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This chapter should be cited as follows:
Berkowitz, K, Garite, T, Glob. libr. women's med.,
(ISSN: 1756-2228) 2008; DOI 10.3843/GLOWM.10123
This chapter was last updated:
October 2008




The classically postmature infant, described by Clifford1 is characterized by loss of subcutaneous fat reserves and meconium staining caused by placental dysfunction.  The syndrome occurs in about 20% of pregnancies progressing beyond 42 weeks gestation, but is rarely seen in today's obstetric practice.  Nevertheless, there are recognized increases in perinatal morbidity and mortality that occur in the postdate pregnancy.  As patients have become more pro-active in expressing concerns about delivering past their due date, these concerns have pressured physicians to re-evaluate the wisdom of continuing a pregnancy to the classically defined post date mark of 42 weeks' gestation. The threshold of 42 weeks became established because the incidence of macrosomia, oligohydramnios, meconium aspiration, and cesarean section performed for fetal distress are significantly increased after 42 weeks of gestation.2, 3, 4  Perinatal mortality rates, as determined by the National Birthday Trust data5 begin to increase after 42 weeks and quintuple by 44 weeks of gestation.  As obstetric practices conerning induction of labor and tolerance of a high cesarean section rate have evolved, many have re-evaluated the risk/benefit ratio and advocated a new threshold represented by 41 weeks' gestation. There is increasing recognition that the occurence of fetal and neonatal complications is a continuum, without clear thresholds determining an absolute limit beyond which pregnancy should not be allowed to progress.6  Increasingly, research has focused on the complications occuring during the "late term" period of 40-42 week' gestation.  Induction of labor at 41 weeks' gestation has been shown to decrease risks of perinatal death.7 The obstetrician must place the risk of this rare but serious complication in the context of maternal and fetal risk of complications incurred by induction of labor.  This chapter discusses what constitutes a postdate pregnancy, how to diagnose and manage its complications, what methods of fetal surveillance should be used, and how to decide the timing of induction and route of delivery.


The accepted normal duration of pregnancy is 266 days after ovulation. The timing of an ovulatory event may be estimated as occurring 14 days after the first day of the last menstrual period if cycles occur at 28-day intervals. Ovulation occurring during longer or shorter cycles also can be estimated, providing the cycles are regular in length.

Postdate pregnancy, prolonged pregnancy, and postmaturity syndrome should not be used as interchangeable terms. A postdate pregnancy usually is defined as a pregnancy lasting more than 294 days, or 42 completed weeks after the first day of the last menstrual period. Whereas some physicians consider prolonged pregnancy and postdate pregnancy to be the same entity, others believe that the term prolonged pregnancy should be reserved for well-dated pregnancies known to exceed 42 weeks of gestation and that the term postdate should be used for the more global group of patients for whom reliable dating criteria may not be available. The postmaturity syndrome was described in detail by Clifford1 and advocates the use of a staging system to quantify increasingly severe clinical manifestations of placental dysfunction. Stage I is typified by a long, lean infant with wrinkled, peeling skin. Stage II includes the clinical findings of stage I and adds greenish meconium staining of amniotic fluid, fetal skin, and placental membranes. Stage III is characterized by a high incidence of fetal distress and yellow-brown meconium staining, indicative of the presence of meconium for several days. The incidence of the postmaturity syndrome increases with the length of pregnancy; at 42 weeks, about 20% of fetuses have stigmata of postmaturity.


The incidence of postdatism decreases as the accuracy of the dating criteria used increases.8 The reported incidence of postdate pregnancy ranges from 3 to 17%.3, 9, 10 The advent of sensitive over-the-counter pregnancy test kits and the common use of early ultrasound for dating have improved the clinical estimation of conception in women who present early for prenatal care. Sonography is most useful when performed before the 20th week of gestation, with measurement of the crown-rump length in the first trimester as the most accurate parameter. Menstrual recall, early palpation of uterine size, and Doppler auscultation of fetal heart tones are less accurate but helpful methods used to determine the estimated date of delivery. Menstrual dating biases towards an overestimation of gestational age compared to ultrasound dating.  It is also less accurate than ultrasound dating due to errors in the patient's ability to correctly recall the timing of her last menstrual period.  Amenorrhea caused by recent abortion, discontinuation of contraceptive pill use, or breast-feeding also obscure the timing of ovulation and conception.  Early palpation of uterine size can lead to overestimation of gestational age in the presence of myomas.  Other factors which obscure accurate identification of the estimated date of delivery include late presentation for obstetric care, switching providers with subsequent loss of early prenatal care records, and a history of irregular menstrual cycles.  When menstrual dating is the prevailing criteria, the incidence of postdate pregnancies is 8.8%.11  When early ultrasound corroborates the menstrual dating, the incidence of postdate pregnancies falls to about 6.9%.6  At a patient's first visit, all available clinical data should be gathered and correlated to reach the best estimate of gestational age.  Once an estimated date of delivery is established, it should remain unchanged by the acquisition of later or less accurate means of estimation.  For instance, if a patient's menstrual dates and first trimester sonography agree on a estimated due date, later measurements obtained by ultrasound in the third trimester should not alter that established due date. 


