Post-term Pregnancy

Aaron B. Caughey

Department of Obstetrics and Gynecology, Oregon Health and Science University, Portland, Oregon, USA

Gestational age is an important determinant of perinatal outcomes. Most attention to this issue has been focused on predicting and preventing preterm births, defined as delivery prior to 37 weeks of gestation. This seems entirely appropriate as preterm birth is the greatest cause of perinatal morbidity, mortality and costs [1,2]. However, post‐term births are also associated with increased perinatal morbidity and mortality [3]. Furthermore, post‐term pregnancy is easily preventable by delivery of the neonate by induction of labour. Thus this potentially problematic condition of pregnancy deserves further attention, research and careful consideration. This chapter discusses what is known about the existing epidemiology of post‐term birth and associated outcomes, the methodological issues related to studying post‐term pregnancy, that complications associated with post‐term pregnancy rise in a continuous manner as opposed to suddenly at any specific threshold, and the management and prevention of post‐term births and future directions for research and clinical care.

Definitions

Post‐term pregnancy is currently defined as a pregnancy progressing to 42 weeks (294 days) of gestation or beyond [4]. Other terms such as ‘prolonged’ or ‘post‐dates’ have also been used but for the sake of nomenclature ‘post‐term’ should be used [5]. Further, although 42 weeks is the current threshold designation for post‐term pregnancy, up until the 1980s 43 weeks was the threshold while many clinicians currently use the term to describe pregnancies of 41 weeks’ gestation and beyond.

It is sensible that there should be a term to describe the range of 41 to 41⁺⁶ weeks of gestation, and recently the designation ‘late term’ was agreed upon and endorsed by the American College of Obstetricians and Gynecologists (ACOG) and the Society for Maternal–Fetal Medicine (SMFM) in the USA. This term is in contrast to ‘full term’, describing pregnancies from 39⁺⁰ to 40⁺⁶ weeks of gestation, and ‘early term’, describing pregnancies from 37⁺⁰ to 38⁺⁶ weeks of gestation [6].

Given the wide range of terminology, it is best to always include the gestational age along with the descriptor for clarity, for example ‘post‐term pregnancy at 42⁺¹ weeks gestation’ or ‘late term pregnancy at 41⁺² weeks gestation’.

Incidence

In order to accurately determine the ‘natural’ incidence of post‐term pregnancy, there must be meticulous early pregnancy dating, universal follow‐up of all pregnancies, and absence of obstetric intervention.

The 14% post‐term pregnancy rate quoted for the Hawaiian island Kauai [7] may be regarded as informative because of low rates of obstetric intervention and full follow‐up, but lacks correction for potential gestational age dating error. In the UK, the fall in incidence of post‐term pregnancy from 11.5% in 1958 [8] to 4.4% in 1970 [9] illustrates the effect of the rise in rates of induction of labour from 13 to 26% over the same period. More recently, in the USA in 2005, 14% of all pregnancies progressed beyond 41 weeks of gestation and just under 6% progressed beyond 42 weeks of gestation [10]. This is lower than the approximately 18% of pregnancies beyond 41 weeks and 10% beyond 42 weeks in 1998, with these changes attributed to increases in the use of induction of labour, but are also partly due to improved early gestational age dating [11,12]. An analysis of 171 527 births in residents of the North‐east Thames region in 1989–1991 gave an incidence of 6.2% for post‐term pregnancy [13]. In a study of 1514 healthy pregnant women in whom the discrepancy between date of last menstrual period (LMP) and dating based on first‐trimester crown–rump length (CRL) was less than −1 to +1 days, the duration of pregnancy was estimated using time‐to‐event analysis: non‐elective delivery was taken to be the event while elective delivery was taken to be censoring [14]. The median time to non‐elective delivery was 283 days from LMP. The life‐table graph published in this study gives an incidence of post‐term pregnancy of about 6%. This study likely underscores the importance of accurate dating in the actual incidence of post‐term pregnancy.

As noted earlier, accuracy of gestational age is an important component of determining whether a pregnancy is post‐term. This has been demonstrated in several studies of pregnancy dating. For example, one study found that reliance on menstrual dates gave an incidence of post‐term pregnancy of 10.7%, whereas the use of basal body temperature (BBT) charts gave a much lower rate of 4.7% [15]. In another study, the routine use of ultrasound to confirm pregnancy dating decreased the overall incidence of post‐term pregnancy from 12 to 3% [16]. The impact of BBT or ultrasound dating is likely because women are far more likely to be oligo‐ovulatory and have delayed ovulation than polyovulatory with earlier ovulation. Delayed ovulation in any given menstrual cycle would place a pregnancy at an earlier gestational age than that predicted by the first day of the LMP.

Other studies have demonstrated that the use of ultrasound to establish gestational age lowers the incidence of post‐term pregnancy. Eik‐Nes et al. [17] showed that adjustment of dates following measurement of the biparietal diameter at 17 weeks’ gestation led to an incidence of post‐term pregnancy of 3.9%. Three other studies of routine ultrasound examination for dating have demonstrated a reduction in the rate of false‐positive diagnoses of post‐term pregnancy, and thereby the overall rate of post‐term pregnancy, from 10–15% to approximately 2–5% [18–20]. In a Cochrane review of randomized trials of routine versus selective second‐trimester ultrasound, routine second‐trimester biometry was found to reduce the number of pregnancies classified as post‐term [21].

Moreover, early ultrasound for pregnancy dating may be superior to mid‐trimester ultrasound in this regard. In a small prospective randomized trial, Bennett et al. [22] demonstrated that routine first‐trimester ultrasound for pregnancy dating reduced the incidence of post‐term pregnancy from 13% to 5% compared with second‐trimester ultrasound dating. In another study, it was demonstrated that not only did first‐trimester ultrasound dating lead to lower rates of post‐term pregnancy beyond 42 weeks’ gestation, but the same was true for diagnosis of pregnancy beyond 41 weeks’ gestation [23]. Improved dating also reveals a greater difference in the rate of perinatal complications between term and post‐term pregnancies. This is due to the misclassification bias that usually occurs with misdating. Such misclassification of women who are term as post‐term and women who are post‐term as term both lead to a smaller difference in the rate of complications between term and post‐term pregnancies. Thus, older studies of women whose pregnancies did not have dating confirmation by ultrasound underestimate the rates of complications seen in post‐term pregnancies. The multicentre First and Second Trimester Evaluation for Aneuploidy Trial (FASTER) studied 3588 women undergoing first‐trimester ultrasound [24]. Gestational age determination using CRL as opposed to LMP reduced the apparent incidence of pregnancies greater than 41 weeks’ gestation from 22.1 to 8.2% (P <0.001). Of note, ultrasound at 12–14 weeks’ gestation, while considered early, can often lead to worse estimates of gestational age than ultrasound at 18–22 weeks. Thus, reliance on standard nuchal translucency ultrasound over an earlier first‐trimester ultrasound may be problematic and requires further research.

