The prevalence of post-term pregnancy (those exceeding 294 days
or 42 weeks of gestation) is about 10% when dating is based on the
first day of the last menstrual period, but this is only about 5%
when dating is by an early ultrasound scan. In about 30% of post-term
pregnancies, the fetuses develop a postmaturity syndrome, characterized
by growth restriction, dehydration, severe desquamation of the epidermis,
bile-stained nails and amnion, advanced hardness of the skull, absence
of the vernix caseosa and lanugo hair.
1: Intrauterine death (black), neonatal death and post-neonatal
death (white) per 1000 ongoing pregnancies at each gestation.
Adapted by permission from Hilder et al. 1
pregnancy is associated with increased risk of both intrauterine
and postnatal death. Hilder et al. examined 171 527 births
in the North East Thames Region in London and reported that the
rate of stillbirth increased six-fold from 0.35 per 1000 ongoing
pregnancies at 37 weeks of gestation to 2.12 per 1000 pregnancies
at 43 weeks (Figure 1). When neonatal and post-neonatal mortality
rates are included, the overall risk of death increased from 0.7
per 1000 ongoing pregnancies at 37 weeks to 5.8 per 1000 pregnancies
at 43 weeks1.
are no morphological features that could indicate an aging process
of the term or post-term placenta, either by light or by electron
microscopy; furthermore, placental DNA increases linearly with gestation
beyond the 40th week of pregnancy2. In contrast, the
amniotic fluid volume decreases from about 37 weeks, and, during
the post-dates period, it is estimated that there is a decrease
in amniotic fluid volume of about 33% per week3,4. This
decrease in amniotic fluid volume, combined with the increased incidence
of meconium staining of the amniotic fluid in post-term pregnancies,
results in an increased risk of meconium aspiration syndrome. The
risk of perinatal death is mainly in the small, postmature, growth-restricted
fetus, and the main aim of antenatal monitoring is to identify the
onset of uteroplacental insufficiency and the development of fetal
Post-term pregnancies are associated with the development of oligohydramnios
and non-reactive fetal heart rate patterns. One possible explanation
for the oligohydramnios is decreased fetal renal perfusion due to
impaired fetal cardiac function.
alternative hypothesis for the reduction in renal perfusion and
urinary output is redistribution in the fetal circulation, as in
intrauterine growth restriction. Supportive evidence for impaired
fetal renal perfusion as a cause of oligohydramnios in post-term
pregnancies was provided by the study of Veille et al. who
examined 50 pregnancies at or after 40 weeks of gestation. In the
17 with oligohydramnios (amniotic fluid index of less than 5 cm)
impedance to flow in the fetal renal artery was significantly higher
than in the 33 pregnancies with normal amniotic fluid5.
Several studies have examined the potential value of Doppler assessment
in the prediction of adverse outcome (usually defined as fetal distress
in labor) in post-term pregnancies and provided conflicting results
(Table 1). All four studies examining uterine arteries reported
no significant changes in pregnancies with adverse outcome. Impedance
to flow in the umbilical arteries of pregnancies with adverse outcomes
was normal in five studies, increased in three studies and decreased
in one study. Impedance in the fetal cerebral circulation was reported
as being decreased in three studies andnormal in two studies.
fetal cardiac function
There is evidence that the oligohydramnios and abnormal fetal heart
rate pattern in post-term fetuses are caused by impaired fetal cardiac
function. Thus, Weiner et al. examined 120 post-term pregnancies
and reported that the pregnancies with oligohydramnios had a significantly
lower peak velocity and velocity–time integral in the fetal aortic
outflow tract and mitral valve. Post-term fetuses with reduced fetal
heart rate variation had a significantly lower peak velocity and
velocity–time integral in the aortic and pulmonic outflow tracts
and mitral valve6. In a further study, Weiner et
al. examined 45 pregnancies at 41–43 weeks of gestation. In
eight fetuses that subsequently developed an abnormal fetal heart
rate pattern in labor, there was a decrease in peak velocity and
velocity–time integral in the fetal aortic and pulmonic outflow
tracts7. It was suggested that, in prolonged pregnancies,
cardiac function deteriorates in fetuses that subsequently develop
an abnormal fetal heart rate pattern. Similarly, Horenstein et
al. examined post-term pregnancies and reported an inverse relationship
between fetal ventricular function and amniotic fluid volume8.
