| SMALL
FOR GESTATIONAL AGE |
Small
for gestational age fetuses are defined by the finding that the abdominal
circumference is bolow the 5th centile for gestation. About
80% of such fetuses are constitutionally small, with no increased
perinatal death or morbidity, 15% are growth restricted due to reduced
placental perfusion and "utero‑placental insufficiency",
and 5% are growth restricted due to low growth potential, the result
of genetic disease or enviromental damage. |
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BPD
/ OFD / HC
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TCD
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AC
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FL
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In cases of wrong dates, there may be a suggestive history
(uncertain last menstrual period, irregular cycle, conception within
three months of stopping the contraceptive pill or breast feeding),
all measurements symmetrically small, no obvious anatomical defects,
normal amniotic fluid volume and fetal activity. A repeat ultrasound
examination in two weeks will demonstrate an increase in fetal measurements
and the rate of growth is normal (the lines joining the measurements
are parallel to the appropriate normal mean for gestation).
In normal small fetuses, the mother is usually small (the main
determinant of fetal size is maternal size), and the ultrasound findings
are similar to pregnancies with wrong dates. However, a repeat scan
in two weeks may demonstrate a further deviation from normal in the
various fetal measurements.
In starving small fetuses, the fetal measurements demonstrate
asymmetry (the greatest deficit is observed in the abdominal circumference,
then the femur length and finally the head circumference with the
transverse cerebellar diameter being the least affected), there are
no obvious fetal anatomical defects, the amniotic fluid and fetal
movements are dreduced, the placenta is often thickened with translucent
areas (placental lakes) and there are abnormal Doppler waveforms in
the uterine and / or umbilical arteries.
In abnormal small fetuses there may be anatomical defects suggestive
of chromosomal abnormalities (in triploidy there may be a molar placenta
or in the presence of a normal placenta the fetus demonstrates severe
asymmetrical growth retardation, mild ventriculomegaly, micrognathia,
cardiac abnormalities, myelomeningocoele, syndactyly, or 'hitch-hiker'
toe deformity; trisomy is characterised by strawberry-shaped head,
choroid plexus cysts, absent corpus callosum, enlarged cisterna magna,
facial cleft, micrognathia, nuchal oedema, heart defects, diaphragmatic
hernia, oesophageal atresia, exomphalos, renal defects, myelomeningocoele,
growth retardation and shortening of the limbs, radial aplasia, overlapping
fingers and talipes or rocker bottom feet). The amniotic fluid may
be normal decreased or often increased. In congenital infection growth
retardation may be associated with features of hydrops and brain abnormalities
(ventriculomegaly, microcephaly or cerebral calcifications).
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Doppler
ultrasound provides a non-invasive method for the study of fetal haemodynamics.
Investigation of the uterine and umbilical arteries provide information
on the perfusion of the utero-placental and feto-placental circulations
respectively, while Doppler studies of selected fetal organs are valuable
in detecting the hemodynamic rearrangements that occur in response
to fetal hypoxaemia. In normal pregnancy, impedance to flow in the
uterine artery decreases with gestation and this presumably reflects
the trophoblastic invasion of the spiral arteries and their conversion
into low resistance vessels. Similarly, there is a decrease in impedance
to flow in the umbilical arteries due to progressive maturation of
the placenta and increase in the number of tertiary stem villi. |
In
constitutionally small fetuses Doppler studies of the placental and
fetal circulations are normal. Similarly in growth restricted fetuses
due to genetic disease the results are often normal. In growth restriction
due to placental insufficiency there is increased impedance to flow
in the uterine arteries (with the characteristic waveform of early
diastolic notching) and umbilical arteries (high pulsatility index
and in severe cases absence of reversal of end diastolic frequencies).
These data support the findings from histopathologic studies that
in this condition there is failure of the normal development of maternal
placental arteries into low resistance vessels (and therefore reduced
oxygen and nutrient supply to the intervillous space), and reduction
in the number of placental terminal capillaries and small muscular
arteries in the tertiary stem villi (and therefore impaired maternal-fetal
transfer).
Doppler studies of the fetal circulation demonstrate decrease in impedance
to flow in the middle cerebral arteries and increase in impedance
in the descending thoracic aorta and renal artery. These findings
suggest that in fetal hypoxemia there is an increase in the blood
supply to the brain and reduction in the perfusion of the kidneys,
gastro-intestinal tract and the lower extremities. Although knowledge
of the factors governing circulatory readjustments and their mechanism
of action is incomplete, it appears that partial pressures of oxygen
and carbon dioxide play a role, presumably through their action on
chemoreceptors. In severe fetal hypoxemia there is decompenation in
the cardiovascular system and right heart failure. This is manifested
by the absence or reversal of forward flow during atrial contraction
in the ductus venosus and this is a sign of impendinf fetal death. |
Although
low birtweight is a common feature of many chromosomal abnormalities,
the incidence of chromosomal defects in small for gestational age
neonates is less than 1-2%. However, data derived from postnatal studies
underestimate the association between chromosomal abnormalitites and
growth retardation, since many pregnancies with chromosomally abnormal
fetuses result in intrauterine death. Thus in fetuses presenting with
growth retardation in the second trimester the incidence of chromosomal
abnormalities is 10-20%. The chromosomal abnormalities associated
with severe growth restriction are triploidy, trisomy 18 and deletion
of the short arm of chromosome 4.
The incidence of chromosomal defects is much higher in (a) fetuses
with multiple malformations, than in those with no structural defects,
(b) the group with normal or increased amniotic fluid volume, than
in those with reduced or absent amniotic fluid, and (c) in the group
with normal waveforms from both uterine and umbilical arteries, than
in those with abnormal waveforms from either or both vessels. A substantial
proportion of the chromosomally abnormal fetuses demonstrate the asymmetry
(high head to abdomen circumference ratio), thought to be typical
for uteroplacental insufficiency; indeed the most severe form of asymmetrical
growth retardation is found in fetuses with triploidy.
Growth restriction can also be caused by confined placental mosaicism.
In this condition, which is found in about 1% of pregnancies, the
fetal karyotype is normal but there are two different chromosomal
complements in the placenta (one is usually normal and the other an
autosomal trisomy). Placental mosaicism is also associated with uniparental
disomy (inheritance of two homologous chromosomes from one parent),
which often results in growth restriction. |
Copyright
© 2000 by Pilu, Nicolaides, Ximenes & Jeanty
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