Small babies

Published on 09/03/2015 by admin

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Last modified 09/03/2015

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35

Small babies

Introduction

Babies have a wide range of birth weights. While those born prematurely are more likely to be of low birth weight, the focus of this chapter is on fetuses and neonates who appear to be, or are, small for their gestational age (SGA). These babies may simply be small, in other words they are normal babies who just happen to be at the smaller end of a normal range (constitutionally or genetically small), or are small for a pathological reason. These latter fetuses are referred to as being affected by fetal growth restriction (FGR, previously called intrauterine growth restriction or IUGR).

The key issues are how to screen a low-risk population in order to identify these small fetuses and, once identified, how best to identify those that are risk of developing problems in utero or in labour.

Accuracy of dating

It is not possible to reliably diagnose SGA or FGR without accurate knowledge of gestation. Menstrual dating has significant inherent inaccuracies. The dates may be inaccurately recalled, the cycle may be irregular and bleeding in early pregnancy may be mistaken for menses. Gestation is most accurately determined by an ultrasound scan undertaken before 20 weeks’ gestation, as it is reasonable to assume that all fetuses are of similar size, up until this point. The natural variation in size after this stage makes accurate dating very difficult. The most reliable measurements are based on the crown–rump length between the 8th and 14th weeks, and the head circumference between the 15th and 20th weeks.

The estimated date of delivery is taken as 40 weeks after the date of the start of the last menstrual period (LMP), providing the cycle length is 28 days. A correction may be made for those with regular longer or shorter cycles; for example, if the cycle is 35 days long, then 7 days should be added to the date of the LMP. Abdominal palpation is an inaccurate way of establishing gestational age, as is the date that fetal movements were first noted. The rest of this chapter will assume that gestational age is reliably established.

Small-for-gestational-age (SGA)

Small-for-gestational-age describes the fetus or baby whose birth weight or estimated fetal weight is below a specified centile for its gestation at birth. The chosen centile may be the 10th, 5th or 3rd, depending on different policies, and this choice reflects a trade-off between sensitivity and specificity. If the 10th centile is chosen, it will correctly identify most fetuses liable to be at risk due to their small size but will also include many other fetuses who are not at risk. If the 3rd centile is chosen, then specificity will be good, in other words a greater proportion of identified babies will be at risk, but more ‘at-risk’ fetuses might be missed. The most commonly used threshold is the 10th centile.

Fetal growth restriction (FGR)

The term fetal growth restriction indicates ‘a fetus which fails to reach its genetic growth potential’. FGR presents as a fetus whose growth on serial ultrasound scanning falls below a certain threshold. This threshold is poorly defined and is often implied as the crossing of centiles on a chart of fetal biometry (see later).

Babies with FGR appear thin, as measured by the ponderal index (the ratio of body weight to length) and their skin-fold thickness, a measure of subcutaneous fat, is reduced. There is clearly an overlap in the categorization of small and/or growth-restricted fetuses; a proportion of SGA fetuses will be growth restricted but the majority will be constitutionally small, i.e. genetically determined to be small. Some growth-restricted fetuses will not be SGA, i.e. their growth is failing but they do not have a size below the 10th centile.

Aetiology

Fetal growth is determined by the baby’s intrinsic genetic potential, which is then modified by various fetal, maternal and placental factors (Box 35.1).

Box 35.1

Factors affecting fetal growth

Fetal factors

icon01.gif Genetic – depends on ethnic background and personal characteristics. Maternal genes are more relevant than paternal genes

icon01.gif Chromosomal – decreased growth in association with fetal aneuploidy

icon01.gif Fetal anomaly

Maternal factors

icon01.gif Pre-pregnancy maternal disease, e.g. renal disease, essential hypertension

icon01.gif Drugs/cigarette smoking

icon01.gif Maternal disease in pregnancy, e.g. pre-eclampsia

Placental factors

icon01.gif Adequate/inadequate invasion

icon01.gif Adequate/inadequate vascular function

Fetal factors affecting fetal growth

The genetic make-up of the fetus is the main determinant of its growth and is related to a number of factors, including ethnicity. Asian mothers, for example, have smaller babies than their European counterparts.

This intrinsic genetic drive to grow is more related to the maternal genome than the genome of the father, and involves ‘genomic imprinting’. It is well recognized that while large women often have correspondingly large babies, the correlation between large men and the size of their baby is poor.

Many developmentally abnormal fetuses are small, presumably as a result of a decreased intrinsic drive. This is particularly seen with chromosomal abnormalities, for instance trisomies 18, 13, 21 and triploidy. Small babies are also found in association with structural abnormalities of all the major organ systems as well as with fetal infection. These infections include toxoplasmosis, cytomegalovirus and rubella, but worldwide, the main association is with malaria.

Maternal factors affecting fetal growth

Small variations in diet do not have a measurable effect on fetal growth, but extreme starvation does cause significant growth impairment. This was observed in the Dutch winter famine of 1944 and during the Siege of Leningrad from 1941 to 1944. There is no evidence, however, that food supplementation above a normal diet can improve growth in utero.

Oxygen supply is important. Babies born at high altitude are small, presumably as a result of the decreased oxygen content found in the rarefied atmosphere. This is also true of babies born to mothers with chronic hypoxia secondary to congenital heart disease. The fetus is able to partly compensate through placental hypertrophy, but this compensation is incomplete.

Drugs such as tobacco, heroin, cocaine and alcohol may decrease fetal growth. It has been estimated that smoking, for example, will decrease neonatal weight by an average of approximately 150 g. Maternal chronic disease also has an adverse effect on fetal growth, particularly if there is renal impairment.

Placental factors affecting fetal growth

Adequate placental function depends on adequate trophoblastic invasion. In the first trimester, trophoblast cells invade the maternal spiral arteries in the decidua. In the second trimester, a secondary wave of trophoblast extends this invasion along the spiral arteries and into the myometrium. This results in the conversion of thick-walled muscular vessels with a relatively high vascular resistance to flaccid thin-walled vessels with a low resistance to flow. In certain conditions, such as pre-eclampsia, it would appear that there has been failure of this secondary trophoblastic invasion, the consequences being subsequent placental ischaemia, atheromatous changes and secondary placental insufficiency. Why this failure should occur is unclear, but may be related to the immunological interface between the fetal and maternal cells. In pre-eclampsia, there may be additional impaired placental flow from vasoconstriction. Local placental blood flow is under the control of prostacyclin and thromboxane A2, with thromboxane causing vasoconstriction and prostacyclin vasodilatation. There is a relative deficiency of prostacyclin in pre-eclampsia and an increase in the production of thromboxane A2, the net result being placental vessel vasoconstriction.

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