Energy expenditure and plasma catecholamines in preterm infants with mild chronic lung disease

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Early Human Development 72 (2003) 147–157

Energy expenditure and plasma catecholamines in

preterm infants with mild chronic lung disease

Jacqueline Bauer a,*, Kathrin Maier b, Bernd Muehlbauer c,Johannes Poeschl a, Otwin Linderkamp a

aDivision of Neonatology, Department of Pediatrics, University of Heidelberg, Im Neuenheimer Feld 150,

D-69120 Heidelberg, GermanybDepartment of Pediatrics, University of Freiburg, Freiburg, Germany

cDepartment of Pharmacology, University of Tuebingen, Tuebingen, Germany

Accepted 13 March 2003

Abstract

The present study examined the hypothesis that the energy expenditure (EE) increases during the

development of chronic lung disease (CLD) together with serum catecholamines as indicator of stress.

Sixteen spontaneously breathing infants with gestational age of 28–34 weeks and birth weight of

870–1920 g were studied. Eight patients were at risk for CLD, eight were healthy controls.

Measurements of indirect calorimetry were done weekly at postnatal ages of 2, 3, 4 and 5 weeks.

Serum concentrations of adrenaline and noradrenaline were measured by means of a high-pressure

liquid chromatography (HPLC) method. The eight CLD risk infants developed mild CLDwith FiO2 of

0.27–0.31 and characteristic radiographic signs at 28 days. Compared to the healthy controls, preterm

infants with mild CLD showed increases in EE from week 3 (+67%) to week 5 (+46%). Plasma

noradrenaline was increased significantly in the CLD infants when compared to the controls at week 3

(0.7F0.3 vs. 0.5F0.1 ng/ml; P<0.05) and more pronounced at week 4 (1.4F0.2 vs. 0.6F0.2 ng/ml;

P<0.001) and 5 (1.1F0.3 vs. 0.7F0.2 ng/ml; P<0.01). Plasma adrenaline was markedly higher in the

CLD risk group (mean overall value: 0.64F0.1 ng/ml) than in the controls (<0.1 ng/ml in all controls)

from week 2 to 5. Regression analysis for the combined values of the infants with and without CLD

showed that EE was directly correlated with heart rate, noradrenaline and adrenaline concentration at

each of the four study weeks and with respiratory rate at weeks 2 and 3. Increased plasma

catecholamine concentrations in preterm infants with CLD suggest that these infants experienced

marked stress during the early stages of the disease. Increased EE may in part be a result of this stress.

D 2003 Elsevier Science Ireland Ltd. All rights reserved.

Keywords: Catecholamines; Energy expenditure; Chronic lung disease; Stress; Preterm infants

* Corresponding author. Tel.: +49-6221-5639369/562308; fax: +49-6221-565602.

0378-3782/03/$ - see front matter D 2003 Elsevier Science Ireland Ltd. All rights reserved.

doi:10.1016/S0378-3782(03)00046-X

E-mail address: [email protected] (J. Bauer).

J. Bauer et al. / Early Human Development 72 (2003) 147–157148

1. Introduction

Approximately 30% of preterm infants with birth weight below 1500 g that suffer from

respiratory distress syndrome develop chronic lung disease (CLD) [1]. In recent years, less

severe forms of CLD have been observed after the introduction of antenatal steroids and

postnatal surfactant therapy, and the application of early CPAP [2]. However, the incidence

of mild CLD did not change [1,2].

Growth failure is common in infants with CLD [3] and may be associated with

impaired long-term outcome [4]. Undernutrition of preterm infants with CLD may result

from fluid and nutrient restriction and increased resting energy expenditure (EE).