Aetiology

It is likely that the majority of post‐term pregnancies represent the upper range of a normal distribution. Further, as noted above, the most common ‘cause’ of post‐term pregnancy is inaccurate pregnancy dating. However, it does appear that there are specific associations with a range of predictors that may help point to potential aetiologies of post‐term pregnancy.

Rare but classically described causes of post‐term pregnancy include placental sulfatase deficiency (an X‐linked recessive disorder characterized by low circulating estriol levels), fetal adrenal insufficiency or hypoplasia, and fetal anencephaly (in the absence of polyhydramnios) [25,26].

Genetic factors may also play a role in prolonging pregnancy. In one study, women who were the product of a pregnancy beyond 41 weeks’ gestation were more likely themselves to have a pregnancy progress beyond 41 weeks’ gestation (relative risk, RR 1.3) [27]. Similarly, women who have had a prior post‐term pregnancy are more likely to have another such pregnancy [27,28]. For example, after one pregnancy beyond 41⁺⁰ weeks of gestation, the risk of a second such pregnancy in the subsequent birth is increased 2.7‐fold (from 10 to 27%). If there have been two successive prolonged pregnancies, the incidence rises to 39% [29]. Paternal genes expressed in the fetoplacental unit also appear to influence length of gestation. In a recent Danish case–control study [30] of women with two consecutive births, the risk of a second post‐term pregnancy among 21 746 women whose first delivery was post‐term was 20% as compared with 7.7% among 7009 women whose first delivery was at term. However, the risk of recurrent post‐term delivery was reduced to 15% when the first and second child had different fathers (odds ratio, OR 0.73, 95% CI 0.63–0.84).

Low vaginal levels of fetal fibronectin at 39 weeks are predictive of an increased likelihood of post‐term pregnancy [31]. Ramanathan et al. [32] showed how transvaginal measurement of cervical length at 37 weeks predicts both post‐term pregnancy and failed induction. These observations suggest that a defect or delay in the remodelling of the cervix that takes place prior to successful initiation of labour may cause post‐term pregnancy and may also be associated with some of the apparent increase in dystocia associated with post‐term pregnancy.

Post‐term pregnancy could result from variations in the corticotrophin‐releasing hormone (CRH) system during pregnancy, such as alteration in the number or expression of myometrial receptor subtypes, altered signal transduction mechanisms or increase in the capacity of CRH‐binding protein to bind and inactivate CRH. Prospective longitudinal studies have shown that women destined to deliver before term tend to have a more rapid exponential rise in CRH in mid‐pregnancy while women who go on to deliver post‐term babies have a slower rate of rise [33]. Efforts currently directed towards researching the initiation of labour before term may lead to greater understanding of the aetiology of post‐term pregnancy.

Epidemiology

There are a number of risk factors associated with post‐term pregnancy which may have biological causal association. First among these is nulliparity, with a greater proportion of nulliparas reaching 40, 41 or 42 weeks’ gestation and the median duration of pregnancy being 2 days longer in nulliparas compared with multiparas. Recent data have also shown an association with male fetuses [34]. Additionally, it has been described that African‐American women have higher rates of preterm delivery [35], raising the possibility that race/ethnicity may be associated with overall gestational age and prolonged pregnancy in particular. One recent study found a decreased risk of post‐term pregnancy among African Americans, Asians and Latinas compared with white women [36]. Further, some effects of race/ethnicity have been described to vary between obese and non‐obese patients [37]. Obesity has been found to be associated with post‐term pregnancy in several studies [38,39]. The association may have actual causality: studies have demonstrated this finding consistently and have shown a dose–response effect, with greater response among women who are obese than those who are overweight.

The theoretical mechanisms for the association between obesity and post‐term pregnancy remain unclear. Since adipose tissue is hormonally active [40] and since obese women may have an altered metabolic status, it is possible that endocrine factors involved in the initiation of labour are altered in obese women. The long‐noted associations between lower pre‐pregnancy body mass index (BMI) and increased spontaneous preterm birth [41,42] are consistent with our findings and may be explained by a common, as yet unknown, mechanism regarding parturition, potentially related to circulating levels of oestrogen or progesterone. Since, evolutionarily, as a species we have evolved to face the environmental pressures of food scarcity, it is likely that the outcomes of a post‐term pregnancy rarely served as an evolutionary pressure related to obesity 10 000 years ago when we existed primarily as nomadic tribes with a lower median BMI than today. Thus there is likely little benefit to the fetus for the pregnancy to proceed beyond 42 weeks’ gestation, and such post‐term pregnancies may be a product of current intrinsic and environmental factors.

Risks associated with post‐term pregnancy

Perinatal mortality

Post‐term pregnancy is associated with an increased risk of perinatal mortality, both antepartum stillbirth as well as infant death. There is an important methodological distinction to make when measuring complications by gestational age. Some complications can only happen to women and infants who are delivered at that week of gestation. Other complications can occur to all women who are pregnant at that week of gestation, both those delivering as well as those who remain pregnant. For example, an antepartum stillbirth can occur in anyone who is pregnant at a given gestational age, i.e. in ongoing pregnancies. Alternatively, a neonatal death can only occur to the group that actually delivers at that week of gestation [43]. When considering the outcomes related to post‐term pregnancy, we see the association with antepartum stillbirth regardless of how the effect is measured, but when the appropriate denominator of ongoing pregnancies is used, we see the risk of antepartum stillbirth begin to increase earlier at 39 and 40 weeks’ gestation. Yudkin et al. [44] questioned the validity of using perinatal mortality rates as a means of relating outcome to gestational age, arguing that the population at risk of intrauterine fetal death at a given gestational age is the population of fetuses in utero at that gestational week and not those delivered at that week. However, the population at risk of intrapartum and neonatal complications such as cord prolapse or meconium aspiration syndrome is clearly the population of babies delivered at that week of pregnancy [45]. These issues are clearly explained by Smith [45], who related the perinatal risks at each gestational week to the appropriate denominators. Antepartum deaths were related to the number of ongoing pregnancies, intrapartum deaths to all births at that gestational age, excluding antepartum stillbirths, and neonatal deaths were related to the number of live births. Yudkin et al. [44] expressed the prospective risk of stillbirth for the next 2 weeks of the pregnancy; Hilder et al. [13] expressed the risk as a rate over the next week; Cotzias et al. [3] generated considerable controversy [46,47] by expressing the risk of prospective stillbirth for the remainder of the pregnancy. This is a counter‐intuitive concept for most obstetricians, whereas many find the concept of the prospective risk of stillbirth over the coming week an accessible concept, particularly in pregnancies of 40–42 weeks’ gestation (‘If this woman remains undelivered in the next 7 days, what is the chance of a fetal death occurring in utero?’).

