Body Composition in the Fetus and Newborn: Effects of Intrauterine Growth Aberration

Abstract

The body compositions of infants born large (LGA) or small (SGA) for gestational age are different from those of appropriately grown (AGA) infants. When compared with AGA infants, LGA infants have higher fat and lower total body water contents. SGA infants on the other hand have higher total body water and lower fat contents. During the first week of life, all newborn infants experience a reduction of extracellular body fluid with a maximum of 10% to 15% as reflected in the reduction of body weights. This physiologic transition is accompanied by diuresis. Excessive fluid intakes in very low birth weight infants may result in the lack of this physiologic transition (reflected as lack of postnatal weight loss) and lead to undesirable clinical morbidity such as patent ductus arteriosus or bronchopulmonary dysplasia. Daily monitoring of weight changes assuring appropriate weight loss in the course of fluid and electrolyte management of these high risk infants is essential.

Keywords

body composition, postnatal weight loss, macrosomia, intrauterine growth restriction, small for gestational age

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Body Fluid Compartments
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Body Water in Fetal Growth Aberration
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Transitional Changes of Body Water After Birth
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Clinical Implications of Transitional Body Water Changes in Preterm Very Low Birth Weight Infants

Body Fluid Compartments

Water is the most abundant element of body composition. It is divided into two compartments: intracellular water (ICW) and extracellular water (ECW); the latter is further divided into interstitial fluid and plasma volume ( Fig. 2.1 ). Several methods are available for the measurements of body water in human infants. The general principle has been the use of an indicator that is infused to the subject, allowing for equilibration, and then obtaining a plasma sample to calculate the volume of interest using the principle of dilution with the following formula: V = I ÷ Pl I, in which V is volume of the compartment being measured, I is the amount of indicator infused, and Pl I is plasma concentration of infused indicator. Various indicators measure different body water compartments depending on their location of distribution. Table 2.1 shows the water compartments that can be measured with various indicators used.

Table 2.1

INDICATORS USED FOR BODY WATER IN HUMANS

Body Water Compartment	Indicator
Total body water	Antipyrine stable isotope of water (D ₂O or H ₂¹⁸O)
Extracellular water	Bromide, sucrose, inulin
Plasma volume	Evans blue

The other body composition can be calculated by using the following formula:

Solids = Body weight − Total body water

Intracellular water = Total body water − Extracellular water

Interstitial water = Extracellular water − Plasma volume

In early gestation (24 weeks), the total body water (TBW) is very high (~86% of body weight), and most of it (60%) is in the ECW compartment. With increasing gestational age and growth, the TBW content decreases. The decline is primarily attributable to an increase in solid components of the body composition with growth as evidenced by an increase in the ICW compartment and a decline of the ECW compartment. At term, the TBW is down to 78% of body weight, with 44% being in the ECW compartment, 34% in the ICW compartment, and the rest (22%) being solid body mass. At 1 year of age the TBW is approximately 70% of body weight; most of it is in the ICW (42%), and the rest is in the ECW. Solids account for approximately 30% of body weight. These changes also mean that a preterm infant born at 28 weeks’ gestation will have a high TBW and ECW.

It should be noted that the aforementioned changes in body composition do not distinguish the variation as a result of intrauterine growth aberration and the effects of maternal nutrition and lifestyle. The aberration in intrauterine growth can be in the form of macrosomia (large for gestational age [LGA]) or intrauterine growth restriction (IUGR; also known as small for gestational age [SGA]). Their body fluid characteristics and neonatal adiposity are described later.

Body Water in Fetal Growth Aberration

Large for Gestational Age

This is a heterogeneous group of infants that consists of those with accelerated fetal growth as a result of poorly controlled maternal diabetes mellitus, maternal constitutional obesity without diabetes, and genetic predisposition to enhanced fetal growth.

The data on body water in LGA infants are sparse. The only information published in the literature is that of Clapp and coworkers, who used D ₂O dilution technique to measure TBW and found that in seven infants of diabetic mothers (not all LGA), the value was lower than those of infants with nondiabetic mothers (73% vs. 80% body weight). It should be noted that not all of the infants of diabetic mothers were LGA; they had birth weights ranging from 1430 to 3495 g.

In the absence of good data on directly measured body water content, one may try to make an estimation of this parameter by indirect assessment of the data on body composition in these subjects.

Using dual-energy x-ray absorptiometry (DEXA), Hammami and coworkers measured the body composition of 47 LGA term infants and compared the results with a group of gestational age–matched appropriate-for-gestational-age (AGA) infants. They found that the LGA infants had a higher absolute amount of body fat, lean body mass, and mineral contents. When expressed as a percentage of body weight, the LGA had higher total body fat and mineral contents but less lean body mass. They also found that the increase in total body fat was highest among LGA infants whose mothers had impaired glucose tolerance during pregnancy.

Maternal physical status, lifestyle, and dietary intake may influence the fat contents of the offspring. In a prospective study examining the association between maternal physical measurements and lifestyle, an Irish study involving a large cohort showed that increasing maternal body mass index and waist height ratio were significantly associated with increased neonatal percentage body fat. On the other hand, lifestyle such as smoking during pregnancy is significantly associated with decreased neonatal percentage body fat. These findings are not new, but with a large cohort and rigorous statistical analysis, the data provide important information pointing to the importance of maternal factors affecting neonatal body composition.

