FOR GESTATIONAL AGE
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.
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).
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.
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.
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.
© 2000 by Pilu, Nicolaides, Ximenes & Jeanty