In the broad range of literature, studies which dichotomize gestational age at 42 weeks demonstrate increased perinatal mortality (Table 23.1). The outcomes presented in this table compare pregnancies fulfilling the epidemiological definition of post‐term pregnancy with those delivered at ‘term’. In modern obstetric practice, women with epidemiological and obstetric risk factors are more likely to be delivered before 42 weeks. Thus women with twin pregnancies, pre‐eclampsia, diagnosed intrauterine growth restriction, antepartum haemorrhage or previous perinatal death are likely to be over‐represented in the 37–41 week population and under‐represented among those delivered at 42 weeks and later, potentially underestimating the increased risks from progressing to the post‐term period.

Table 23.1 Perinatal mortality rates in term versus post‐term pregnancies.

Reference	Source	Outcome	37–41 weeks	42 weeks and over
Campbell et al. [58]	444 241 births Norway 1978–1987	Relative risk of perinatal death	1	1.30 (1.13–1.50)
Fabre et al. [133]	547 923 births Spain 1980–1992	Stillbirth rate	3.3	3.6
		Early neonatal mortality rate	1.7	2.8
		Perinatal mortality rate	4.9	6.4
Olesen et al. [28]	78 033 post‐term pregnancies, Danish birth register 1978–1993, 5% sample of deliveries at term	Adjusted odds ratio: stillbirth	1	1.24 (0.93–1.66)
		Adjusted odds ratio: neonatal death	1	1.60 (1.07–2.37)
		Adjusted odds ratio: perinatal death	1	1.36 (1.08–1.72)

Studies have also examined these outcomes by week of gestation across all term pregnancies by week and demonstrate similar findings (Table 23.2). Specifically, this table addresses the argument that the duration of pregnancy is a continuum and that perinatal risks are unlikely to alter abruptly on day 294 of a pregnancy. Outcomes are presented by week of gestational age from 37 weeks up to and including 43 weeks’ gestation. Outcome statistics are presented in a variety of forms as discussed above.

Table 23.2 Perinatal outcomes by week of gestation, 37–43 weeks.

Reference	Source	Outcome	38–39	39–40	40–41	41–42	42–43	≥43
Bakketeig & Bergsjo	157 577 births, Sweden 1977–1978	Perinatal mortality rate	7.2	3.1	2.3	2.4	3	4
Ingemarsson & Kallen [51]	914 702 births, Sweden 1982–1991	Stillbirth rate in nulliparas	2.72	1.53	1.23	1.86	2.26
		Neonatal mortality rate nulliparas	0.62	0.54	0.54	0.9	1.03
		Stillbirth rate in multiparas	2.1	1.42	1.35	1.4	1.51
		Neonatal mortality rate multiparas	0.55	0.45	0.53	0.5	0.86
Divon et al. [134]	181 524 singleton pregnancies, reliable dates, ≥40 weeks, Sweden 1987–1992	Odds ratio for fetal death			1	1.5	1.8	2.9
Hilder et al. [13]	171 527 births, London 1989–1991	Stillbirth rate	3.8	2.2	1.5	1.7	1.9	2.1
		Infant mortality rate	4.7	3.2	2.7	2	4.1	3.7
		Stillbirth rate per 1000 OP*	0.56	0.57	0.86	1.27	1.55	2.12
		Infant mortality rate per 1000 OP	0.7	0.83	1.57	1.48	3.29	3.71
Caughey & Musci [54]	Hospital based, California 1992–2002, 45 673 births after 37 weeks	Fetal death rate per 1000 OP	0.36	0.4	0.26	0.92	3.47
Smith [45]	700 878 births in Scotland 1985–1996, multiple births and congenital anomalies excluded	Cumulative probability of antepartum stillbirth	0.0008	0.0013	0.0022	0.0034	0.0053	0.0115
Smith [45]		Estimated probability of intrapartum and neonatal death	0.0006	0.0005	0.0006	0.0006	0.0006	0.0008

OP, ongoing pregnancies.

At first sight, it might seem that whether studies have used thresholds like 42 and 43 weeks of gestation or examined complications by week was only a matter of whether the strata required increased subgroup sample size due to needs for increased statistical power. However, examining these outcomes by threshold or in a continuous fashion is an important methodological issue. If complication rates increase as gestational age increases, then one would see an increase regardless of what threshold was chosen. And it is true, if one examines stillbirth rates before and after 39, 40, 41, 42 or 43 weeks, there is always a higher rate beyond the threshold. More importantly is how such information can be utilized to inform clinical management. Thus, a comparison of one week to the next is truly what needs to be examined. Are the risks higher of delivering at a given gestational age or of waiting an additional week of gestation? For such comparisons, examining complications week by week is of more use than simply comparing before and after a given threshold.

There are other methodological problems with this literature. Of course, there may be errors or biases in recording of information relating to gestational age. Women with uncertain dates have been repeatedly shown to be at increased risk of perinatal mortality [48,49]. Their inclusion may inflate the apparent perinatal risks of post‐term pregnancy. Older studies of perinatal outcome in post‐term pregnancy showed that about 25% of the excess mortality risk in post‐term pregnancy relates to congenital malformations [25]. Of the studies quoted in Tables 23.1 and 23.2, only that by Smith [45] specifies that cases of lethal congenital malformation have been excluded from the analysis. Hilder et al. [46] reanalysed the data presented in their 1998 study [13] after correcting for congenital malformation, showing that the outcomes presented were not biased by fetuses with congenital malformation being preferentially represented among post‐term pregnancies. Another potential bias is the interval between intrauterine death and delivery. A fetus that dies in utero at 41 weeks and is delivered at 42 weeks will be counted as a perinatal death at 42 weeks’ gestation. If this happened regularly, this would suggest that perinatal mortality risks actually increase half a week to a week earlier.

Both tables show that post‐term pregnancy is associated with an increased risk of perinatal death. However, there is no consistency between studies as to the timing of that increased risk from fetal death before labour, to antepartum death to early neonatal death or even infant mortality. The studies summarized in Table 23.1 suggest that an increased risk of neonatal death is the main source of the increased perinatal risk. This has been further substantiated by a recent study from California which finds higher rates of infant death in births at 41 weeks and beyond even in a low‐risk population [50]. However, Table 23.2 shows that when pregnancies ending at 42 weeks are compared with those delivered at 41 weeks, every adverse outcome is increased with the exception of the ‘estimated probability of intrapartum and neonatal death’ from the Smith study [45]. When pregnancies ending at 41 weeks are compared with those ending at 40 weeks, this outcome is again unchanged, as is the neonatal mortality rate in multiparas in the Ingemarsson and Kallen series [51] and the infant mortality rate in the Hilder series [13]. All other outcomes deteriorate from 40 weeks to 41 weeks and again from 41 weeks to 42 weeks.

