In 2018, the incidence of postterm delivery was estimated to be 0.33% in the United States and as high as 8.1% in Scandinavian countries.^11,12 Many factors may influence the prevalence estimates of term and postterm deliveries. First trimester ultrasound dating may reduce rates of postterm significantly. A meta-analysis demonstrated that early routine ultrasound examination reduced the rate of intervention (ie, induction of labor) for postterm pregnancy in primigravidae by as much as 40%.¹³ Other factors that may influence postterm pregnancy rates in a particular region include the prevalence of primigravid women within the location being assessed, which shifts the curve for gestational age at birth to the right, as first-time mothers are more likely to deliver postterm, and the prevalence of more active management by the location’s health care teams toward induction of labor, which shift the curve for gestational age at birth to the left. It is also important to remember that, when managed conservatively, 40% to 50% of women will deliver within 4 to 5 days of the 42nd week.¹⁴ However, regardless of the variables that may influence rates of postterm pregnancy, accurate pregnancy dating remains a critical factor and perinatal mortality has been noted to increase in pregnancies with unknown dates.¹⁵ It is possible that some of these deaths are due to a failure to diagnose the prolonged pregnancy.

In most postterm gestations, the etiology is unknown, and some cases are misdiagnosed as postterm pregnancies due to poor dating.¹⁶ Although understanding the physiology of parturition may explain the causes of postterm pregnancies, the exact mechanisms of parturition in humans remain unknown, and current knowledge is largely based on studies in animal models, specifically research in pregnant sheep.

In sheep, the release of corticotropin-releasing hormone from the fetal hypothalamus induces secretion of adrenocorticotropic hormone and then cortisol by the adrenal gland in the mother.¹⁷ The rise in maternal cortisol levels causes an increase in prostaglandin and estrogen secretion with a concomitant decrease in progesterone secretion. Together, these are known factors to initiate myometrial contractions.^17,18 Thus, malfunction in the hypothalamic-pituitary-adrenal (HPA) axis results in delay in parturition.

A classical example of HPA dysfunction in pregnancy is X-linked placental sulfatase deficiency (ichthyosis), which is associated with a median pregnancy duration of 1 week longer than normal term.^19,20 The absence of the placental sulfatase enzyme results in low estradiol levels. Ichthyosis may be suspected following a second-trimester screening test for Down syndrome in which low levels of unconjugated serum estradiol are present.²¹ Another example of HPA axis disruption that results in prolonged pregnancy is anencephaly.²²

Prolonged pregnancy is associated with increased maternal anxiety and morbidity. Higher rates of fetal macrosomia and uteroplacental insufficiency may result in greater need for operative vaginal delivery or cesarean delivery in both spontaneous and induced labor.^24,25,26 Other maternal morbidities reported as associated with prolonged pregnancy include endometritis, chorioamnionitis, perineal laceration, and postpartum hemorrhage.²⁷

Multiple studies have demonstrated an increased risk of perinatal mortality after 42 weeks’ gestation.^28,29 Perinatal mortality reaches its nadir at 39 to 40 weeks and then increases as pregnancy exceeds 41 weeks. After 42 weeks, the rate of perinatal mortality is twice the rate at term, increasing to fourfold at 43 weeks and to five- to sevenfold at 44 weeks.^28,29 Deaths associated with postterm pregnancy occur during the antepartum, intrapartum, and neonatal period as the result of events related to uteroplacental insufficiency or to birth trauma caused by the development of fetal macrosomia. During the antepartum period, the fetus may suffer hypoxic ischemic insults resulting in stillbirth or intrauterine growth restriction and the development of the postmature syndrome.

Although stillbirth is discussed in detail in Chapter 4, it warrants mention here in the context of prolonged pregnancy. Traditional reports of stillbirth rates have commonly used the number of deaths per 1000 newborns as the denominator. However, this method of calculation fails to provide a realistic risk assessment, which should more accurately be reported as the number of deaths per continuing pregnancies. Studies have shown that pregnancies that continue beyond 42 weeks have an increased risk of stillbirth,³⁰ but, when the risk of stillbirth is expressed as a function of ongoing pregnancies (stillbirth divided by total births), the mortality rate is even greater. In a large study from the United Kingdom, the rate of stillbirth increased from 0.86 per 1000 live births to 1.08 per 1000 ongoing pregnancies at 40 to 41 weeks; from 1.2 per 1000 live births to 1.272 per 1000 ongoing pregnancies at 41 to 42 weeks; from 1.3 per 1000 live births to 1.9 per 1000 ongoing pregnancies at 42 to 43 weeks; and from 4.58 per 1000 live births to 6.3 per 1000 ongoing pregnancies after 43 weeks.³⁰

Most of the excessive perinatal mortality associated with a prolonged pregnancy occurs in the intrapartum and neonatal periods.³¹ Intrapartum asphyxia and meconium aspiration have been implicated in an estimated 25% of perinatal deaths. In addition, 5.4 per 1000 postterm infants have been reported to exhibit early neonatal seizures compared with 0.9 per 1000 term infants.³¹ Although meconium aspiration can complicate neonate health regardless of gestational age at delivery, in the prolonged pregnancy, meconium-stained
amniotic fluid is more prevalent and results more frequently in meconium aspiration syndrome than in term pregnancy.³²

Oligohydramnios is commonly encountered in prolonged pregnancies. The etiology is uncertain. A possible explanation is fetal hypoxemia, decreased renal perfusion, and diminished urine production.³³ Prolonged pregnancy complicated with oligohydramnios is associated with increased perinatal adverse outcomes, and, thus, induction of labor is favorable in these circumstances.³⁴

The most common complication of prolonged pregnancy is fetal macrosomia, defined as newborn birth weights of 4000 to 4500 g.³⁵ The clinical significance of birth weights between 4000 and 4500 g is unclear, but it has been well established that shoulder dystocia is greatest for infants weighing >4500 g.^36,37

Macrosomia can also result in brachial plexus injuries and fractures.³⁵ In a study by Pollack et al,³⁸ 21% of pregnancies beyond 41 weeks resulted in infants weighing more than 4000 g, and 4% of these fetuses weighed more than 4500 g. Macrosomia suspected according to perinatal ultrasound evaluation of fetal weight is associated with up to 22% cesarean delivery frequency due to arrest of decent.³⁹ Labor induction, cesarean delivery, and shoulder dystocia are also significantly increased in prolonged pregnancy.³⁹

As macrosomia places both mother and fetus at risk, attempts have been made to determine fetal weights in prolonged pregnancies. Chervenak et al³⁹ calculated fetal weights in 317 women followed up conservatively for the management of prolonged pregnancy. In this study, 24% of women had infants born weighing more than 4000 g and, of this group, 22% had cesarean deliveries for protracted disorders versus 10% of the control subjects (P < .01). The sensitivity of ultrasound for predicting birth weight >4000 g was 61% with a specificity of 91%, a positive predictive value of 70%, and a predictive value 87%. However, the diagnosis of fetal macrosomia by ultrasound is not precise, and the ACOG has concluded that ultrasound is better at ruling out macrosomia than ruling it in.³⁵