Maternal age, ethnicity and history of prior pregnancy loss do not seem to be related to the incidence of prolonged pregnancy.8, 12, 13 Primigravidy8, 14 low socioeconomic status,13 maternal weight gain,2 obesity6 and smoking6 are associated with a higher incidence of prolonged pregnancy.  However, these associated clinical conditions do not appear to be causal and thus their predictive power is limited. For instance, the association of low socioeconomic status with an increased incidence of postdatism may reflect delayed initiation of prenatal care and the subsequent use of less accurate dating criteria, rather than a true causal relationship with postdate pregnancy.

Properly timed initiation of labor is a complex process requiring appropriate interactions of the fetal hypothalamo-hypophyseal-adrenal axis, the placenta, fetal membranes, decidua, uterine myometrium, and cervix. Failure to coordinate these interactions impedes labor; several different pathogenic mechanisms may thus result in postdate pregnancy. Simply stated, interactions between the endocrine systems of fetus, placenta, and mother must induce anatomic and functional changes in uterine musculature and cervical resistance. The uterus is transmuted from a quiescent organ suited to retaining its contents to one that actively and rhythmically works to expel the fetus.

Activation of the myometrium is hormonally mediated by withdrawal of inhibitors of myometrial activity. For example, nitric oxide acts to relax the myometrium. At term, levels of messenger ribonucleic acid encoding inducible nitric oxide are decreased.15 The possible role of progesterone withdrawal, a mechanism well established in labor activation in many mammalian species, remains elusive. Whereas no measurable changes in progesterone occur during the phase of uterine activation, the ability of progesterone to maintain uterine relaxation could wane if antagonists to progesterone action increase. The myometrium is rendered more responsive to stimulation of stretch receptors and begins to generate the high-frequency, high-amplitude electrical signals that result in coordinated contractions. Once activated, the uterus is also more receptive to stimulation by prostaglandins and oxytocin.

Cervical ripening is a metabolic process which triggers, or can be triggered by, the intra-uterine or fetal precursors to labor.  Collagen, elastin and smooth muscle cells undergo significant remodeling in a relatively short time period.  Collagen crosslinks dissolve, smooth muscle cells undergo apoptosis and glycosaminoglycan content changes.16  The process of cervical ripening converts the cervix from an inelastic muscular barrier into a compliant portal through which uterine contractile forces can act to expel the intrauterine contents with ease.  Cervical ripening agents potentiate the physiologic changes and can induce uterine contractile activity.   Patients undergoing induction of labor with cervical ripening agents experience a shorter time in labor and less need for uterotonic agents than those not receiving such agents.17 

The fetal hypothalamo-hypophyseal-adrenal axis also must be activated to effect regular contractions. The maturation, size, and function of the fetal adrenal medulla and the provisional zone of the adrenal cortex depend on the release of adrenocorticotropin from the fetal anterior pituitary.18 The adrenocorticotropic hormone also regulates fetal adrenal production of steroid hormones. As cortisol levels increase at term, cortisol increasingly competes with progesterone for binding sites on the glucocorticoid receptor.19 Increased production of other steroid hormones has been described before the onset of labor in normal human pregnancy.20 These increases are absent in anencephalic pregnancies.21 The fetal adrenal appears to be critical in timing the onset of labor because anencephalics with normal fetal adrenal cortical regions usually deliver at or before the due date, whereas those with adrenal hypoplasia classically have a postdate delivery.6 Drost and Holm22 adrenalectomized fetal sheep and were able to prolong pregnancy, whereas McDonald and Nathanielsz23 prolonged ovine gestation by ablation of the fetal paraventricular nuclei. Labor is preceded by increased maternal cortisol levels in sheep.24 Other workers25 have been able to initiate labor by intra-amniotic instillation of cortisol in the human. However, a key difference between sheep and primate models of labor initiation lies in the ability of primate fetal adrenal cortical stimulation to produce cortisol and estrogens, whereas in the sheep estrogen is not produced.

Placental senescence is the root cause for increased morbidity post-dates pregnancies.  Metabolic and circulatory functions degrade as the placenta ages and calcifies.  Genetically programmed apoptosis occurs, leading to specific changes in metabolism and placental hormonal production.  Serum estriol levels increase with advancing gestation until 40 weeks; there is a progressive decline in estriol values that parallels the decline in amniotic fluid level when the term gestation is exceeded.26, 27 Placental sulfatase deficiency, a rare and specific type of placental dysfunction, is characterized by low estriol production. Prolonged pregnancy is common in patients with placental sulfatase deficiency.28 Ballantyne proposed a role for placental dysfunction in 1902 and linked it to the development of the postmaturity syndrome.29 Clifford1 further advanced the theory of placental dysfunction as a cause of postmaturity syndrome, with decreased nutrient transfer to the fetus, resulting from calcification and aging of the placenta. As the placenta ages, increased rates of placental infarction and fibrin deposition decrease placental exchange of wastes and nutrients with the maternal circulation. Placental senescence impairs the transfer of oxygen fuels and the disposition of wastes as the number of villous capillaries and intervillous spaces decline. The postdate fetus experiences a range of physiologic changes that predispose it to the development of hypoxia and acidosis. These stresses in turn activate the fetal hypothalamic-hypophyseal-adrenal axis to produce more cortisol, attempting to trigger the normal process of uterine activation and stimulation leading to labor.