Perinatal morbidity

Epidemiological studies identify birth after 41 weeks or after 42 weeks as a risk factor for a variety of adverse neonatal outcomes. One retrospective cohort study of all low‐risk, term, cephalic and singleton births delivered at the University of California, San Francisco, between 1976 and 2001 examined the incidence of adverse neonatal morbidity outcomes at 40, 41 and 42 weeks’ gestation and compared these with the rates in pregnancies delivered at 39 weeks’ gestation, after controlling for maternal demographics, length of labour, induction, mode of delivery and birthweight (except macrosomia) [52]. Compared with the outcome at 39 weeks’ gestation, the relative risk of meconium aspiration increased significantly from 2.18 at 40 weeks to 3.35 at 41 weeks and 4.09 (95% CI 2.07–8.08) at 42 weeks. A composite outcome of ‘severe neonatal complications’, including skull fracture and brachial plexus injuries, neonatal seizures, intracranial haemorrhage, neonatal sepsis, meconium aspiration syndrome and respiratory distress syndrome, increased from a relative risk of 1.47 at 40 weeks to 2.04 at 41 weeks to 2.37 (95% CI 1.63–3.49) at 42 weeks. Similar findings have been demonstrated in multiple other studies that examined perinatal morbidity including pre‐eclampsia, meconium, meconium aspiration syndrome, macrosomia, neonatal acidaemia, need for neonatal mechanical ventilation, caesarean delivery and perinatal infectious morbidity [53–57].

For example, dystocia, shoulder dystocia and obstetric trauma are all increased in post‐term pregnancy [58]. Here, the risks increase with increasing fetal weight, but gestational age remains a risk factor independent of birthweight. In a case‐matched study of 285 women with uncomplicated singleton post‐term pregnancy and spontaneous onset of labour and 855 women with uncomplicated singleton term pregnancy, Luckas et al. [59] showed that caesarean delivery was significantly more common in women with post‐term pregnancy (RR 1.90, 95% CI 1.29–2.85). The increase was equally distributed between caesarean deliveries performed for failure to progress in labour (RR 0.74, 95% CI 1.02–3.04) and fetal distress (RR 2.00, 95% CI 1.14–3.61). This finding is consistent with the hypothesis that some cases of post‐term pregnancy are associated with a defect in the physiology of labour, in addition to any increase in risk of fetal hypoxia. However, the possibility of bias in management arising out of the knowledge that a pregnancy is post‐term cannot be excluded as a factor in the increase in caesarean delivery rates.

A strong association between neonatal seizures and delivery at 41 weeks’ gestation or more has also been identified in previous case–control studies. Minchom et al. [60] found that delivery after 41 weeks’ gestation was associated with an odds ratio of 2.7 (95% CI 1.6–4.8). Curtis et al. [61] studied 89 babies with early neonatal seizures delivered after 42 weeks’ gestation in Dublin; 27 were delivered after 42 weeks’ gestation compared with 6 of 89 controls (OR 4.73, 95% CI 2.22–10.05).

Cerebral palsy

Neonatal encephalopathy may be followed by the development of cerebral palsy, while other cases of cerebral palsy may occur following a clinically normal neonatal period. It is accepted that the presence of neonatal encephalopathy indicates that a neurological insult has taken place during labour or the early neonatal period, while its absence is thought to indicate an insult at some earlier time in pregnancy [62]. Gaffney et al. [63] examined the obstetric background of 141 children from the Oxford Cerebral Palsy Register; 41 children whose cerebral palsy was preceded by neonatal encephalopathy were compared with 100 who had not suffered from neonatal encephalopathy. The babies with neonatal encephalopathy were more likely to have been delivered at 42 weeks’ gestation or more (OR 3.5, 95% CI 1–12.1). Babies born at 42 weeks or more to nulliparous women were at particular risk of this sequence of events (OR 11.0, 95% CI 1.2–102.5).

Effect of parity and birthweight

Whether these outcomes, their rates, peaks and nadirs are affected by other demographics such as maternal age, race/ethnicity, socioeconomic status and medical complications of pregnancy has been minimally studied. However, it has been examined by parity. One series [51] shows that the increasing risks of adverse outcome associated with advancing age of gestation are more marked in nulliparas than in multiparas (Table 23.2). The aetiology for the modification of these outcomes by parity is unclear and could be due to true biological differences or perhaps differences in dating accuracy between the two groups. Birthweight has also been examined as a modifier of outcomes by gestational age. In an analysis of 181 524 singleton pregnancies with reliable dates delivered at 40 weeks or later in Sweden between 1987 and1992, birthweight of two standard deviations or more below the mean for gestational age was associated with a significantly increased odds ratios for both fetal death (OR 7.1–10.0) and neonatal death (OR 3.4–9.4) [51]. A Norwegian cohort [58] also showed that small‐for‐gestational age babies were more vulnerable to the risks of post‐term pregnancy. In this study, babies weighing less than the 10th centile had a relative risk of 5.68 (95% CI 4.37–7.38) of perinatal death at 42 weeks’ gestation or later compared with babies between the 10th and 90th centile at the same gestational age. In this series, birthweight above the 90th centile was associated with the lowest relative risk of perinatal death (RR 0.51, 95% CI 0.26–1.0). These findings make biological sense in that one might suspect that there would be a subgroup of fetuses whose growth is affected due to intrauterine factors that increase the risk for fetal or neonatal demise. The practice pattern of delivering such fetuses at an earlier gestational age is thus supported by such findings.

Management

Management of post‐term pregnancies actually starts before a pregnancy becomes post‐term. The goals of managing such otherwise low‐risk pregnancies is to prevent the complications of post‐term pregnancy and to prevent post‐term pregnancy itself. Thus, the mainstay of management involves the use of antepartum testing to reduce risks of complications from expectantly managing these pregnancies. It also includes reducing the risk of post‐term pregnancy through good pregnancy dating, outpatient cervical ripening and induction of labour, all before a pregnancy becomes post‐term. These broad topics are discussed next.

Antenatal testing

The evidence of increased perinatal mortality and morbidity in late term and post‐term pregnancy compared with delivery at 39 or 40 weeks’ gestation inevitably leads to the conclusion that some cases of post‐term pregnancy could be prevented by earlier delivery. It would seem logical to use screening tests to identify pregnancies destined to have an adverse outcome and to intervene selectively in these cases.

The ideal test of fetal well‐being in post‐term pregnancy would allow identification of all fetuses at risk of adverse outcome, at a stage where delivery would result in a universally good outcome. Thus a ‘negative’ test would indicate that the fetus is safe in utero for an interval of a few days until either delivery or a repeat test is performed and that the woman would eventually deliver with a good outcome. At present, no method of monitoring post‐term pregnancy is backed up by strong evidence of effectiveness. There is some observational evidence that some pregnancies at risk of adverse outcome can be identified, but less evidence that prediction of the adverse outcome confers prevention.

