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Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN 46202, Indianapolis, IN 46202
3To whom correspondence and reprint requests should be addressed at 699 West Drive, RR 208, Indianapolis, IN 46202. E-mail: sdenne{at}iupui.edu
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONREFERENCES |
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KEY WORDS: • energy expenditure • rate of growth • pulmonary insufficiency
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONREFERENCES |
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, Strangeway et al. 1976
,
Markestad and Fitzhardinge 1981
, Ariagno et al. 1991
); increased rates of energy expenditure would appear to be
a rational explanation to account for diminished growth rates. However,
limitations in study designs and measurement techniques have
complicated the interpretation of energy expenditure determinations in
infants with pulmonary insufficiency.
A variety of studies over the last 20 y have attempted to
answer the question of whether premature infants with chronic lung
disease have higher rates of energy expenditure. The results of most of
the studies measuring energy expenditure with respiratory calorimetry
in infants with chronic lung disease are shown in Figure 1
(Weinstein and Oh 1981
, Kao et al. 1988
,
Yeh et al. 1989
, Yunis and Oh 1989
,
Billeaud et al. 1992
, de Gamarra 1992
,
Wahlig et al. 1994
, Chessex et al. 1995
,
Merth et al. 1997
); from the data presented, it would be
difficult to come to a definitive conclusion about energy expenditure
in these infants. In addition, a number of important points must be
made about these studies. The results of nine studies are shown, but
only five of these studies included control groups. Many of the control
groups were not well matched for postnatal and sometimes gestational
age, both important determinants of energy expenditure (Chessex et al. 1981
, Sauer 1984
). Furthermore, most of
these studies were small (10 or fewer subjects in each group), four of
the studies were conducted prior to the availability to surfactant,
only three studied ventilated infants and very few extremely premature
infants (< 1000 g birth weight) were included in any study. All
these investigations used respiratory calorimetry as the tool to
measure energy expenditure. Although respiratory calorimetry has the
advantage of being noninvasive, because of practical considerations
measurements can usually be obtained for only several hours, and
therefore can examine resting energy expenditure, which then must be
extrapolated to total energy expenditure. Furthermore, the accuracy of
respiratory calorimetry in neonates is questionable in a supplemental
oxygen environment and during mechanical ventilation (Kalhan and Denne 1990
). These limitations in measurement techniques and
study designs have resulted in continuing uncertainty about the rates
of energy expenditure in infants with chronic lung disease.
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). This method requires the oral
administration of trace amounts of deuterium- and oxygen 18–labeled
water. Both labels mix with total body water, and over time both are
lost from the body; however, they are not lost at the same rate. The
deuterium label is lost as water (urine or evaporation). The
18O is also lost as water; however, because of
the action of carbonic anhydrase, some of the 18O
also ends up on carbon dioxide and as thus lost as carbon dioxide.
Therefore, the 18O label is lost at a greater
rate than is the deuterium label. The difference between the two
elimination rates reflects carbon dioxide production, which can then be
used to calculate energy expenditure. This method has been extensively
validated in a variety of populations and clinical circumstances,
including in premature infants (Roberts et al. 1986
).
The doubly labeled water technique is now beginning to be applied
to important questions regarding neonatal energy expenditure.
Preliminary evidence suggests that energy expenditure in critically ill
term infants with severe respiratory disease is not higher than that in
normal healthy infants; the energy requirements of these critically ill
infants can apparently be met by rather modest caloric intakes
(Carr et al. 2000
). In contrast, extremely premature
neonates with minimal respiratory disease seem to have high rates of
energy expenditure (
85 kcal · kg-1 ·
d-1), which typically exceeds the calories typically
provided in early postnatal life (Carr et al. 2000
).
Preliminary information is also emerging regarding energy expenditure
in extremely premature infants with early chronic lung disease; these
data suggest that total energy expenditure is approximately 25%
greater in ventilated extremely premature infants than in their
nonventilated counterparts (Leitch and Denne 2000
).