Placental insufficiency and redistribution in the fetal circulation
Battaglia et al. compared 16 pregnancies at 40 weeks with
16 pregnancies at more than 41 weeks. In the post-term pregnancies,the
time-averaged maximum velocity of the fetal descending thoracic
aorta and the ratio of the impedance in the middle cerebral artery
to that in the umbilical artery were decreased9. Furthermore,
post-term pregnancies were associated with an increased incidence
of oligohydramnios, increased plasma viscosity and coagulation parameters
(decreased fibrinogen, antithrombin III and platelet number). It
was concluded that post-term pregnancy may mimic a mild ‘fetal growth
et al. examined 253 post-term pregnancies for the relation
between impedance to flow in the umbilical artery and histological
findings in the placenta10. Disseminated retarded maturation
of the villi was associated with high impedance in the umbilical
artery and, in this group, there was a high rate of Cesarean section
for fetal distress, low birth weight and high neonatal morbidity.
Disseminated retarded maturation of the placenta was found in 66%
of the cases with pathological umbilical artery flow velocity waveforms,
whereas it occurred only in 6% of the cases with normal flow10.
et al. examined 34 pregnancies that delivered after 43 weeks
of gestation and reported that, at this gestation, compared to 40
weeks, the mean flow velocity and volume flow in the fetal aorta
were lower, the flow velocity in the umbilical vein was higher,
impedance to flow in the umbilical artery was lower and impedance
to flow in the uterine artery was not different11. It
was suggested that these findings are compatible with physiological
circulatory alterations enhancing continued fetal growth until the
late post-term period. There were no signs of any general circulatory
deterioration. In a subsequent study, these authors examined 44
pregnancies at 42–43 weeks of gestation. In cases that developed
fetal distress in labor, the umbilical artery pulsatility index
(PI) was significantly decreased and the fetal aortic volume flow
significantly increased; uterine flow was not significantly different.
It was suggested that, in post-term pregnancies, subclinical fetal
hypoxia may trigger vasodilation of placental vessels (with consequent
decrease in umbilical artery PI) and indicates an increase of cardiac
output with consequent increased aortic volume flow12.
Another similarity between the growth-restricted and the post-term
fetus was highlighted by the study of Arduini et al. who
examined the changes in fetal blood flow velocity waveforms during
maternal hyperoxygenation13. They administered 60% humidified
oxygen in 45 post-term pregnancies. During oxygen treatment, nine
fetuses exhibited a temporary 20% increase in the impedance to flow
in the internal carotid artery and, in this group, there was a higher
incidence of emergency Cesarean delivery due to fetal distress and
more neonatal complications than in the other 36 fetuses that did
not respond to maternal hyperoxygenation. It was concluded that
an increase of at least 20% in the PI of the fetal internal carotid
artery during maternal hyperoxygenation may be a useful marker of
adverse outcome in post-term fetuses.
Some studies reported that the pregnancies which subsequently developed
fetal distress in labor were associated with antepartum evidence
of increased impedance in the umbilical artery, decreased impedance
in the fetal middle cerebral artery, and decreased blood flow velocity
in the fetal aorta. Fischer et al. examined 75 pregnancies
at more than 41 weeks of gestation and reported that impedance to
flow in the umbilical artery was significantly higher in those with
subsequent abnormal perinatal outcomes than in those with normal
outcomes14. Similarly, Hitschold et al. examined
130 pregnancies at 40–42 weeks of gestation and reported that, in
the group with increased impedance in the umbilical artery, the
rate of Cesarean section for fetal distress was 53%, compared to
3% in those with normal impedance15. Rightmire and Campbell examined
35 pregnancies at more than 42 weeks of gestation and reported that
impedance to flow in the uterine and umbilical arteries did not
change with gestation, but impedance in the umbilical artery was
higher in fetuses with a worse clinical outcome16. Blood
flow velocity in the fetal descending aorta decreased with gestation
and velocity was lower in fetuses who passed meconium before delivery.
It was suggested that fetal compromise in prolonged pregnancy is
more a fetal–placental problem than a uteroplacental problem16.
Similarly, Anteby et a. examined 78 women at more than 41
weeks of gestation, who had normal non-stress test and amniotic
fluid volume17. Pregnancies that subsequently developed
signs of fetal distress during labor had increased impedance in
the umbilical artery, decreased impedance in the fetal middle cerebral
artery, and decreased time averaged velocity in the fetal aorta.
It was concluded that, in uncomplicated post-term pregnancies, those
with abnormal Doppler results are prone to need intervention following
fetal distress in labor17.