Fetal movement counting

The least invasive monitoring is maternal assessment of fetal movements, also known as fetal kick counts. This test is used commonly in the supervision of term and post‐term pregnancies (Table 23.3) but is not supported by firm evidence of efficacy. Generally, women are asked to count fetal movements once or twice per day and are expected to experience four to six such movements in 20–30 min. Two randomized trials have addressed the question of whether clinical actions taken on the basis of fetal movement improve fetal outcome [64,65]. The larger of these trials involved over 68 000 women [65]. These trials collectively provide evidence that routine formal fetal movement counting does not reduce the incidence of intrauterine fetal death in late pregnancy. Routine counting results in more frequent reports of diminished fetal activity, with a greater use of other techniques of fetal assessment, more frequent admission to hospital and an increased rate of elective delivery. It may be that fetal movement counting in post‐term pregnancy will perform more effectively than it does in low‐risk pregnancies. However, in the end, if this test did demonstrate reduction in perinatal morbidity or mortality, it is likely that such a protocol also leads to maternal anxiety and high rates of false positives.

Table 23.3 Randomized trials of routine versus selective induction at 41–42 weeks’ gestation.

Reference	No.	Gestation at trial entry (days)	Method of induction	Method of fetal surveillance	Perinatal deaths
Augensen et al. [135]	409	290	Oxytocin and amniotomy	CTG	0
Bergsjo et al. [123]	188	284	Membrane sweep, oxytocin, amniotomy	Fetal movement, ultrasound, urinary estriol	1 in induction arm 2 in selective arm
Cardozo et al. [124]	363	290	PGE₂, oxytocin, amniotomy	Fetal movement, CTG	1 in selective arm 1 in induction arm
Chanrachakul & Herabutya [136]	249	290	Amniotomy and oxytocin	CTG, AFI	0
Dyson et al. [121]	302	287	PGE₂, oxytocin, amniotomy	CTG, AFI	1 in selective arm
Hannah et al. [111]	3407	287	PGE₂, oxytocin, amniotomy	Fetal movement, CTG, AFI	2 in selective arm
Heden et al. [137]	238	295	Amniotomy, oxytocin	CTG, AFI	0
Henry [122]	112	290	Amniotomy and oxytocin	Amnioscopy	2 in selective arm
Herabutya et al. [138]	108	294	PGE₂, oxytocin	CTG	1 in selective arm
James et al. [139]	74	287	Extra‐amniotic saline if Bishop score <5; membrane sweep, amniotomy and oxytocin	Fetal movement, BPS	0
Katz et al. [120]	156	294	Amniotomy, oxytocin	Fetal movement, amnioscopy, oxytocin challenge	1 in each arm
Martin et al. [140]	22	287	Laminaria, oxytocin	CTG, AFI	0
NICHD [141]	440	287	CTG, oxytocin, amniotomy	CTG, AFI	0
Roach & Rogers [142]	201	294	PGE₂	CTG, AFI	0
Suikkari et al. [143]	119	290	Amniotomy, oxytocin	CTG, human placental lactogen, estriol, AFI	0
Witter & Weitz [144]	200	287	Oxytocin, amniotomy	Estriol, oxytocin challenge	0

AFI, amniotic fluid index; BPS, biophysical profile scoring; CTG, cardiotocography.

Cardiotocography

Antenatal cardiotocography (CTG), also known as a non‐stress test, has been widely used for more than 20 years to monitor moderate‐ to high‐risk pregnancies. Observational studies have reported very low rates of perinatal loss in high‐risk pregnancies monitored in this way [66,67]. Six randomized controlled trials comparing CTG with other methods of antepartum fetal monitoring have been the subject of a Cochrane review [68]. Women with post‐term pregnancies were included in these trials. On the basis of the information presented in this review, the antenatal CTG has no significant effect on perinatal outcome or on interventions such as elective delivery. Miyazaki and Miyazaki [69] reported a series of 125 women with post‐term pregnancies where a reactive CTG was recorded within 1 week of delivery. Ten adverse outcomes were reported from this group: four antepartum deaths, one neonatal death, one case of neonatal encephalopathy and four cases of fetal distress on admission in early labour. The poor performance of antenatal CTG in this series and in the randomized trials may relate to errors in interpretation or excessive intervals between tests. Numerical analysis using computerized calculations of the baseline rate and variability may reduce the potential for human error [70]. Weiner et al. [71] compared the value of antenatal testing with computerized CTG, conventional CTG, biophysical profile scores and umbilical artery Doppler; 337 pregnant women who were delivered after 41 weeks’ gestation and who had 610 antenatal tests were included in this study. Of 12 fetuses with reduced fetal heart rate variation on computerized CTG, 10 had a trial of labour. Of these 10 fetuses, nine had fetal distress during labour. Of the 12 fetuses with reduced fetal heart rate variation, seven were acidotic at delivery (umbilical artery pH <7.2). Overall, there were 10 acidotic fetuses at delivery in the study group. Only two of them had an umbilical systolic/diastolic ratio above the 95th percentile, three had an amniotic fluid index greater than 5, and five had fetal heart rate decelerations before labour. Fetuses who demonstrated an abnormal intrapartum fetal heart rate tracing or who were acidotic at delivery had a significantly higher rate of reduced fetal heart rate variation or decelerations before labour. The authors conclude that computerized CTG may improve fetal surveillance in post‐term pregnancy. The obvious criticism of this study is the circular argument of using an antepartum CTG abnormality to predict an intrapartum CTG abnormality.

Ultrasound assessment of amniotic fuid

Ultrasound monitoring of amniotic fluid volume was first described in 1980 when a subjective classification of ‘normal’, ‘reduced’ or ‘absent’ amniotic fluid was described, based on the presence or absence of echo‐free space between the fetal limbs and the fetal trunk or the uterine wall [72]. To test the value of the classification, 150 patients with pregnancies of 42 weeks or more underwent ultrasound examination in the 48 hours prior to delivery. The patients classified as having reduced or absent amniotic fluid had a statistically significant excess incidence of meconium‐stained liquor, fetal acidosis, and birth asphyxia and meconium aspiration. Manning et al. [73] described a semi‐quantitative method based on the largest vertical pool of amniotic fluid and used a 1‐cm pool depth as the cut‐off for intervention in a population of babies with suspected growth restriction. This was subsequently modified to 2 cm to improve detection of the growth‐retarded infant [74]. Crowley et al. [75] found an increase in adverse outcomes in post‐term pregnancies where the maximum pool depth was less than 3 cm. Fischer et al. [76] found that a maximum vertical pool of less than 2.7 cm was the best predictor of abnormal perinatal outcome.