Grannum and coworkers30 advocate using sonography to grade the severity of placental senescence on a scale of 0–3. A grade 3 placenta exhibits sonographic findings of linear echogenic densities, probably representing areas of increased calcium deposition, dividing the placental bed into compartments. Echolucent areas may be seen in the central portion of the compartments. The incidence of grade 3 placentas increases after 40 weeks, but its presence alone cannot be used to predict the occurrence of fetal distress or the postmaturity syndrome. However, Yeh and colleagues31 found that the postmaturity syndrome was more common when both oligohydramnios and a grade 3 placenta were present.

The amniotic fluid volume declines by as much as 33% per week in the postdate pregnancy.32 As placental blood flow decreases, the fetus must redistribute a decreased circulating blood volume to maintain renal blood flow. Diminished fetal ventricular function may also hamper the fetus's efforts to maintain renal perfusion.33 As renal blood flow decreases, so does fetal urinary output. Eventually, the decrease in amniotic fluid leads to umbilical cord compression. Intermittent cord compression can be diagnosed by identifying the presence of variable decelerations during fetal heart rate testing. Cord compression stimulates the passage of meconium by the same vagal reflex that initiates a heart rate deceleration. Meconium passed into a small amniotic fluid volume tends to be thicker, more tenacious, and more difficult to clear after aspiration. A significant amount of cord compression can lead to hypoxia, acidosis, and fetal distress. A fetus already compromised by other factors such as diabetes, hypertension, or intrauterine growth retardation has few reserves available to protect it against the additional stresses imposed by the physiologic changes occurring in the postdate pregnancy. They are particularly at risk for increased perinatal mortality.



Although placental function decreases in the postdate pregnancy, the total placental area increases so that the exchange of nutrients usually continues to support fetal growth. Therefore, the most common problem associated with postdatism is not postmaturity syndrome, but macrosomia. Birth weights in excess of 4000 g are threefold to sevenfold more common in the postdate pregnancy,2 with an overall incidence of 25% at 42 weeks. The delivery of macrosomic infants is associated with increased rates of labor dystocia, birth trauma, cesarean section, and neonatal complications such as hypoglycemia, temperature instability, and jaundice. In a large review of shoulder dystocia, 40% of the cases were noted to occur in the postdate infant.34 In deciding whether to use a liberal policy of induction in the postdate population to decrease the development of macrosomia, the clinician should recognize that there is a crossover point at which the increased cesarean section rate associated with failed induction would negate any advantage of preventing a cesarean section performed for macrosomia.

Although ultrasound may be helpful in identifying macrosomic infants at risk for birth trauma, clinicians should be aware of the limitations of this modality in predicting birth weight. The formulas currently used to estimate fetal size are less accurate in macrosomic infants because of variations in head shape and adiposity found in this group. Formulas predicted on estimates of macrosomic populations or which depend less on fetal head size may carry greater accuracy in identifying the fetus at risk for shoulder dystocia.35

Fetal Asphyxia

Intrauterine asphyxia results from a deficit in the required amount of oxygen being delivered to the fetus. The deficit results from chronic conditions such as uteroplacental insufficiency or from acute, intermittent cord compression seen in conjunction with oligohydramnios. Pregnancies complicated by chronic hypertension or diabetes mellitus, already compromised by suboptimal placental function before term, carry a fourfold to fivefold greater risk of perinatal mortality when allowed to continue after the delivery date.12 The clinical manifestations of asphyxia may range from fairly innocuous changes in fetal heart rate patterns to the development of permanent neurologic sequelae. Antepartum testing is meant to detect the fetus with hypoxia, but often a dysmature or otherwise compromised fetus exists in a prehypoxic state. Tests that could consistently identify the prehypoxic fetus at risk for asphyxia would allow this group to be delivered before complications arise. Estriol levels correlate inversely with the rate of fetal heart rate decelerations and the occurrence of fetal distress,27 but the inconvenience of performing frequent 24-hour urine collections has led to the use of other predictive tests such as the amniotic fluid index. The reliable identification of a subset of postdate pregnancies at risk for fetal hypoxia and asphyxia obviates routine induction in the low-risk postdate patient.

Meconium Aspiration

The mechanisms of meconium passage described earlier are more likely to be found in the postdate pregnancy. The meconium also is likely to be thicker and more tenacious because of the frequency of oligohydramnios. Meconium aspiration is eight times more common in postdatism, and its complications include pneumonia, pneumothorax, a requirement for assisted ventilation, and the development of pulmonary hypertension.36 The intrapartum identification of meconium should be accompanied by preparations to suction both the mouth and nares to clear meconium from the pharynx before delivery of the fetal body. Personnel trained in neonatal intubation should be available to intubate and continue suctioning as required. Intrapartum meconium aspiration can be decreased by the use of saline amnioinfusion, which dilutes the meconium and helps to prevent occlusion of the respiratory passages.37 An intrauterine pressure catheter is used to introduce a specific bolus amount of saline solution, followed by a variable rate of infusion as determined by baseline uterine tonus. The pressure catheter continues to provide accurate readings of the intrauterine pressure being generated by contractions.

Postmaturity Syndrome

The hallmarks of the postmature infant as described by Clifford1 include meconium staining, loss of subcutaneous fat reserves, and skin peeling. The infant's appearance is like that of a wizened old gnome—long, thin, and wrinkled with decreased muscle mass and long nails on the toes and fingers. The decreased stores of fat and glucose predispose these infants to metabolic disturbances such as hypoglycemia, hypothermia, and polycythemia. Currently, there is no way of predicting in utero which infants will develop the syndrome, although it is more commonly seen after 42 weeks and in conjunction with oligohydramnios.