Further evidence for centralization of the fetal circulation was
provided by the study of Devine et al., who examined 49 pregnancies
at more than 41 weeks of gestation and reported that decreased fetal
middle cerebral artery to umbilical artery impedance to flow ratio
is an accurate method of predicting post-date-related adverse outcome
(the occurrence of meconium aspiration syndrome, Cesarean delivery
for fetal distress, or fetal acidosis)18. A middle cerebral
artery to umbilical artery ratio of less than 1.05 predicted an
adverse outcome, with a sensitivity of 80%, specificity of 95% and
positive predictive value of 80%. In contrast, the sensitivities
of oligohydramnios (amniotic fluid index of less than 5 cm), non-reactive
fetal heart rate pattern, and a biophysical profile score equal
to or less than 6, had sensitivities equal to or less than 40%18.
Similarly, Brar et al. examined 45 pregnancies at more than
41 weeks of gestation and reported that the incidence of fetal distress
in labor was higher in patients with antepartum oligohydramnios
(amniotic fluid index less than 5 cm) or non-reactive fetal heart
rate pattern. In this group, compared to those with normal amniotic
fluid and reactive fetal heart rate pattern, there was no significant
difference in impedance to flow in the umbilical and uterine arteries,
but impedance in the fetal internal cerebral artery was significantly
Normal placental and fetal Doppler
Some studies suggested that the pathophysiology of placental insufficiency
in post-term pregnancies differs from that observed in cases of
fetal growth restriction at earlier gestational ages, because, in
post-term pregnancies, both placental and fetal Doppler indices
are normal. Thus, Farmakides et al. examined 149 pregnancies
at more than 41 weeks of gestation and reported that impedance to
flow in the uterine and umbilical arteries was not altered, even
in the presence of other signs suggestive of fetal compromise20.
Similarly, Stokes et al. examined 70 pregnancies at more
than 41 weeks of gestation and reported that impedance to flow in
the umbilical and uteroplacental arteries was not significantly
different in pregnancies associated with fetal compromise and abnormal
neonatal outcome from those with normal outcome21.
et al. examined 153 pregnancies at 41–43 weeks of gestation
and reported that impedance to flow in the umbilical artery, uteroplacental
arteries and fetal middle cerebral artery did not change significantly
within this gestational range22. The majority of Doppler
measurements in pregnancies with subsequent asphyxia or otherwise
complicated fetal outcome were within the 95% prediction interval
for patients with normal fetal outcome. This study also reported
that, in the prediction of asphyxia, the sensitivity for oligohydramnios
and antepartum cardiotocography was less than 20%.
Bar-Hava et al. examined 57 pregnancies at more than 41 weeks
of gestation23. They measured impedance to flow in the
umbilical arteries and the fetal middle cerebral and renal arteries.
In 15 pregnancies, there was oligohydramnios and, although in this
group the mean birth weight was significantly lower than in the
42 pregnancies with normal amniotic fluid, there were no significant
differences between the groups in the Doppler indices. It was concluded
that, in post-term pregnancies, oligohydramnios is not associated
with a major redistribution in the fetal circulation.
Post-term pregnancy is associated with increased risk of both
intrauterine and postnatal death.
In post-term pregnancies, impedance to flow in the uterine arteries
In post-term pregnancies with adverse outcomes, impedance to
flow in the umbilical arteries may be increased or normal.
In post-term pregnancies with adverse outcome, impedance to
flow in the fetal middle cerebral arteries may be decreased.
post-term pregnancies with adverse outcome, blood flow velocity
in the fetal descending aorta may be decreased.
In post-term pregnancies with oligohydramnios, impedance to
flow in the fetal renal arteries may be increased.
In post-term pregnancies with adverse outcome, there is decreased
blood flow velocity in fetal aortic and pulmonic outflow tracts
and across the mitral valve.
Hilder L, Costeloe K, Thilaganathan B. Prolonged pregnancy: evaluating
gestation-specific risks of fetal and infant mortality. Br J Obstet Gynaecol
Fox H. Placental pathology. In Progress in Obstetrics and Gynaecology. Edinburgh: Churchill Livingstone,
Phelan JP, Platt LD, Yeh SY, Broussard P, Paul RH. The role of ultrasound
assessment of amniotic fluid volume in the management of the postdate
pregnancy. Am J Obstet Gynecol 1985;151:304–8
Beischer NA, Brown JB, Townsend L. Studies in prolonged pregnancy.