Phelan et al. [77] described the amniotic fluid index (AFI), the sum of the maximum pool depth in four quadrants. Fischer et al. [76] found that maximum pool depth performed better than AFI in predicting adverse outcomes in post‐term pregnancies. Alfirevic and Walkinshaw [78] randomly allocated women with post‐term pregnancy to monitoring using either maximum pool depth or AFI. Both groups underwent computerized fetal heart rate monitoring every 3 days in addition to amniotic fluid measurements. The threshold for intervention was a maximum pool depth of less than 1.8 cm or an AFI of less than 7.3 cm. These figures had been identified as the third centiles for the local population. The number of women found to have an abnormal AFI was significantly higher than the number found to have an abnormal maximum pool depth and more women underwent induction of labour in the AFI arm of the trial. There were no perinatal deaths and no statistically significant differences in perinatal outcome between the two groups.

Morris et al. [79] performed an observational study of 1584 pregnant women at or beyond 40 weeks’ gestation in Oxford. Women underwent measurement of amniotic fluid, using both the single deepest pool and AFI. The results of these ultrasound measurements were concealed from caregivers. These authors agreed with Alfirevic and Walkinshaw [78] that more women ‘test positive’ using AFI than with single deepest pool; 125 women (7.9%) had an AFI of less than 5 cm in contrast to 22 women (1.4%) who had single deepest pool less than 2 cm. There were no perinatal deaths. There were seven cases of severe perinatal morbidity, an incidence of 0.44%. Two of these had an AFI below 5 cm and four had an AFI of less than 6 cm. None of the seven cases had a deepest pool measurement of less than 2 cm, thus emphasizing the trade‐off between specificity and sensitivity.

Locatelli et al. [80] conducted a similar study, but measured AFI twice weekly from 40 weeks until delivery. A composite adverse outcome of fetal death, 5‐min Apgar score less than 7, umbilical artery pH less than 7 and caesarean delivery for fetal distress occurred in 19.8% of those with an AFI below 5 compared with 10.7% of those with an AFI above 5 (P = 0.001).

These studies of amniotic fluid after 40 weeks suggest some association between reduction in volume and adverse outcome, but overall it performs with poor sensitivity and specificity. There is no evidence to suggest that it can be relied on as a means of monitoring pregnancies after 41 weeks’ gestation. In a meta‐analysis of studies on the relationship of amniotic fluid with adverse fetal outcome, Chauhan et al. [81] concluded that there was some association between oligohydramnios and an increased risk of caesarean delivery for non‐reassuring fetal heart rate patterns and low Apgar scores; however, the data relating to neonatal acidosis were insufficient. Fundamentally, while there is biological plausibility that decreases in amniotic fluid volume may pre‐date complications in the term and post‐term pregnancy, there are inadequate data to definitively state that such assessment followed by intervention will necessarily affect perinatal outcomes, by how much and with what timing. Furthermore, confidence in ultrasound assessment of amniotic fluid volume is undermined by studies which show a poor correlation between ultrasound AFI and actual amniotic fluid volumes measured by dye‐dilution studies [82,83]. Development of a better test to identify the senescent placenta or changing fetal–placental–maternal physiology at term and post‐term that will prevent perinatal complications is paramount.

Biophysical profile

Observational studies indicate that low biophysical scores identify babies at higher risk of adverse outcome [84]. However, evidence of ability to predict adverse outcome must not be interpreted as proof of the ability to prevent these outcomes.

A systematic review of four trials, comparing biophysical profile scoring with other forms of antepartum fetal monitoring, yields insufficient data to show that the biophysical profile is better than any other form of fetal monitoring [85]. Only one of these randomized controlled trials deals specifically with post‐term pregnancy [78]. This trial compares monitoring of post‐term pregnancy using a modified biophysical profile score (consisting of computerized CTG, AFI and the rest of the components of the conventional biophysical profile) with simple monitoring using CTG and measurement of amniotic fluid depth. The more complex method of monitoring post‐term pregnancy is more likely to yield an abnormal result, but does not improve pregnancy outcome as evidenced by umbilical cord pH.

An observational study of biophysical profile scoring in the management of post‐term pregnancy showed that 32 of 293 women who had abnormal biophysical profiles had significantly higher rates of neonatal morbidity, caesarean delivery for fetal distress and meconium aspiration than the women with reassuring biophysical profiles [86]. A further observational study of 131 post‐term pregnancies showed that a normal biophysical profile score was highly predictive of normal outcome, but an abnormal test had only a 14% predictive value of poor neonatal outcome [87].

Doppler velocimetry

Two studies of routine umbilical artery Doppler velocimetry [88,89] in post‐term pregnancy indicate that it is of no benefit. In a small observational study comparing the predictive values of CTG, AFI, biophysical profile scoring and the ratio of middle cerebral artery (MCA) Doppler to umbilical artery Doppler, Devine et al. [90] found that the ratio of MCA Doppler to umbilical artery Doppler was the best predictor of ‘adverse outcome’ in this study, defined by meconium aspiration syndrome or caesarean delivery for fetal distress or fetal acidosis.

Prevention of post‐term pregnancy

The prevention of post‐term pregnancy centres around efforts to ensure that a misdiagnosis is not made from improper pregnancy dating and encouraging the onset of labour prior to post‐term pregnancy developing. While the first demands public health action to ensure that all patients have the option to obtain first‐trimester ultrasound dating confirmation, widespread adoption of this practice seems limited at this point. However, most women undergo second‐trimester ultrasound, which also reduces the risk of being misdiagnosed with a post‐term pregnancy, though not as much as first‐trimester ultrasound.

Post‐term pregnancy can absolutely be prevented by simply inducing all patients before they reach 42 weeks of gestation. This appears to be a reasonable approach, but does carry some costs due to the prolonged admissions to labour and delivery units for induction of labour. A better way of preventing such post‐term pregnancies would use techniques to encourage spontaneous labour. Several minimally invasive interventions have been recommended to encourage the onset of labour at term and prevent post‐term pregnancy, including membrane stripping, unprotected coitus and acupuncture. Stripping or sweeping of the fetal membranes refers to digital separation of the membranes from the wall of the cervix and lower uterine segment. This technique, which likely acts by releasing endogenous prostaglandins from the cervix, requires the cervix to be sufficiently dilated to admit the practitioner’s finger. Although stripping of the membranes may be able to reduce the time interval to spontaneous onset of labour, there is no consistent evidence of a reduction in operative vaginal delivery, caesarean delivery rates, or maternal or neonatal morbidity [91–93]. Unprotected sexual intercourse causes uterine contractions through the action of prostaglandins in semen and potential release of endogenous prostaglandins similar to stripping of the membranes. Indeed, prostaglandins were originally isolated from extracts of prostate and seminal vesicle glands, hence their name. Despite some conflicting data, it appears that unprotected coitus may lead to the earlier onset of labour, reduction in post‐term pregnancy rates, and less induction of labour [94–96]. In one small randomized trial which attempted to address this question, women were randomized to a group advised to have coitus versus a control group which was not. In this study, the women advised to have coitus did so more often (60% vs. 40%), but there was no measurable difference in the rate of spontaneous labour in this underpowered study [97]. Similarly, the efficacy of acupuncture for induction of labour cannot be definitively assessed because of the paucity of trial data and requires further examination [98,99].