Long-Term Outcome

Early reports suggest that the postmature infant experienced quantifiable delays of either mental or physical development that lasted up to the fifth year of life.38, 39 Mothers reported increased incidence of sleep and feeding difficulties. However, other studies that used rigorous pregnancy dating criteria and stratified infants based on their Clifford staging showed that once the infant passed the perinatal period, its development was comparable with term control infants.40, 41


The development of simple, reliable methods for fetal surveillance, the use of ultrasound to determine fetal size and amniotic fluid volume, and the introduction of cervical ripening agents have improved the clinician's ability to manage the postdate pregnancy safely. Before the introduction of adequate methods of fetal surveillance in the 1970s, routine induction of labor at 42 weeks was commonly practiced to improve the perinatal outcome.42, 43 This management strategy predictably led to a high incidence of cesarean section for failed induction of labor, and many practitioners began to advocate expectant management for patients with an unfavorable cervix and who were at low risk for poor perinatal outcome.44  Postdate patients with an unfavorable cervix have benefitted from the introduction of cervical ripening agents. Prostaglandin preparations to ripen the cervix are available as a gel (dinoprostone [Prepidil]), as a removable sustained-release suppository (Cervidil), or as a vaginal tablet (misoprostol). These agents sensitize the uterus to the action of uterotonic agents, as well as remodel the cervix, and have encouraged physicians to undertake induction of labor in postdate patients when delivery is indicated.  It should be noted that induced labor roughly doubles the risk for cesarean delivery.45, 46  The use of cervical ripening agents speeds progress through the induction process, but does not decrease the overall risk for cesarean delivery when compared to spontaneous labor.

Antepartum Testing

The development of simple, inexpensive, and easily interpreted methods of antepartum fetal testing has led to the current practice of watchful waiting in patients with an unfavorable cervix and reassuring antepartum test results, reserving routine induction for patients with an inducible cervix, non-reassuring test results, or other risks for a poor outcome. Antepartum surveillance generally begins at 41 weeks, or 287 days from the first day of the last menstrual period, because perinatal morbidity and mortality begin to rise before 42 weeks of amenorrhea.47, 48 Several antenatal surveillance schemes are in current use49, 50, 51, 52, 53, 54 (Table 1). The ideal test would be easily administered and easily interpreted, noninvasive, cost-effective, sensitive enough to identify the fetus at risk, and yet specific enough to prevent excessive intervention. Use of the contraction stress test, the nonstress test, or the biophysical profile for antepartum testing decreases the perinatal morbidity and mortality associated with postdatism. The relative merits of each testing scheme have led to considerable debate as to which is the single “best” test.

Table1. Antenatal surveillance testing methods



Contraction stress test49


Patient placed in semi-Fowler position and BP recorded every 10 min

Negative: no late decelerations, contraction frequency 3/10 min

FHR and uterine contractions monitored for 30 min

Positive: consistent late decelerations, regardless of contraction frequency but without uterine hyper-stimulation

If spontaneous contraction frequency <3/10 min, begin oxytocin infusion until a contraction frequency of 3/10 min is achieved

Equivocal: nonpersistent late decelerations or FHR decelerations occurring with uterine hyperstimulation (CTX > 5/10 min or CTX lasting >90 sec)

If no late decelerations occur, discontinue stimulation and observe FHR until return to baseline uterine activity


If late decelerations occur, continue stimulation until decelerations can be determined to be persistent or transient


Negative test: repeat weekly


Positive test: deliver patient


Equivocal test: retest in 24 hours


Nonstress testing50, 51, 52


FHR monitoring in postprandial period with patient in semi-Fowler position

Reactive: two FHR accelerations of 15 beats/min lasting 15 sec in a period of 10 min

Monitor for reactivity for 20 min; if nonreactive, stimulate fetus with abdominal palpation or glucose administration

Nonreactive: absence of qualifying FHR acceleration after 40 min of monitoring

Nonreactive: proceed to contraction stress test

Deceleration: fifteen beats/min lasting 30 sec

Biophysical profile53, 54


Ultrasound observation for 30 min, recording parameters of fetal breathing for 1 min, three fetal movements, fetal tone, and normal amniotic fluid volume (>2 cm vertical pocket or amniotic fluid index greater than 5)

Normal: all ultrasound parameters normal or an abnormal ultrasound parameter with a reactive nonstress test

Normal: repeat test twice-weekly

Abnormal: abnormal ultrasound parameter with nonreactive nonstress test or decreased amniotic fluid volume

Abnormal: consider delivery


BP, blood pressure; CTX, contractions; FHR, fetal heart rate.

The contraction stress test remains the gold standard for antepartum fetal surveillance.4, 55 Freeman49 conducted a prospective study of over 700 postdate pregnancies using weekly contraction stress testing to identify fetuses at risk for intrapartum distress. There were no perinatal deaths using this methodology. However, only 57.9% of patients had a normal result for the last test before delivery. Many (38.5%) patients had equivocal test results that required either frequent retesting or other intervention. Although the low rates of perinatal mortality and morbidity achieved using the contraction stress test attest to its sensitivity, the high percentage of equivocal results obtained can make the test cumbersome to administer to numerous patients. The test also frequently requires the intravenous administration of oxytocin, although sometimes this can be obviated by use of nipple stimulation rather than oxytocin infusion.