Increased EE in infants with CLD may be caused by increased work of breathing,

increased heart rate, impaired growth, hypoxia, inflammation and tissue repair. Resting EE

may be markedly increased in preterm infants already during the acute phase of respiratory

illness, that is, during the first week after birth [5,6]. In ten 6–49 days old ventilated

preterm infants, EE increased linearly with the extent of ventilatory support required to

maintain adequate gas exchange [7]. Several groups determined EE in premature infants

with severe CLD at more than 4 weeks of postnatal age and found EE elevated by 20–

30% [5–7]. Little is known about catecholamines in preterm infants with acute or chronic

lung disease. Barker and Rutter [8] found a marked rise in plasma catecholamines in

preterm infants with severe acute respiratory illness. Kallio et al. [9] observed that

antenatal dexamethasone treatment decreases plasma noradrenaline and adrenaline con-

centrations in preterm infants. They explain their results by improved surfactant produc-

tion. Greenough et al. [10] reported that plasma catecholamines increased in preterm

infants with low Apgar score and umbilical artery pH<7.25. Weinstein et al. [11] found a

positive correlation between urinary noradrenaline excretion and oxygen consumption in

preterm infants with 3–15 days of postnatal age.

The purpose of our investigation was to study whether relationships between EE and

plasma catecholamines exist in preterm infants with CLD risk from 2 to 5 weeks of

postnatal age. Catecholamines were studied as indicators of stress.

2. Patients and methods

2.1. Patients

Sixteen spontaneously breathing preterm infants with gestational age of 28–33 weeks

(median, 30 weeks) and birth weight of 870–1920 g were enrolled for the study at

postnatal age of 2 weeks. All patients were recruited from the preterm population admitted

in the NICU of the University of Freiburg during the study period. Eight infants had CLD

and eight healthy preterm infants matched for birthweight and gestational age served as

control group. Excluded were all infants with FiO2>35% because of technical limitations

of the measurement of VO2. Moreover, infants with infection, malformations, erythro-

blastosis and diabetic mothers were excluded. Because infants with intrauterine growth

retardation may show increased EE [12], only infants appropriate for gestational age were

included. All the infants were treated with caffeine for apnoea until they reached 34 weeks

J. Bauer et al. / Early Human Development 72 (2003) 147–157 149

of gestational plus postnatal age [13]. Serum concentrations of caffeine ranged from 10 to

15 Ag/ml. No corticosteroids, catecholamines, sedatives, diuretics or other drugs that could

affect EE or catecholamine values were given during the study period. Approval for the

study was obtained from the Ethical Committee of the University of Freiburg. Consent

was obtained from the parents of each infant studied.

Criteria for enrollment of the infants at increased risk for CLD included prematurity at

birth (gestational age below 34 weeks), a history of respiratory distress syndrome,

exposure to mechanical ventilation and/or prolonged CPAP support, supplemental oxygen

in the first 2 weeks of life to maintain oxygen saturation (SaO2) above 92%, and chest

roentgenographic findings according to the criteria described by Bancalari [14]. Roent-

genographic signs at 2 weeks of postnatal age included diffuse haziness and densities. On

the first day of life, three infants required mechanical ventilation and surfactant therapy for

respiratory distress syndrome. These three infants were extubated at 2 days after birth. Five

infants were only treated with CPAP. During the study period (from 2 to 5 weeks of age),

no respiratory support with mechanical ventilation or CPAP was required in any of the

infants. At 2 weeks of age, all CLD-risk infants received oxygen supplementation with

FiO2 of 0.27–0.31. All CLD risk infants had oxygen supplementation until 4 weeks of

age. At 28 days, FiO2 ranged from 0.23 to 0.27 to maintain oxygen saturation (SaO2)

above 92%. Chest radiographs demonstrated characteristic abnormalities (persistent

diffuse haziness and densities in both lungs) in all CLD-risk infants at 28 days. Based

on the requirement of supplemental oxygen and moderate radiographic findings at 28 days

[14], we diagnosed mild CLD in all infants with CLD risk.

Infants in the control group were comparable to the infants with CLD risk for birth

weight and gestational age, but had no evidence of respiratory distress after birth, did not

need supplemental oxygen or ventilatory support and had no clinical or radiographic signs

of CLD.