3. Amniocentesis in prolonged pregnancy. Am J Obstet Gynecol 1969;103:496–503
Veille JC, PenryM, Mueller-Heubach E. Fetal renal pulsed Doppler
waveform in prolonged pregnancies. Am
J Obstet Gynecol 1993;169:882–4
Weiner Z, Farmakides G, Schulman H, Casale A, Itskovitz-Eldor J.
Central and peripheral haemodynamic changes in post-term fetuses:
correlation with oligohydramnios and abnormal fetal heart rate pattern.
Br J Obstet Gynaecol
Weiner Z, Farmakides G, Barnhard Y, Bar-Hava I, Divon MY. Doppler
study of the fetal cardiac function in prolonged pregnancies. Obstet Gynecol 1996;88:200–2
Horenstein J, Brar H, DeVore G. Cardiovascular evaluation of the
post-termfetus. Presented at the 34 Annual Meeting of the Society of Gynaecologic Investigation,
Atlanta, GA, 1987
Battaglia C, Artini PG, Ballestri M, Bonucchi D, Galli PA, Bencini
S, Genazzani AP. Hemodynamic, ematological and hemorrheological
evaluation of post-term pregnancy. Acta Obstet Gynecol Scand 1995;74:336–40
Hitschold T, Weiss E, Berle P, Muntefering H. Histologic placenta
findings in prolonged pregnancy: correlation of placental retarded
maturation, fetal outcome and Doppler sonographic findings in the
umbilical artery. Z Geburtshilfe Perinatol 1989;193:42–6
Olofsson P, Saldeen P, Marsal K. Fetal and uteroplacental circulatory
changes in pregnancies proceeding beyond 43 weeks. Early Hum Dev 1996;46:1–13
Olofsson P, Saldeen P, Marsal K. Association between a low umbilical
artery pulsatility index and fetal distress in labor in very prolonged
pregnancies. Eur J Obstet Gynecol Reprod
Arduini D, Rizzo G, Romanini C, Mancuso S. Doppler assessment of
fetal blood flow velocity waveforms during acute maternal oxygen
administration as predictor of fetal outcome in post-term pregnancy.
Am J Perinatol 1990;7:258–62
Fischer RL, Kuhlman KA, Depp R, Wapner RJ. Doppler evaluation of
umbilical and uterinearcuate arteries in the postdates pregnancy.
Obstet Gynecol 1991;78:363–8
Hitschold T, Weiss E, Berle P. Doppler sonography of the umbilical
artery, mode of delivery and perinatal morbidity in prolonged pregnancy.
Z Geburtshilfe Perinatol 1988;192:197–202
Rightmire DA, Campbell S. Fetal and maternal Doppler blood flow
parameters in postterm pregnancies. Obstet
Anteby EY, Tadmor O, Revel A, Yagel S. Post-term pregnancies with
normal cardiotocographs and amniotic fluid columns: the role of
Doppler evaluation in predicting perinatal outcome. Eur J Obstet Gynecol Reprod Biol 1994;54:93–8
Devine PA, Bracero LA, Lysikiewicz A, Evans R, Womack S, Byrne DW.
Middle cerebral to umbilical artery Doppler ratio in post-date pregnancies.
Obstet Gynecol 1994;84:856–60
Brar HS, Horenstein J, Medearis AL, Platt LD, Phelan JP, Paul RH.
Cerebral, umbilical, and uterine resistance using Doppler velocimetry
in postterm pregnancy. J
Ultrasound Med 1989;8:
Farmakides G, Schulman H, Ducey J, Guzman E, Saladana L, Penny B,
Winter D. Uterine and umbilical artery Doppler velocimetry in postterm
pregnancy. J Reprod Med 1988;33:259–61
Stokes HJ, Roberts RV, Newnham JP. Doppler flow velocity waveform
analysis in postdate pregnancies. Aust N Z J Obstet Gynaecol 1991;31:27–30
Zimmermann P, Alback T, Koskinen J, Vaalamo P, Tuimala R, Ranta
T. Doppler flow velocimetry of the umbilical artery, uteroplacental
arteries and fetal middle cerebral artery in prolonged pregnancy.
Ultrasound Obstet Gynecol 1995;5:189–97
Bar-Hava I, DivonMY, Sardo M, Barnhard Y Is oligohydramnios in posttermpregnancy
associated with redistribution of fetal blood flow? Am J Obstet Gynecol 1995;173:519–22