The nonstress test now is the most widely used method of antepartum fetal surveillance because of its simplicity and noninvasive nature. Analysis of a fetal heart tracing requires the identification of accelerations, spontaneous decelerations, baseline heart rate, and uterine activity before classifying the tracing as reactive, reactive with decelerations, or nonreactive. Fetal stimulation by palpation or the use of vibroacoustic stimuli can be used to induce reactivity without compromising the validity of the test. When the nonstress test is performed weekly, perinatal outcome is not as favorable as when the contraction stress test is performed weekly.50 Performance of the test twice-weekly improves perinatal outcome.56 Estimation of the amniotic fluid volume in conjunction with the use of the nonstress test provides outcomes very similar to those achieved with a weekly contraction stress test57.  This is the most widely used form of testing currently.  If there are equivocal findings using the nonstress test in conjunction with amniotic fluid index evaluation, a "back-up test" , consisting of either a contraction stress test or a biophysical profile can be performed.  The biophysical profile53 is unique in its primary reliance on ultrasound parameters rather than fetal heart rate patterns. A normal biophysical profile with all ultrasound parameters identified during the test period of 30 minutes was associated with no perinatal mortality and low rates of perinatal morbidity. An abnormal test requires the use of nonstress testing in addition to ultrasound, with appropriate intervention predicated on the results of the nonstress test.

Doppler velocimetry studies have not been helpful in identifying the postdate infant at risk for intrapartum distress, perhaps because the umbilical arterial and venous diameters are increased in the postdate fetus.58 Middle cerebral artery velocity or a ratio between middle cerebral and umbilical arterial velocities has been helpful in identification of the fetus most at risk for complications from postdate pregnancy.59

Antepartum testing protocols are all designed to signify increased fetal risk.  Once the maternal and fetal risks to continuation of the pregnancy are no longer acceptable, the physician will effect delivery.  Perinatal fetal morbidity and mortality nadir at 39–40 weeks' gestation.60  Maternal morbidity increases with induction of labor and with pregnancy prolonged more than 41 weeks' gestation.  Several studies have challenged the need to continue with antepartum testing to 42 weeks' gestation, comparing outcomes to a policy of induction once 41 weeks' gestation is achieved. One observational study found that neither policy gave a clear reduction in fetal risks, but did significantly increase the cesarean section rate among nulliparous women undergoing induction at 41 weeks' gestation.61  A retrospective study compared the outcomes of over 5000 deliveries when the hospital policy changed to induction of labor at 41 weeks' gestation.  While the rate of labor induction nearly doubled, from 29 to 58%, there were no significant improvements in mode of delivery, Apgar scores or stillbirth rates.62  A study of the timing of induced labor in Canada from 1980 to 1995 showed a significant increase in deliveries between 41 and 42 weeks, with a concomitant decline in births after 42 weeks' gestation.  The stillbirth rate declined over this time period, but it is uncertain how much of the benefit is attributable to the shift in delivery timing, as the decline in stillbirth rate was seen at 40, 41 and 42 weeks' gestation.63  Overall, it appears that fetuses of multiparous patients with a prior vaginal delivery may benefit by delivering at 41 as compared to 42 weeks' gestation.  Nulliparous patients undergoing induction can expect an increase in medical interventions and cesarean section rate when interventions begin at 41 weeks' gestation.

Use of Ultrasound

Fetal macrosomia occurs at least three times more frequently in postdate pregnancy than in term deliveries.2 There is increased morbidity to both mother and infant because of an increased frequency of birth trauma and cesarean delivery. Approximately 40% of shoulder dystocia cases occur in postterm deliveries.64 Use of ultrasound to estimate fetal weight represents a significant improvement over clinical estimation of fetal size by the Leopold method65 because it is less dependent on the mother's size and the skill of the examiner. However, the formulas currently available for estimation of fetal size are less accurate in the upper range of the birth weight spectrum because of fetal variation in head shape, adiposity, and muscle mass. The average margin of error is 10–15%. Even when this margin remains stable, the absolute value of the difference between estimated and actual weight is greater in larger infants. Ultrasound identification of a fetus with an estimated weight in excess of 4500 g should prompt the physician to consider cesarean delivery, although this remains controversial.


Once the timing and route of delivery has been selected, the clinician may be stymied by the presence of an unfavorable cervix. Most patients with documented postterm pregnancy have a low Bishop score.57 When expectant management is no longer an option, cervical ripening techniques may help to attain a safe vaginal delivery. Membrane stripping by vigorous cervical examination is a widely practiced technique that many practitioners subjectively believe decreases the incidence of postdate pregnancy.58 Theoretically, a low-grade deciduitis ensues and leads to the initiation of labor by release of prostaglandins near the cervical os. A prospective study involving 180 subjects was conducted in which women were randomized to either gentle cervical examination to assess Bishop score or to vigorous membrane stripping. The authors found a statistically decreased frequency of postterm delivery in patients who had undergone membrane stripping.59 Laminaria tents quickly accomplish the goal of cervical dilation but have been associated with a higher incidence of infectious complications such as neonatal group B streptococcal infection.60 Synthetic laminaria do not appear to be associated with increased infectious morbidity, but their efficacy as cervical ripening agents in postterm pregnancy has not been studied widely. The use of a Foley catheter, relaxin, or breast stimulation also has been advocated for cervical priming.59