The CRIB score was obtained according to the criteria of Baumer et al. [15] (see Table

1). The infants were monitored continuously using a cardiorespiratory monitor (Mar-

quette-Hellige, model VICOM-SMU, Freiburg, Germany) and by a pulse oxymeter

(Hellige or Nellcor, Hayward, USA). Heart rate, respiratory rate and oxygen saturation

were monitored continuously. Skin (lower leg) and rectal temperatures (Exacon System

4000, Roskilde, Denmark) were measured continuously for 2 h before, during, and for 2 h

after, indirect calorimetry. Room humidity and temperature were recorded during the

observation periods. Indirect calorimetry was measured in the neonates in an air temper-

ature-controlled incubator (model 8000, Draeger, Lubeck, Germany) at thermoneutral

temperatures according to published recommendations [16]. All of the infants were treated

in the same type of incubator.

During the whole study period, all infants were fed every 2 h at weeks 2 and 3 and

every 4 h at weeks 4 and 5 on either breast milk fortified with FM 85 (Nestle, Vevey,

Switzerland) or a preterm formula. At the first study week, all infants received

approximately only 5–10% of the nutrition parenterally and 90–95% via a gastric tube.

Because VO2 and VCO2 are influenced strongly by feeding, each period of indirect

calorimetry began 45 min after feeding according to published recommendations [17].

Measurements were started after an equilibration time of 15 min as described by the

manufacturer. Therefore, each period of calorimetry began 60 min after feeding to


minimise effects of postprandial thermogenesis on the results and lasted for 60 min in

infants with 2-h feedings and for 180 min in infants with 4-h feedings. Measurements were

not interrupted by the nursing routine. In infants with 2-h feedings, measurements were

repeated after the next feeding under identical conditions, to obtain a total measure period

of 120 min. Both groups received the same energy intake, but different fluid intake during

the study periods (see Table 2). Body weight was measured daily at 8 a.m. by using a scale

with a resolution of 5 g.

The behavioural states of the infants were recorded throughout the observation period,

based on the modified Freymond Behavioural State Scale [18]. Four different behavioural

states were distinguished: (0) eyes open or closed, regular respiration, no movements; (1)

small movements; (2) vigorous movements; and (3) crying. Both groups of infants were

studied only during sleep (state 0–1).

2.2. Methods

If the inclusion criteria were fulfilled, indirect calorimetry (oxygen consumption and

carbon dioxide production) was started at 2 weeks. The measurements were repeated under

identical conditions at 3, 4 and 5 weeks of postnatal age. Before respiratory gas analysis,

blood samples (60 Al of blood) were obtained via a central catheter in an umbilical vessel

(in two CLD-risk infants at 2 weeks) or a plastic cannula placed in a superficial vein. One

hour after, the cannula was inserted. Blood was sampled for catecholamines. Blood

samples were also used for weekly routine laboratory analyses performed in all infants.

Venous blood samples were taken in all preterm infants with 28–34 weeks of gestation

from 2 to 5 weeks of age for routine laboratory analyses. If necessary, more blood samples

were taken (e.g., signs of infection). The blood samples for catecholamines were collected

into EDTA tubes, placed on ice, and centrifuged promptly to separate the plasma. Plasma

samples were stored at �70 jC until analysed for adrenaline and noradrenaline by high-

pressure liquid chromatography (HPLC) [19]. The lower limit of detection of adrenaline

and noradrenaline was 0.1 ng/ml. All patients have completed the set of four longitudinal

measurements of EE and catecholamines.

2.3. Indirect calorimetry

Oxygen consumption (VO2) and carbon dioxide production (VCO2) were measured by

means of a portable open-circuit continuous indirect calorimetry device, Deltatrac II

metabolic monitor (Datex-Ohmeda, Instrumentarium, Helsinki, Finland) [20]. Details of

the technique, the precision of the VO2 measurement device and its validation for indirect

calorimetry in neonates were as previously described [20–22]. The accuracy of the device

was tested as a mean experimental error for VO2 measurements of 2% (S.D. 2%) [23]. The

device does not measure inspiratory and expiratory oxygen concentration separately, but

measures 0.01% (vol.) O2 differences as a 1-min average very accurately. Calibration of

the device was performed before each measurement by a standard calibration gas (5% O2

and 95% CO2). The analyser was set at zero according to room air. Calibration gases were

prepared to an accuracy of F0.03% and certified gravimetrically. For the measurements in

the preterm infants, a facemask (silicon) was used instead of a hood as previously

Table 1

Clinical data of preterm infants with mild chronic lung disease (CLD) and control infants

CLD (n=8) Controls (n=8)

Gestational age (weeks) 31F4 32F3

Birth weight (g) 1360F110 1310F119

Apgar score

at 1 min 4.4F1.6* 6.7F0.5

at 5 min 7.1F1.2 8.6F0.6

Umbilical artery pH 7.26F0.05* 7.33F0.03

CRIB score [15] 3.8F1.4* 1.5F0.5

FiO2 at 2 weeks 0.32F0.01* 0.21F0.00

Data are given as means (S.D.).