The doubly labeled water method has also been used to examine
whether dexamethasone therapy in extremely premature infants alters
energy expenditure and balance. Dexamethasone therapy substantially
reduces growth rates in premature infants (Yeh et al. 1990
, Papile et al. 1998
), and steroids have
been shown to increase energy expenditure in adults (Tataranni et al. 1996
); therefore, increased energy expenditure in
premature infants in response to dexamethasone therapy would be a
plausible explanation for altered rates of weight gain. Using a
cross-over, double-blind, placebo-controlled study design,
Leitch and colleagues (1999
) determined total energy
expenditure and balance in twelve 26-wk-gestation premature infants
during treatment with dexamethasone and placebo. Although the rate of
weight gain was reduced 70% during dexamethasone treatment, total
energy expenditure was unchanged (Fig. 2
). Furthermore, energy balance during dexamethasone treatment and
placebo treatment was virtually identical. This result of similar
energy balance and substantially altered weight gain strongly suggests
that dexamethasone alters the composition of newly accreted tissue
toward fat and away from protein; studies in preterm infants, human
adults and animals support this probability (Van Goudoever et al. 1994
, Tataranni et al. 1996
, Weiler et al. 1997
). Based on the findings from this study, it seems
unlikely that a strategy directed simply at increasing caloric intakes
in infants receiving dexamethasone will be successful in achieving
normal growth.
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)
measured higher rates of energy expenditure in 2-mo-old 29-wk gestation
infants with chronic lung disease (73 kcal · kg-1 ·
d-1) compared to 1-mo-old control infants (63 kcal ·
kg-1 · d-1). The fact that the control and
chronic lung disease groups were not well matched for postnatal age is
a limitation; nevertheless total energy expenditure determinations in
both early and established chronic lung disease suggest energy needs in
this population are increased 15–25% over controls, although further
work is clearly necessary.
It is an attractive hypothesis to attribute the increase in
energy expenditure in infants with chronic lung disease to increased
work of breathing. Indeed, a number of studies have observed a
correlation between energy expenditure and some measure of respiratory
status (Billeaud et al. 1992
, Wahlig et al. 1994
, de Meer et al. 1997
). However, Kao and
colleagues (1988
) examined the relationship between work
of breathing and energy expenditure more rigorously. Energy expenditure
and the mechanical power of breathing was measured in 4-mo-old infants
with oxygen-dependent chronic lung disease at baseline and then in
response to diuretic therapy or theophyline plus diuretic therapy.
Although the mechanical power of breathing decreased 40–50% in
response to either therapy, no change in energy expenditure was
measured. The energy cost of breathing was calculated at approximately
1–2 kcal · kg-1 · d-1, unlikely to
contribute significantly to increased energy expenditure in infants
with chronic lung disease. Alternative explanations for increased
energy expenditure, such as inflammation, appear more likely.
Recent studies using the doubly labeled water technique to measure
total energy expenditure in infants with congenital heart disease have
begun to better establish the energy needs of this population; previous
studies investigating energy metabolism in this population have been
difficult to interpret because of limitations in study design and
measurement techniques (Lees et al. 1965
, Krieger 1970
, Menon and Poskitt 1985
). A recent study
has reported total energy expenditure (using doubly labeled water),
resting energy expenditure (using respiratory calorimetry) and energy
intake in infants with cyanotic congenital heart disease and healthy
control infants (Leitch et al. 1998
). Subjects were
studied at both 2 wk and 3 mo of age. Although growth rates were
significantly lower in infants with cyanotic heart disease, no
significant difference was observed in energy intake or resting energy
expenditure between groups at either age. In contrast, total energy
expenditure was slightly but not statistically increased in the infants
with cyanotic congenital heart disease at 2 wk of age and significantly
increased at 3 mo of age (94 vs. 72 kcal · kg-1 · d-1). This study demonstrated the significant influence of
age at measurement as well as the importance of measuring total energy
expenditure and not just resting energy expenditure to determine energy
requirements. In addition, it appears that increased total energy
expenditure rather than deficiencies in dietary intake may be the
primary factor influencing growth in infants with cyanotic congenital
heart disease.
A similar study was carried out in 4-mo-old infants with moderate
to large ventricular septal defects (Ackerman et al. 1998
). Resting energy expenditure and energy intake were
virtually identical in infants with ventricular septal defects and
age-matched healthy control infants (Fig. 3
). Total energy expenditure, however, was 40% higher in the ventricular
septal defect (VSD) group (88 vs. 62 kcal · kg-1 ·
d-1). In addition, the difference between total energy
expenditure and resting energy expenditure, reflecting the energy of
activity, was 2.5-fold greater in the VSD group. These data suggest
that the high rates of total energy expenditure in infants with VSD may
primarily result from increased energy cost of physical activity.
Additional preliminary work in this population has demonstrated a
direct relationship between the energy of activity and the size of the
shunt in VSD infants (Leitch et al, 2000
).
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FOOTNOTES |
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2 Supported by PHS Grants RO1-HD29153, MO1RR750, S10 RR07269 and the James Whitcomb Riley Memorial Association.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONREFERENCES |
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