The use of cervical ripening agents is now the standard of care for patients undergoing induction of labor who present with a Bishop score under 7.  Dyson and coworkers61 conducted a prospective randomized trial involving 302 patients with documented postdate pregnancies and unfavorable Bishop scores. Rates of meconium passage, fetal distress, duration of labor, and cesarean section were higher in the group assigned to expectant management with antepartum testing than in the group who received intravaginal or intracervical prostaglandin gel as outpatients. However, other studies have not shown benefit.62 Great variation exists in the dosage, timing, and route of administration of prostaglandin gel. Even the type of gel used to suspend the prostaglandin may affect the rate of systemic absorption. Rapid absorption is associated with uterine hyperstimulation and fetal distress that may be difficult to treat because prostaglandin gel, once administered, cannot be removed easily.  Gel preparations have been largely replaced now by the use of vaginal pessaries, composed of timed-release lozenges of dinoprostone, or use of misoprostol tablets.  Patients treated with either medication experience a quicker time to vaginal delivery and less need for subsequent use of oxytocin than women with unfavorable Bishop scores who are not treated 60. The dinoprostone product has the advantage of FDA approval and ease of removal should tachysystole occur; misoprostol has the advantage of very low cost. 

It is important to minimize the time spent in the process of labor, as the postdate fetus has little uteroplacental reserve and may rapidly become hypoxic or asphyxiated.  Fetal heart rate patterns reflect the fetus's ability to withstand the stresses of intermittent hypoxia and may be classified as reassuring or nonreassuring. In general, a normal baseline fetal heart rate with good variability or a pattern of spontaneous deceleration with rapid recovery and good interval variability are indicative of a fetus who is tolerating labor without any ominous problems. Spontaneous variable decelerations are indicative of intermittent cord compression and can be seen frequently either in labor or during antepartum testing. The presence of variable decelerations is associated with oligohydramnios. Late decelerations are suggestive of uteroplacental insufficiency and are associated with increased rates of fetal distress, low Apgar scores, and perinatal morbidity. Persistent late decelerations, especially when associated with a loss of reactivity, are particularly ominous. A fetus displaying such a fetal heart rate pattern requires expeditious delivery in an environment equipped for neonatal resuscitation. Maternal positional changes, hydration, and oxygen administration may alleviate fetal heart rate patterns associated with intermittent cord compression.  The use of standardized definitions of fetal heart rate patterns help identify the fetus at risk for intrapartum asphyxia.66  The use of standardized protocols for pitocin administration also decrease the risk of low apgar scores and cesarean section for fetal distress11 and should be considered for all women undergoing induction of labor. 

The use of saline amniofusion may alleviate some abnormalities of fetal heart rate patterns and has been reported to decrease the rate of meconium aspiration.34, 64 The obstetrician should be alert to the probability of thick meconium passage by the postdate infant and be ready to manage the airway properly after delivery of the fetal head. Fetal scalp blood sampling is of little value in identifying an acidotic fetus, as the acidosis may be a transient respiratory acidosis of little clinical significance rather than a metabolic acidosis.65 Additionally, fetal scalp puncture may lead to hemorrhage, scalp infection, and increased rates of vertical transmission of human immunodeficiency virus or hepatitis to the fetus.

These techniques combined with appropriate induction of labor allow many women to experience a safe vaginal delivery. Cesarean delivery still is required for many women with a postterm pregnancy; the perinatal morbidity of the procedure should be weighed against the likelihood of fetal asphyxia and birth trauma before proceeding.


Whereas the diagnosis of postdatism remains a challenge, the clinician's ability to identify a potentially compromised fetus has been improved by the introduction of reliable antepartum surveillance methods. The most important controversy that needs to be addressed is the issue of whether to use routine induction for all postdate patients or to selectively induce patients who have favorable cervices, nonreassuring antepartum test results, macrosomia, or other antepartum complications. While labor induction at 41 weeks' gestation may decrease the risk of stillbirth, it does so at the cost of increased maternal morbidity--especially in the nulliparous patient.  Although physicians differ in their beliefs as to the reliability of antepartum testing in preventing all perinatal complications and in the likelihood of success using prostaglandin cervical ripening, evidence indicates that the use of routine induction in the postdate pregnancy leads to a significantly increased rate of cesarean section without a concomitant improvement in outcome. Watchful waiting can safely be used in most postdate pregnancies with normal antepartum test results and without other risk factors, and the subset of women who require delivery can be reliably predicted using current methodology. Ultrasound can improve the selection of women in whom a vaginal delivery may lead to increased birth trauma. When induction of labor is indicated, the use of cervical ripening agents and checklist-based protocols for oxytocin use improve the rate of labor and decrease the risk for fetal compromise during the labor process.  Finally, intrapartum treatment of fetal heart rate abnormalities may decrease the rates of cesarean section for fetal distress and for meconium aspiration syndrome. A satisfactory outcome can be reasonably expected in the postdate pregnancy managed appropriately.