* P<0.05 when compared with controls (Mann–Whitney Rank Sum test).


described [13,21,22]. The mean experimental error for VO2 measurements was shown to

be 2F2% [23]. In infants with increased oxygen concentration, expired air was sampled

completely. Only VCO2 was measured and VO2 was calculated because the inspiratory

oxygen concentration was unstable and VO2 measurements are difficult and can produce

errors [24]. In previous studies, it was shown that calculated VO2 from VCO2 and food

quotient agrees closely with measured VO2 [25–27]. The error was given within F2% in

children and adults [27] and F3% in premature infants [25]. At the end of the measure-

ment cycle, the values were transmitted to a personal computer and processed using SAS

for Windows (SAS Institute, Cary, NC, USA). Energy expenditure (EE) was calculated as

EE=5.50 VO2+1.76 VCO2 (in kilocalories per kilogram per day) [28].

Table 2

Age-dependent changes in clinical parameters in preterm infants with mild chronic lung disease (CLD) and

controls (C)

Age (weeks)

2 3 4 5

Body weight (g) CLD 1190F106 1320F110 1400F202 1490F208

C 1200F98 1290F88 1420F103 1570F115

Heart rate (min�1) CLD 139F14 137F15 134F8 129F14

C 134F15 133F16 130F13 126F12

Respiratory rate (min�1) CLD 68F12 69F14 63F16 60F17

C 61F15 58F12 62F12 62F10

FiO2 CLD 0.29F0.01** 0.23F0.01** 0.23F0.01** 0.21F0.01

C 0.21F0.00 0.21F0.00 0.21F0.00 0.21F0.00

Energy intake (kcal/kg/day) CLD 70F12 92F13 119F15 124F15

C 69F9 90F12 123F14 126F10

Fluid intake (ml/kg/day) CLD 89F12 108F15 116F17* 119F13**

C 92F10 119F14 126F12 138F15

Behavioural state CLD 0.0F0.0 0.0F0.0 0.0F0.0 0.0F0.0

C 0.0F0.0 0.0F0.0 0.0F0.0 0.1F0.3



** P<0.001 when compared with controls (Mann–Whitney Rank Sum test).

Table 3

Age-dependent changes in calorimetry values and plasma catecholamines in preterm infants with mild chronic

lung disease (CLD) and controls (C)

Age (weeks)

2 3 4 5

VO2 (ml/kg/min) CLD 6.3F0.3** 6.0F0.5** 8.5F0.4** 9.9F0.3**

C 4.7F0.4 5.0F0.5 6.1F0.3 6.8F0.4

VCO2 (ml/kg/min) CLD 6.4F0.3** 6.7F0.4** 7.9F0.5** 9.8F0.5**

C 4.4F0.3 4.9F0.3 5.9F0.4 6.3F0.4

EE (kcal/kg/day) CLD 46F7 80F10** 82F7** 102F12**

C 41F5 48F10 58F10 70F12

Adrenaline (ng/ml) CLD 0.6F0.1** 0.6F0.2** 0.8F0.1** 0.7F0.2**

C <0.1F0.0 <0.1F0.0 <0.1F0.0 <0.1F0.0

Noradrenaline (ng/ml) CLD 0.8F0.2 0.7F0.3* 1.4F0.2** 1.1F0.3**

C 0.8F0.2 0.5F0.1 0.6F0.2 0.7F0.2


VO2: oxygen consumption; VCO2: carbon dioxide production; EE: energy expenditure.


