational Agea Test(s) Monitoring schedule
#25 weeks Na, K, Cl, tCO2b By 8–12 h; then every 8–12 h until stable or trending towards reference
range; then daily
Glucose Usually estimated frequently at the bedside with dry-reagent test strips;
estimated values in the lower portion of the reference range must be
confirmed with a serum glucose concentration to reliably identify
hypoglycemiac,d
Ca At 12–24 h; then every 8–12 h until nadir is reached; then every 24 h until
the value is within reference range without calcium supplementation
Creatinine By 8–12 h, then daily
26–30 weeks Na, K, CL, tCO2b By 12–24 h; then every 12–24 h until stable or trending towards reference
range; then daily
Glucose As above
Ca At 12–24 h; then every 24 h until nadir is reached; then every 24 h until
value is within reference range without calcium supplementation
Creatinine By 12–24 h, then daily
30–34 weeks Na, K, Cl, tCO2b By 18–24 h, then daily
Glucose As above
Ca At 18–24 h, then daily until value is within reference range without
supplementation
Creatinine By 18–24 h, then only if renal insufficiency is anticipated or suspected
$34 weeks on Na, K, Cl, tCO2b At 18–24 h, then daily
intravenous Glucose As above
maintenance Ca As above, but only with risk factor (in addition to prematurity) or signs
consistent with hypocalcemia
Creatinine At 18–24 h, then only if renal insufficiency is anticipated or suspected
$34 weeks Na, K, Cl, tCO2b Only as indicated by excessive weight loss or unusual water and electrolyte
without loss
intravenous Glucose As above, but only with risk factor or signs consistent with hypoglycemia
maintenance Ca As above
Creatinine Only if renal insufficiency is anticipated or suspected
a
These gestational age ranges are provided as approximations; they are not meant as strict cutoffs.
b
If acid– base status is being simultaneously assessed with blood gases, regular assessment of Cl and tCO2 (total carbon dioxide) is probably unnecessary unless
calculation of the anion gap is of interest. Unfortunately there is little information available regarding the usefulness of the anion gap in the neonate. Furthermore, if
the sample is obtained from a skin stick without prewarming, then the tCO2 may be spuriously low.
c
Ref. 38.
d
Other methods that involve very small sample volumes are available that offer accuracy and precision comparable with conventional laboratory methods [39,40].

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 potas-
sium 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 inter-
preting the results of subsequent analyses because the
perfusate can contaminate the sample. For example, sam-
pling 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 mini-
mized 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 ob-
tained 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
208 Lorenz: Assessing fluid and electrolyte status

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 knowl-
edgeable 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 in-
struments (to avoid delays associated with changing work
shifts), and morning patient rounds to expedite return of
results in a timely manner.
Analytic Concerns
As discussed previously, minimization of sample volume
is required for laboratory analyses. Therefore, micro-
method 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 impreci-
sion and interlaboratory inaccuracy. Table 3 lists the
allowable error specified for analytical equipment perfor-
mance 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]. Preci-
sion 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

Table 2. Example of sample volume information that should be available in the newborn intensive care unit.
Test Container Blood volume, mL
Na, K, Cl, CO2 1 microtainer 0.6
Na, K, Cl, CO2, BUN, Creat, Glu 1 microtainer 0.6
Na, K, Cl, CO2, BUN, Creat, Glu, Ca 1 microtainer 0.6
Na, K, Cl, CO2, Creat, T/D Bili 1 microtainer 0.6
Na, K, Cl, CO2, Creat, Ca, Mg 1 microtainer 0.6
Any other combination of analytes in the chemistry profile 6 Mg and Trig 2 microtainers 1.2
Ionized calcium Na-Heparin tube 0.6
Hgb 1 EDTA microtainer 0.6
Hgb 1 Retic 1 EDTA microtainer 0.6
PBC (includes platelets) 6 Diff 1 EDTA microtainer 0.6
PBC 1 Retic 1 EDTA microtainer 0.6
CBC (PBC 1 Diff) 1 Retic 1 EDTA microtainer 0.6
PT/PTT 1.8 mL citrate tube 1.8
PT/PTT 1 Fibrinogen 1.8 mL citrate tube 1.8
PT/PTT 1 Fibr. 1 D-dimer 1.8 mL citrate tube 1.8
Lactic acid 1 Na-F microtainer 0.5
Ammonia 1 EDTA microtainer 0.6
Karyotype Na-Heparin tube 1.0
Platelet antibodies 2 microtainers 1.2
Theophylline 1 microtainer 0.6
Vancomycin 1 microtainer 0.6
Gentamicin 1 microtainer 0.6
Phenobarbital 1 microtainer 0.6
Phenytoin 1 microtainer 0.6
BUN, blood urea nitrogen; Creat, creatinine; Glu, glucose; T/D Bili, total/direct bilirubin; Trig, triglycerides; Hgb, hemoglobin; PBC, partial blood count; Diff, differential
count; Retic, reticulocytes; CBC, complete blood count; PT, prothrombin time; PTT, partial thromboplastin time.
 Clinical Chemistry 43, No. 1, 1997 209

Reference Ranges (Table 4)

Table 3. Allowable error as specified by CLIA ’88.
Reference ranges are usually established on the basis of
Na 64 mmol/L
the statistical distribution of results within a sample of the
K 60.5 mmol/L
population. Values within these ranges have no adverse
Cl 65%
consequences under usual circumstances; values outside
Glucose 610%
Total calcium 60.25 mmol/L
these ranges may or may not have pathophysiological
Creatinine 626 mmol/L or 15% (whichever is greater) 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 gesta-
important that clinicians be aware of the total error of tional and (or) postnatal age. Furthermore, even values
analyte measurements in their own institutions, so that they that are not statistically unusual for gestational/postnatal
can appropriately interpret the significance of differences age may have pathophysiologic consequences that require
in values over time. intervention. However, in most cases, there is little infor-
mation specific to the neonate about the likelihood of
clinically significant effects with degree of deviation from
normal.
Table 4. Reference ranges.
Plasma concentrationa
Analyte SI units Conventional units
Sodiumb 135–145 mmol/L 135–145 meq/L I am grateful for the assistance of Anthony Koller in the
Potassium 3.6–6.7 mmol/L 3.6–6.7c meq/L preparation of this manuscript.
Chlorideb 101–111 mmol/L 101–111 meq/L
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