Clifford S: Postmaturity with placental dysfunction: Clinical syndrome and pathologic findings. J Pediatr 44: 1, 1954


Eden RD, Seifert LS, Winegar A et al: Perinatal characteristics of uncomplicated postdate pregnancies. Obstet Gynecol 69: 296, 1987


Sachs BP, Friedman EA: Results of an epidemiologic study of postdate pregnancy. J Reprod Med 31: 162, 1986


Freeman RK, Garite TJ, Modanlow H et al: Postdate pregnancy: Utilization of the contraction stress test for primary fetal surveillance. Am J Obstet Gynecol 140: 128, 1981


McClure-Browne JC: Postmaturity. Am J Obstet Gynecol 85: 573, 1963


Naeye RL: Causes of perinatal mortality excess in prolonged gestations. Am J Epidemiol 108: 429, 1978


AMG; Imezoglu. Induction of labour for improving birth outcomes for women at or beyond term. Cochrane Rev Abstract. 2007:2007 The Cochrane Collection, posted 7/1/07.


Zwerdling MA: Factors pertaining to prolonged pregnancy and its outcome. Pediatrics 40: 202, 1967


Hovi M, Raatikainen K, Heiskanen N, Heinonen S. Obstetric outcome in post-term pregnancies:time for reappraisal in clinical management. Acta Obstet Gynecol Scand 2006; 85(7):805-9


Beischer NA, Evans JH, Townsend L: Studies in prolonged pregnancy. I: Incidence of prolonged pregnancy. Am J Obstet Gynecol 103: 476, 1969


Clark S, Belfort M, Saade G et al: Implementation of a conservative checklist-based protocol for oxytocin administration: maternal and newborn outcomes. Am J Obstet Gynecol. 2007 Nov;197(5):480.e1-5.


Evans TN, Koeff ST, Morley GW: Fetal effects of prolonged pregnancy. Am J Obstet Gynecol 85: 701, 1965


Magram HM, Cavanaugh WV: The problem of postmaturity: A statistical analysis. Am J Obstet Gynecol 79: 216, 1963


Bruckner TA, Chen YW, Caughey AB. Increased neonatal mortality among normal weight births beyond 41 weeks of gestation in California. Am J Obstet Gynecol 2008; 199:421.e1-421.e7.


Bansal RK, Goldsmith PC, He Y et al: A decline in myometrial nitric oxide synthase expression is associated with labor and delivery. J Clin Invest 99: 2502, 1997


Leppert PC. Anatomy and physiology of cervical ripening. Clin Obstet Gynecol 1995; 38(2):267-79


Hofmeyr GJ, Gulmezoglu AM: Vaginal misoprostol for cervical ripening and induction of labour. Cochrane Database Syst Rev 2003;(1):CD000941


Young MC, Laurence KM, Hughes IA: Relationship between fetal adrenal morphology and anterior pituitary function. Horm Res 32: 130, 1989


Patel FA, Clifton VL, Chwalisz K et al: Steroid regulation of prostaglandin dehydrogenase activity and expression in human term placenta and chorio-decidua in relation to labor. J Clin Endocrinol Metab 84: 291, 1999


Oku M: Steroids' action on dependence of outset, maintenance of gravidity and onset of labor. Nippon Naibunpi Gakkai Zasshi 64: 51, 1988


Kawamura E, Hashino M, Akiyama T et al: Serum concentrations of delta 5C21 steroids during pregnancy and at delivery. Nippon Naibunpi Gakkai Zasshi 65: 1, 1989


Drost M, Holm LW: Prolonged gestation in ewes after foetal adrenalectomy. J Endocrinol 40: 293, 1968


McDonald TJ, Nathanielsz PW: Bilateral destruction of the fetal paraventricular nuclei prolongs gestation in sheep. Am J Obstet Gynecol 165: 764, 1991


Basset JM, Thorburn GD: Foetal plasma corticosteroids and initiation of parturition in sheep. J Endocrinol 44: 285, 1969


Nwosu VC, Wallach EE, Bolognese RJ: Initiation of labor by intraamniotic cortisol instillation in prolonged human pregnancy. Ostet Gynecol 47: 137, 1976


Gauthier RJ, Griego BD, Goebelsman U: Estriol in pregnancy. VII: Unconjugated plamsa estriol in prolonged gestation. Am J Obstet Gynecol 139: 382, 1981


Phelan JP: The postdate pregnancy: An overview. Clin Obstet Gynecol 32: 221, 1989


Flint APT: Regulation of placental enzymes. In MacDonald PD, Porter JC (eds): Initiation of Parturition: Prevention of Postmaturity. Fourth Ross Conference on Obstetrics Research. Columbus, OH, Ross Laboratories, 1983


Ballantyne JW: The problem of the postmature infant. Br J Obstet Gynaecol 2: 521, 1902


Grannum P, Berkowitz RL, Hobbins JC: The ultrasonic changes in the maturing placenta and their relation to fetal pulmonary maturity. Am J Obstet Gynecol 113: 915, 1979


Yeh S, Petrucha R, Platt LD: Possible role of ultrasonic placental grading in predicting fetal dysmaturity in postterm pregnancies. Proc Soc Perinat Obstet 139, 1982


Phelan JP, Smith CV, Broussard P et al: Amniotic fluid volume assessment using the four quadrant technique in the pregnancy between 36 and 42 weeks. J Reprod Med 32: 540, 1987


Horenstein JH, Brar HS, Devore GR et al: Cardiovascular evaluation of the postterm fetus. 34th Annual Meeting of the Society of Gynecologic Investigation. Atlanta, GA, March 18–21, 1987


Hopewood HG Jr: Shoulder dystocia: Fifteen years' experience in a community hospital. Am J Obstet Gynecol 142: 47, 1982