** P<0.001 when compared with controls (Mann–Whitney Rank Sum test).


2.4. Statistical analyses

Data were expressed as group means and standard deviations of the mean. Comparisons

of values of the CLD risk and control group were performed by the Mann–Whitney Rank

Sum test (Tables 1–4). Because of the multiple comparisons, P values <0.001 were

considered significant. Several regression equations were calculated between EE (as

dependent variable) and the variables heart rate, respiratory rate, FiO2, energy intake,

noradrenaline and adrenaline concentrations. For multiple regression analysis, an addi-

Fig. 1. Energy expenditure age-dependent changes in calorimetry values and plasma catecholamines in preterm

infants with mild chronic lung disease (CLD) and controls (C). Data are given as means (S.D.), **P<0.001 when

compared with controls (Mann–Whitney Rank Sum test).


tional independent variable was assumed to improve the relationship, if either the

significance of the additional regression coefficient was <0.1 or the correlation coefficient

(r) increased by more than 0.05.

3. Results

Clinical data are summarised in Table 1. Apgar scores at 1 and 5 min of birth and

umbilical artery pH were significantly lower in the CLD group than in the controls. The

Table 4

Regression equations for infants with and without CLD risk (energy expenditure as dependent variable; n=16)

Regression equation r P

Week 2

EE=0.276EI+24.7 0.436 0.0916

EE=0.38RR+19.5 0.774 0.00042

EE=0.722FiO2+25.6 0.471 0.0657

EE=0.600HR�38.2 0.894 0.0000031

EE=37.0NA+15.7 0.807 0.00103

EE=14.31A+38.6 0.614 0.0150

EE=14.5NA+0.476HR�32.3 0.921 0.0000047

Week 3

EE=0.403EI+27.2 0.277 0.2997

EE=1.017RR�0.817 0.761 0.00062

EE=16.0FiO2�287 0.869 0.000013

EE=0.981HR�69.8 0.597 0.0145

EE=81.1NA+14.7 0.807 0.000157

EE=59.1A+46.1 0.879 0.0000072

EE=0.10HR+76.5NA+2.811 0.809 0.00101

Week 4

EE=0.222EI+43.2 0.218 0.418

EE=0.524RR�37.3 0.484 0.058

EE=12.7FiO2�208 0.848 0.000033

EE=0.939HR�54.6 0.623 0.0099

EE=34.1NA+36.3 0.902 0.0000018

EE=35.1A+56.2 0.853 0.0000262

EE=29.4NA+0.434HR�16.7 0.938 0.00000101

Week 5

EE=0.149EI+67.7 0.096 0.723

EE=0.617RR+48.4 0.429 0.098

EE=16.3FiO2�267 0.814 0.00013

EE=1.063HR�50.6 0.534 0.033

EE=77.5NA+17.0 0.918 0.00000052

EE=53.1A+67.81 0.854 0.0000259

EE=74.3NA+0.469RR�8.85 0.918 0.0000000045

EE=72.2NA+0.297RR+0.299HR�35.0 0.977 0.000000023

EE: energy expenditure; EI: energy intake; RR: respiratory rate; HR: heart rate; NA: noradrenaline; A: adrenaline.


FiO2 values in the CLD-risk group decreased in all infants during the study period, but

were still increased at 5 weeks in six of the eight infants with CLD. Prenatal steroids were

given to four mothers in the CLD group and to six in the control group.

The type and frequency of intensive care were documented during all study weeks in

both groups. There were no differences for parenteral nutrition, frequency of blood

sampling or other invasive procedures during the observation period. There was no

occurrence of infection or sepsis in any of the 16 infants during the entire study period.

Serial values obtained from week 2 to 5 are shown in Table 2. Body weight, heart

and respiratory rate showed no meaningful differences between the two groups. The

mean values of VO2 and VCO2 were significantly (P<0.005) increased in the CLD

group when compared to the control infants during the entire observation period (Table

3). Values of EE were increased from week 3 to 5 (Fig. 1). Plasma adrenaline values

were below the limit of detection of 0.1 ng/ml in all healthy preterm infants. The mean

values of adrenaline in the CLD group were significantly higher than in the controls

from week 2 to 5 (P<0.005). Noradrenaline concentrations were higher in the CLD

group from 3 to 5 weeks.

