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.

Figure 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

Post-term 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.

There 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 week^3,4. 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 hypoxia.

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.

The 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.

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 restriction’ ⁹.

Hitschold 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.

Olofsson 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 lower¹⁹.

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.

Zimmermann 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.

1. Hilder L, Costeloe K, Thilaganathan B. Prolonged pregnancy: evaluating gestation-specific risks of fetal and infant mortality. Br J Obstet Gynaecol 1998;105:169–73

2. Fox H. Placental pathology. In Progress in Obstetrics and Gynaecology. Edinburgh: Churchill Livingstone, 1983;3

3. 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

4. Beischer NA, Brown JB, Townsend L. Studies in prolonged pregnancy. 3. Amniocentesis in prolonged pregnancy. Am J Obstet Gynecol 1969;103:496–503

5. Veille JC, PenryM, Mueller-Heubach E. Fetal renal pulsed Doppler waveform in prolonged pregnancies. Am J Obstet Gynecol 1993;169:882–4

6. 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 1996;103:541–6

7. 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

8. 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

9. 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

10. 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

11. Olofsson P, Saldeen P, Marsal K. Fetal and uteroplacental circulatory changes in pregnancies proceeding beyond 43 weeks. Early Hum Dev 1996;46:1–13

12. 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 Biol 1997;73:23–9

13. 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

14. 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

15. 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

16. Rightmire DA, Campbell S. Fetal and maternal Doppler blood flow parameters in postterm pregnancies. Obstet Gynecol 1987;69:891–4

17. 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

18. 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

19. 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: 187–91

20. 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

21. Stokes HJ, Roberts RV, Newnham JP. Doppler flow velocity waveform analysis in postdate pregnancies. Aust N Z J Obstet Gynaecol 1991;31:27–30

22. 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

23. 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