Ultrasound to establish accurate gestational age

The first step towards managing post‐term pregnancy is to reduce the number of cases of post‐term pregnancy by providing ultrasound verification of gestational age for all pregnancies. A systematic review shows that routine second‐trimester ultrasound reduces the number of cases of post‐term pregnancy [21]. A recent randomized controlled trial of first‐ versus second‐trimester ultrasound showed a lower rate of post‐term pregnancy in pregnancies dated by first‐trimester ultrasound [22]. A secondary analysis of data from the FASTER trial showed that first‐trimester ultrasound determination of gestational age by CRL as opposed to LMP reduces the apparent incidence of pregnancies greater than 41 weeks from 22.1% to 8.2% [24]. It does seem that obtaining a first‐trimester ultrasound to assess viability and gestational age at the first visit is a good idea and may impact the overall number of diagnosed post‐term pregnancies.

Induction of labour for post‐term pregnancy

Given that a patient cannot have a stillbirth at 42 weeks if she is induced at 41 weeks, induction of labour has been identified as the principal intervention to reduce perinatal morbidity from post‐term pregnancy. However, there is concern that such inductions of labour are in turn driving up the caesarean delivery rate. Thus, obstetric providers have responded in various ways to the apparently increased perinatal mortality and morbidity associated with post‐term pregnancy. Such potential clinical options include induction at term to prevent pregnancies reaching 42 weeks, routine induction at 41 or 42 weeks or shortly before, and selective induction at 41 or 42 weeks in cases identified by tests as being at risk of adverse outcome. Fortunately, the benefits and hazards of some of these strategies have been evaluated in randomized controlled trials. Randomized or quasi‐random trials comparing elective induction at term versus expectant management, and elective induction after 41 weeks versus monitoring of post‐term pregnancies were identified using the search strategy described by the Cochrane Pregnancy and Childbirth Group and formed the basis of a systematic review of management options in post‐term pregnancy [100]. The main outcomes of interest are those already identified in the analysis of post‐term pregnancy risks: perinatal mortality, neonatal encephalopathy, meconium‐stained amniotic fluid, caesarean delivery. In addition, evidence was sought relating to the effect of the various management options on maternal satisfaction. Subsequently, there have been other systematic reviews of randomized trials comparing induction of labour with expectant management in pregnancies of 41 weeks’ gestation and more [101] or 41 weeks’ gestation or less [102].

One major concern regarding induction of labour has been that of increased risk of caesarean delivery. However, this conclusion has not been universally accepted [103]. One component of the concern regarding induction of labour is the large number of retrospective studies which demonstrate higher rates of caesarean delivery in the induced patients [104,105]. The methodological problem with these studies is that they generally compare women who are induced to those in spontaneous labour [106]. A recent study which compared women who were induced with those who underwent expectant management actually found lower rates of caesarean delivery in the women who were induced [107]. Further, in a recent meta‐analysis of three small studies of elective induction of labour prior to 41 weeks’ gestation, induction of labour led to lower rates of caesarean delivery [108].

An alternative approach to the prevention of post‐term pregnancy is selective or preventive rather than routine induction of labour at an earlier gestational age. In a small preliminary study of active management of risk in pregnancy at term (AMOR‐IPAT) in which induction of labour at 41 weeks was recommended for all women with risk factors for cephalopelvic disproportion or intrapartum non‐reassuring fetal testing, Nicholson et al. [109] were able to decrease the caesarean delivery rate from 17% in the expectantly managed group (induction rate, 26%) to 4% in the risk‐factor managed group (induction rate, 63%).In a recent, prospective, randomized controlled trial, there was a trend towards lower caesarean rates in the risk‐factor managed group, but the study was underpowered for this outcome [110]. However, it did find lower rates of admission to neonatal intensive care and an improved adverse outcome index in the risk‐factor managed group, which was induced in the majority of cases.

Induction of labour at 41 weeks

Sixteen randomized trials comparing ‘routine’ induction of labour at a specified gestational age with a policy of selective induction of labour in response to an abnormal antepartum test are summarized in Table 23.3. These trials form the basis of a systematic review by Sanchez‐Ramos et al. [101]. Twelve of them had been previously included in the Cochrane review by Crowley [100]. One trial is larger than all others and contributes considerable weight to both meta‐analyses [111]. Both meta‐analyses adopt an inclusive approach and include trials of variable size and quality. The gestational age at trial entry varies from 287 to 294 days’ gestation. A variety of methods of antepartum fetal testing are used to supervise pregnancies in the expectant arm of the trials.

As noted above, it could be costly to routinely induce all women at 41 weeks’ gestation. However, a study found routine induction of labour at 41 weeks’ gestation to be cost‐effective (i.e. more costly than not, but worth the improved outcomes) when compared with expectant management [112]. Routine induction of labour at 41 weeks’ gestation was also included in recent recommendations from ACOG to safely reduce the primary caesarean delivery [113].

Induction at or before 40 weeks

Pre‐emptive induction of labour, where women with uncomplicated pregnancies were routinely offered induction at or before 40 weeks, was practised in some obstetric units in some countries in the 1970s. Six randomized trials compare a policy of ‘routine’ induction at 39 weeks [114,115] or 40 weeks [116–119], with either ‘expectant’ management of an indefinite duration or expectant management until 42 weeks’ gestation. These trials reveal no evidence of any major benefit or risk to ‘routine’ induction at 40 weeks. Two perinatal deaths of normally formed babies occurred in the expectant arm of these trials and none in the induction arm. Obviously, this is not a significant difference. There was no effect on rate of caesarean delivery (OR 0.60, 95% CI 0.35–1.03), instrumental delivery or use of analgesia in labour. Not surprisingly, given the relationship between gestational age and meconium staining of the amniotic fluid in labour, induction around 40 weeks reduces the incidence of meconium staining in labour (OR 0.50, 95% CI 0.31–0.86). Unfortunately, the authors of these trials did not address the important question of women’s views of induction of labour at this stage of pregnancy. The authors therefore missed a golden opportunity in failing to measure women’s satisfaction with their care. ‘Routine’ induction of labour at 40 weeks would no longer be considered a realistic option for the prevention of post‐term pregnancy. The number of inductions at 40 weeks required to prevent an adverse outcome at 41 or 42 weeks would be excessive and intervention at this level would be unlikely to be welcomed by women, obstetricians or midwives. Currently, a large prospective trial of this question – routine induction of labour at 39 or 40 weeks’ gestation versus expectant management – is being conducted in the USA.