Several regression equations were calculated with EE as the dependent variable. In the

infants with CLD risk, EE was significantly (r=0.836) related to energy intake, respiratory

rate, heart rate and noradrenaline concentration at all study days. Adrenaline was

significantly related to EE at weeks 2, 3 and 4 (r=0.664). In the infants without CLD,

only the heart rate was significantly related to EE at all study days (r=0.815). EE was

significantly related to heart rate (r=0.835), noradrenaline (r=0.862) and adrenaline

(r=0.656) concentrations at all study days, to respiratory rate at weeks 2 and 3

(r=0.876), and to FiO2 from week 3 to 5 (r=0.704). Table 4 shows the regression

equations calculated for the combined values of CLD and control infants. Multiple

regression analysis showed that heart rate and noradrenaline concentration were significant

independent variables from week 2 to 4, whereas at week 5, respiratory rate (P<0.098)

improved the relationship between EE and noradrenaline (P<0.001, r=0.918). The

addition of heart rate to noradrenaline and respiratory rate increased the correlation

coefficient from 0.918 to 0.977 (P<0.001) at week 5.

4. Discussion

The preterm infants studied in the present investigation developed mild CLD with

marked increase in EE by about 50% from 3 to 5 weeks of age (Table 3). Increased EE

has previously been shown in preterm infants with acute respiratory illness shortly after

birth and in preterm infants with CLD several weeks after birth. In infants with acute

respiratory illness, EE was related to the degree of respiratory impairment [5]. A number

of studies demonstrated increased EE in preterm infants with CLD [5–7,28,29], but

none of the previous studies was performed longitudinally during the development of

CLD. Our study was designed to obtain serial EE values during the development of

CLD, and we could demonstrate that infants with mild CLD had elevated EE compared

with healthy preterm patients from 3 to 5 weeks of age. The CLD of the preterm infants

described in our study may be different from that seen in the years 1985–1992 when


many of the prior studies of EE in CLD patients were conducted. Presently, many

preterm infants develop CLD although they have been mechanically ventilated for very

short periods or not at all, whereas previous CLD was mainly a result of mechanical

ventilation for 7 days or longer. Mild CLD does, therefore, prevail presently in preterm

infants [14].

In the present study, infants with mild CLD showed higher noradrenaline concen-

trations at 3 and 5 weeks and increased adrenaline values during the entire observation

period (Table 3). Our multiple regression analysis demonstrated that noradrenaline

concentration was the most important determinant of EE at weeks 2, 4 and 5 and the

second most important factor at week 3. Catecholamines may be involved in elevation of

EE in several ways. Increased VO2 may result in intervals of inadequate oxygen supply at

the cellular level, thereby stimulating catecholamine release [7]. Stress during periods of

hypoxia [10] and intensive care interventions [30] may stimulate catecholamine release,

thereby contributing to increased VO2 and EE. Moreover, inflammatory processes and

release of cytokines as tumour necrosis factor have been shown to increase catechol-

amines [31].

Multiple regression analysis showed that noradrenaline and heart rate were the most

powerful determinant of EE from week 2 to 4. At 5 weeks, respiratory rate was a more

powerful factor of EE than heart rate. Previous studies suggest that the increase of heart

rate by one beat increases EE by 0.37 kcal/kg/day [32]. From the regression coefficients of

the multiple regression equations in our study, a mean rise in EE by 0.33 kcal/kg/day/heart

beat can be calculated.

The preterm infants with moderate CLD had similar energy intake as the controls

(Table 2). We can calculate from our data that preterm infants with mild CLD showed

a deficit of energy storage of about 30 kcal/kg/day from 3 to 5 weeks of postnatal

age.

We conclude that both EE and plasma catecholamine levels may be markedly increased

in infants with mild CLD. However, at present, it is unclear whether increases in EE and

catecholamines in infants with mild CLD are causally related or merely reflect independ-

ent consequences of the illness. Growth failure can be a significant problem in this patient

population. Interventional studies with the intention to reduce energy expenditure are

needed.

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Energy expenditure and plasma catecholamines in preterm infants with mild chronic lung disease

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