Maternal dietary intake during early pregnancy can also affect neonatal body fat composition. Low glycemic index dietary intervention in pregnancy was found to have a beneficial effect on neonatal central adiposity. In addition, central adiposity was positively associated with maternal dietary fat intake and postprandial glucose, highlighting the important role of healthful diet in pregnancy in promoting normal neonatal adiposity.

Intrauterine Growth Restriction or Small for Gestational Age

In contrast to LGA infants, there is abundant information regarding the body water and body composition of infants with IUGR.

As in LGA infants, infants with IUGR comprise a heterogeneous group resulting from maternal factors, placental pathology, or fetal causes. Maternal factors include such conditions as maternal undernutrition; maternal disease (e.g., preeclampsia, toxemia of pregnancy); or maternal exposure to adverse environmental factors such as smoking, alcohol, or substance abuse. Placental pathology includes such conditions as placental vascular disease (e.g., preeclampsia resulting in placental vascular insufficiency and placental anomalies). Fetal causes include genetic abnormalities and fetal infection. The clinical diagnosis of an SGA infant, which is also used in most body composition studies, does not differentiate between the different etiologies for impaired growth and is a categorical rather than a continuous description of growth impairment. All of these limitations complicate the interpretation of body composition measurements.

Body Water and Solids in Intrauterine Growth Restriction or Small for Gestational Age Infants

During normal intrauterine growth, TBW content decreases from 94% of body weight in the first trimester of pregnancy to 78% at term, caused by the accumulation of body solids during growth. In the first two-thirds of gestation, body solids increase because of the accretion of protein and minerals, and there is little fat deposition. We know from postmortem chemical analyses that at 27 weeks’ gestation, 86% of body weight is water, 12% is fat-free dry solids, and only 2% is fat. In vivo measurements in AGA preterm infants with a birth weight less than 1500 g showed a TBW content of 83%, and no fat was detectable by dual photon absorptiometry using ¹⁵³Gd magnetic resonance tomography (MRT) in preterm infants. During the last trimester of gestation, the proportion of body solids increases from 14% to 24% of body weight because of the deposition of body fat, which is 2% of body weight at 27 weeks’ gestation and 10% to 15% of body weight at birth.

Normal intrauterine growth critically depends on the delivery of sufficient nutrients to the fetus via the placenta. When nutrient delivery was reduced by uterine artery ligation during experimental IUGR in rats, TBW was increased, reflecting the reduced deposition of body fat and protein. In human IUGR neonates the TBW content of the body was also increased compared with normal intrauterine growth. In SGA preterm neonates the mean TBW content was 62 mL/kg higher than in AGA preterm neonates, and in SGA term neonates, the mean TBW content was increased by 76 mL/kg or by 102 mL/kg, respectively. No reduction in TBW was found in only one study of a small group of SGA neonates with a wide range of gestational ages ( Table 2.2 ).

Table 2.2

TOTAL BODY WATER AND EXTRACELLULAR VOLUME IN APPROPRIATE FOR GESTATIONAL AGE AND SMALL FOR GESTATIONAL AGE HUMAN NEONATES

Authors (Year)	Subjects	Patients n		TBW (mL/kg)	Significance	Method
Cassady and Milstead (1971)	Term (37–43 weeks)	AGA	12	688 ± 16	P < .001	Indicator dilution (antipyrine)
Cassady and Milstead (1971)	Term (37–43 weeks)	SGA	23	790 ± 13	P < .001	Indicator dilution (antipyrine)
Hartnoll and coworkers (2000)	Preterm (25–30 weeks)	AGA	35	906 (833–954)	P = .019	Indicator dilution (H ₂¹⁸O)
Hartnoll and coworkers (2000)	Preterm (25–30 weeks)	SGA	7	844 (637–958)	P = .019	Indicator dilution (H ₂¹⁸O)
Cheek and coworkers (1984)	Term (≥37 weeks)	AGA	7	749	Not reported	Indicator dilution (D ₂O)
Cheek and coworkers (1984)	Term (≥37 weeks)	SGA	6	825	Not reported	Indicator dilution (D ₂O)
Wagen and coworkers (1986)	GA (34–40 weeks)	AGA	11	780 ± 38	NS	Indicator dilution (D ₂O)
Wagen and coworkers (1986)	GA (34–40 weeks)	SGA	10	776 ± 13	NS	Indicator dilution (D ₂O)
Authors (Year)	Subjects	Patients n		ECV (mL/kg)	Significance	Method
Cassady (1970)	Term (≥37 weeks)	AGA	13	376 ± 20	P = .025	Indicator dilution (bromide)
Cassady (1970)	Term (≥37 weeks)	SGA	20	419 ± 45	P = .025	Indicator dilution (bromide)
Cheek and coworkers (1984)	Term (≥37 weeks)	AGA	7	361 ± 16	Not reported	Indicator dilution (bromide)
Cheek and coworkers (1984)	Term (≥37 weeks)	SGA	6	395 ± 35	Not reported	Indicator dilution (bromide)
Wagen and coworkers (1986)	GA (34–40 weeks)	AGA	11	355 ± 55	NS	Indicator dilution (sucrose)
Wagen and coworkers (1986)	GA (34–40 weeks)	SGA	10	344 ± 35	NS	Indicator dilution (sucrose)