Warsof SL, Wolf P, Coulehan J et al: Comparison of fetal weight estimation formulas with and without head measurements. Obstet Gynecol 153: 57, 1985


Usher RH, Boyd ME, McLean FH, Kramer MS: Assessment of fetal risk in postdate pregnancies. Am J Obstet Gynecol 158: 259, 1988


Wenstrom KD, Parsons MT: The prevention of meconium aspiration in labor using amnioinfusion. Obstet Gynecol 73: 647, 1989


Lovell KE: The effect of postmaturity on the developing child. Med J Aust 1: 13, 1973


Field T, Dempsey J, Shumann HH: Five year follow-up of preterm respiratory distress syndrome and post-term postmaturity infants. In Field T, Sostek (eds): Infants Born at Risk. Philadelphia, Grune & Stratton, 1983


Ting RY, Wang MH, McNair-Scott TF: The dysmature infant: Associated factors and outcome at seven years of age. J Pediatr 90: 943, 1977


Shime J: Influence of prolonged pregnancy on infant development. J Reprod Med 33: 277, 1988


McKiddle JM: Fetal maturity in postmaturity. Br J Obstet Gynaecol 56: 386, 1949


Rathburn LS: An analysis of 250 cases of postmaturity. Am J Obstet Gynecol 46: 278, 1943


Martins CD, Marques AMD: Guidelines for induction of labor in prolonged pregnancy. Obstet Gynecol 34: 830, 1969


Dublin S, Lydon-Rochelle M, Kaplan RC et al: Maternal and neonatal outcomes after induction of labor without an identified indication. Am J Obstet Gynecol 2000; 183(4):986-94


Yeast JD, Jones A, Poskin M. Induction of labor and the relationship to cesarean delivery: A review of 7001 consecutive inductions. Am J Obstet Gynecol 1999; 180(3 Pt 1):628-33


Ahn MO, Phelan JP: Epidemiolgoic aspects of the postdate pregnancy. Clin Obstet Gynecol 32: 228, 1989


Guidetti DA, Divon MY, Langer O: Postdate fetal surveillance: Is 41 weeks too early? Am J Obstet Gynecol 161: 91, 1989


Freeman RK: The use of the oxytocin challenge test for antepartum clinical evaluation of uteroplacental respiratory function. Am J Obstet Gynecol 121: 481, 1975


Eden RD, Gergely RZ, Schifrin BS et al: Comparison of antepartum testing schemes for the management of the postdate pregnancy. Am J Obstet Gynecol 144: 683, 1983


Rochard F, Schifrin BS, Sureau C: Nonstressed fetal heart rate monitoring in the antepartum period. Am J Obstet Gynecol 126: 699, 1976


Schifrin BS, Guntes V, Gergely RZ et al: The role of real-time scanning in antenatal fetal surveillance. Am J Obstet Gynecol 140: 525, 1981


Johnson JM, Harman CR, Lange IR et al: Biophysical profile study in the management of the postterm pregnancy: An analysis of 307 patients. Am J Obstet Gynecol 154: 269, 1986


Manning FA, Platt LD, Sipos L: Antepartum fetal evaluation: Development of a fetal biophysical profile. Am J Obstet Gynecol 136: 787, 1980


Lagrew DC, Freeman RK: Management of the postdate pregnancy. Am J Obstet Gynecol 154: 1, 1986


Phelan JP, Platt LD, Yeh S et al: The role of ultrasound assessment of amniotic fluid volume in the management of the postdate pregnancy. Am J Obstet Gynecol 151: 304, 1985


Crowley P: Nonquantitative estimation of amniotic fluid volume in suspected prolonged pregnancy. J Perinat Med 8: 249, 1980


Erskine RL, Ritchie JW: Quantitative measurement of fetal blood flow using Doppler ultrasound. Br J Obstet Gynaecol 92: 600, 1985


Devine PA, Bracero LA, Lysikiewicz A et al: Middle cerebral to umbilical artery Doppler ratio in postdate pregnancies. Obstet Gynecol 84: 856, 1994


Sanchez Ramos L, Kaunitz, AM, Wears RL et al: Misoprostol for cervical ripening and labor induction: a meta-analysis. Obstet Gynecol 1997; 89:633-42


Parry E, Parry D, Pattison N: Induction of labour for post term pregnancy: an observational study. Aust N Z J Obstet Gynaecol 1998; 38(3):275-80


Fok WY, Chan LY, Tsui MH et al: When to induce labor for post-term? A study of induction at 41 weeks versus 42 weeks. Eur J Obstet Gynecol Reprod Biol 2006; 125(2):206-10. Epub 2005 Aug 31


Sue-A-Quan AK, Hannah ME, Cohen MM et al: Effect of labour induction on rates of stillbirth and cesarean section. CMAJ. 1999; 160(8):1145-9


Hopewood HG Jr: Shoulder dystocia: Fifteen years of experience in a community hospital. Am J Obstet Gynecol 144: 162, 1982


Chevernak JL, Divon MY, Hirsch J et al: Macrosomia in the postdate pregnancy: Is routine ultrasonographic screening indicated? Am J Obstet Gynecol 161: 753, 1989


National Institute of Child Health and Human Development Research Planning Workshop: Electronic fetal heart rate monitoring: Research guidelines for interpretation. Am J Obstet Gynecol 1997; 177(6):1385-90