Induction of labour and perinatal morbidity and mortality

Even the largest trial [111] has insufficient statistical power to detect a significant reduction in the perinatal mortality rate. To have an 80% chance of detecting a 50% reduction in a perinatal mortality rate of 3 per 1000, a sample size of 16 000 is required. Table 23.3 records the 13 perinatal deaths that occurred in the randomized trials, three among 3159 women allocated to induction and 10 among 3067 women allocated to selective induction. One normally formed baby, among those allocated to induction [120], died from asphyxia following emergency caesarean delivery for meconium‐stained amniotic fluid and bradycardia 2 hours after induction of labour. The other two deaths among those allocated to routine induction occurred in babies with lethal congenital anomalies. Three further deaths occurred in babies with anomalies among those allocated to selective induction. The other seven deaths occurred in normally formed babies. Two deaths in the Canadian Post‐term Pregnancy Trial [111] occurred despite adherence to the monitoring protocol of daily movement counting and three times weekly CTG and ultrasound assessment of amniotic fluid volume. These babies were both small, weighing 2600 and 3175 g. In the trial by Dyson et al. [121], a neonatal death from meconium aspiration occurred in a 43‐week baby delivered for acute fetal bradycardia following spontaneous labour. Fetal heart rate monitoring and ultrasound assessment of amniotic fluid had been reassuring 48 hours before the spontaneous onset of labour. One of the deaths in the trial by Henry [122] was attributed to gestational diabetes. The second occurred due to meconium aspiration in a woman who refused induction following detection of meconium at amnioscopy. The deaths in the trials by Bergsjo et al. [123] and Cardozo et al. [124] were due to pneumonia and abruptio placentae, respectively.

The authors of systematic reviews adopt a different approach to the inclusion of perinatal deaths in babies with fetal abnormalities. These are excluded in the Cochrane review [100] and included by Sanchez‐Ramos et al. [101]. Thus, the Cochrane systematic review shows that induction of labour is associated with a significant reduction in perinatal mortality in normally formed babies (OR 0.23, 95% CI 0.06–0.90), while Sanchez‐Ramos et al. confirm the reduction in risk of perinatal death (0.9 vs. 0.33%) but with the 95% confidence intervals for the odds ratio of 0.41 crossing unity (95% CI 0.14–1.28).

Both systematic reviews report a significant reduction in the incidence of meconium‐stained amniotic fluid but this does not affect the rate of meconium aspiration (0.82, 95% CI 0.49–1.37) [100]. There is no effect on fetal heart rate abnormalities during labour. The odds ratio for neonatal jaundice (3.39, 95% CI 1.42–8.09), based on the small number of trials that reported this outcome, indicate that it is increased by induction. The systematic reviews do not show any beneficial or hazardous effects on Apgar scores, neonatal intensive care admission or neonatal encephalopathy.

Effect of induction of labour on risk of caesarean delivery

Sanchez‐Ramos et al. [101] report that induction of labour is associated with a reduction in the rate of caesarean delivery (OR 0.88, 95% CI 0.78–0.99). Crowley [100] reported a similar outcome, but interpreted it as evidence that a policy of ‘routine’ induction of labour does not increase the likelihood of caesarean delivery. She believed that a post‐randomization bias in the Hannah trial [111] may have weighted the results towards a spurious reduction in risk of caesarean delivery. Women in the expectant arm of the Hannah trial who required induction because of abnormal antenatal tests were denied vaginal prostaglandins whereas those allocated to ‘routine’ induction were treated with prostaglandin E₂. This could potentially lead to an increase in dystocia or failed induction in those denied prostaglandins. However, this does not account for the 8.3% rate of caesarean delivery for fetal distress in the selective induction arm of the Hannah trial compared with 5.7% in the routine induction arm. The effect of a policy of induction of labour on reducing the rate of caesarean delivery for fetal distress is consistent across the trials reviewed. No significant heterogeneity was detected by Sanchez‐Ramos et al. [101]. These authors also performed funnel plots, which were symmetric, indicating no evidence of publications bias.

Because the reduced rate of caesarean delivery associated with induction of labour is contrary to a traditionally held view among obstetricians that induction of labour increases the likelihood of delivery by caesarean section, a number of secondary analyses were carried out by Crowley [100]. These showed that induction of labour for post‐term pregnancy does not increase the caesarean delivery rate, irrespective of parity, cervical ripeness, method of induction or ambient caesarean delivery rates. As noted above, routine induction of labour at 41 weeks’ gestation was also included in recent recommendations from ACOG to safely reduce the primary caesarean delivery [113].

Women’s views of induction for post‐term pregnancy

Regrettably, randomized trials give little information on women’s views of induction versus conservative management. Only one trial assessed maternal satisfaction with induction of labour [124]. These authors showed that satisfaction was related to the eventual outcome of labour and delivery, rather than to the mode of onset of labour. Women’s views are likely to be influenced by the local culture, by the attitude of their caregivers and by practical considerations such as the duration of paid maternity leave. Few obstetricians, midwives or childbirth educators are capable of giving women unbiased information about the risks of post‐term pregnancy and the benefits and hazards of induction of labour. In a prospective questionnaire study of women’s attitudes towards induction of labour for post‐term pregnancy, Roberts and Young [125] found that despite a stated obstetric preference for conservative management, only 45% of women at 37 weeks’ gestation were agreeable to conservative management if undelivered by 41 weeks. Of those undelivered by 41 weeks’ gestation, 31% still desired conservative management. This significant decrease was unaffected by parity or certainty of gestational age. In a subsequent study, Roberts et al. [126] offered women a choice between induction and conservative management at 42 weeks; 45% of women opted for conservative management. Certainly, an intervention that is common practice in more than 20–25% of pregnancies in most developed countries deserves more study with respect to its impact on women as well as the neonates who are the product of these pregnancies.

Post‐term pregnancy and home birth

There is a lack of good‐quality epidemiological evidence on the outcome of post‐term pregnancy when delivery occurs at home. Bastian et al. [127] used multiple methods of case identification and follow‐up to assemble a population‐based cohort of 7002 home births in Australia; 50 perinatal deaths occurred, giving a perinatal mortality rate of 7.1 per 1000. Of 44 perinatal deaths in women of known gestational age, seven (15.9%) occurred post‐term (≥42 weeks). A study conducted among Native Americans examined an increase in perinatal mortality in home births attended by midwives compared with those attended by doctors and identified post‐dates pregnancies, breech deliveries and twins as the source of the difference in mortality rates between the two groups [128]. Given these relatively weak findings combined with the overall evidence regarding post‐term pregnancy and intrapartum complications and perinatal morbidity and mortality, many home birth providers will refer such patients to an in‐hospital practice.

Tags: Dewhursts Textbook of Obstetrics and Gynaecology

Sep 7, 2020 | Posted by admin in GYNECOLOGY | Comments Off

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