Which of the following would be the best method for delaying the onset of labor?

Fetal Participation in the Onset of Labor

A fetal signal contributes to the onset of labor in animals and humans. Destruction of the paraventricular nucleus of the fetal hypothalamus results in prolongation of pregnancy in sheep. The human counterpart to this animal experiment is anencephaly, which is also characterized by prolonged pregnancy when women with polyhydramnios are excluded. The current paradigm is thatonce maturity has been reached, the fetal brain—specifically the hypothalamus—increases CRH secretion that, in turn, stimulates ACTH and cortisol production by the fetal adrenals. This increase of cortisol in sheep and of dehydroepiandrosterone sulfate in primates eventually leads to activation of the common pathway of parturition.

Maternal Factors

Premature onset of labor, prolonged (>24 hours) rupture of the membrane, clinically proven chorioamnionitis, colonization of the genital tract with pathogenic bacteria (e.g., group B streptococcus or E. coli), urinary tract infection, and sexual intercourse near the time of delivery are all independent risk factors for the development of neonatal infection. They increase the risk of infection by exposing the neonate to pathogens in utero as well as during vaginal delivery. In fact, these risk factors increase the rate of systemic infection more than 10-fold.129

Labor Progress: The Labor Curve

One of the central tasks of those providing intrapartum care is to determine whether labor is progressing normally and, if not, to determine the significance of the delay and what the response should be. Parity is an important determinant of labor length. (Parity refers to previous pregnancies of at least 20 weeks’ gestation. A pregnant woman who is gravida 2, para 1, is pregnant for the second time, and her first pregnancy resulted in delivery after 20 weeks’ gestation.)

A generation of obstetricians is indebted to Emanuel Friedman, whose landmark studies of labor provide a framework for judging labor progress. Friedman's approach was straightforward: He graphed cervical dilation on they-axis and elapsed time on thex-axis for thousands of labors. He considered nulliparous and parous patients separately, and he determined the statistical limits of normal.5 The curve of cervical dilation over time is sigmoid shaped (Fig. 18.5).

Most authorities consider Friedman's most important contribution to be his separation of the latent phase from the active phase of the first stage of labor. Many hours of regular, painful uterine contractions may take place with little appreciable change in the cervix. During this latent (or preparatory) phase, the cervix may efface and become softer. Quite abruptly, the active (or dilation) phase begins, and regular increases in cervical dilation are expected over time. The transition from the latent to the active phase of the first stage of labor does not occur at an arbitrary cervical dilation but rather is known—in retrospect—by change in slope of the cervical dilation curve. Peisner and Rosen6 evaluated the progress of labor for 1060 nulliparous women and 639 parous women. After excluding women with protracted or arrested labor, these researchers noted that 60% of the women had reached the latent-active phase transition by 4 cm of cervical dilation and 89% did so by 5 cm.

Anulliparous woman may labor for 20 hours without achieving appreciable cervical dilation; 14 hours is the limit of the latent phase in theparous woman. Difficulty in assigning length to the latent phase lies not with its end (determined from the change in slope of the cervical dilation curve) but rather with its beginning. The onset of labor is self-reported by the parturient. The uterus contracts throughout gestation, and the level of prelabor uterine activity and its perception are variable. Often both the patient and the physician are uncertain as to exactly when labor started.

According to Friedman, in the active phase of the first stage of labor, a nulliparous woman's cervix should dilate at a rate of at least 1.2 cm per hour, and a parous woman's cervix should dilate at least 1.5 cm per hour. (The slopes of the dilation curves inFig. 18.5 represent the lower limits of normal.) If a woman's cervix fails to dilate at the appropriate rate during the active phase of labor, she is said to haveprimary dysfunctional labor. Graphically, her cervical dilation “falls off the curve.” If cervical dilation ceases during a 2-hour period in the active phase of labor,secondary arrest of dilation has occurred.

I. DEFINITION, CAUSES, AND EFFECTS

The OP position occurs when the occipital portion of the fetal head presents in the posterior portion of the birth canal. This malposition is a common challenge for the clinician to recognize and manage.

Key Points

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Neuraxial analgesia is the most effective form of intrapartum analgesia currently available.

In most cases, maternal request for pain relief represents a sufficient indication for the administration of neuraxial analgesia.

The safe administration of neuraxial analgesia requires a thorough (albeit directed) preanesthetic evaluation and the immediate availability of appropriate resuscitation equipment.

Neuraxial labor analgesia is not a generic procedure. The procedure should be tailored to individual patient needs.

The administration of the epidural test dose should allow the anesthesia provider to recognize most cases of unintentional intravascular or intrathecal placement of the epidural catheter. All therapeutic doses of local anesthetic should be administered incrementally.

Bupivacaine is the local anesthetic most often used for epidural analgesia during labor in the United States. Ropivacaine and levobupivacaine are satisfactory alternatives. Most anesthesia providers reserve 2-chloroprocaine and lidocaine for cases that require the rapid extension of epidural anesthesia for vaginal or cesarean delivery.

The addition of a lipid-soluble opioid to a neuraxial local anesthetic allows the anesthesia provider to provide excellent analgesia while reducing the total dose of local anesthetic and minimizing the side effects of each agent. Perhaps the major advantage of this technique is that the severity of motor block can be minimized during labor.

Intrathecal opioids alone may provide complete analgesia during the early first stage of labor. Epidural opioids without local anesthetic do not provide complete analgesia during labor.

Administration of a local anesthetic (with or without an opioid) is necessary to provide complete neuraxial analgesia for the late first stage and the second stage of labor. Although a neuraxial local anesthetic alone can provide complete analgesia, the required dose is often associated with an undesirably dense degree of motor blockade.

Hypotension is a common side effect of neuraxial analgesia. Prophylaxis and treatment involve the avoidance of aortocaval compression and the administration of a vasopressor as needed. The administration of an intravenous fluid “preload” does not significantly decrease the incidence of hypotension in euvolemic patients.

Other potential side effects of neuraxial analgesia include pruritus, shivering, urinary retention, delayed gastric emptying, maternal fever, and fetal heart rate changes.

Complications of neuraxial analgesia include inadequate analgesia, unintentional dural puncture, respiratory depression, unintentional intravenous injection, and extensive or total spinal anesthesia.

The presence of severe pain during early labor—and/or an increase in local anesthetic/opioid dose requirement—may signal a higher risk for prolonged labor and operative delivery.

Neuraxial labor analgesia does not result in a higher rate of cesarean delivery than systemic opioid analgesia.

Initiation of neuraxial analgesia in early labor (cervical dilation less than 4 to 5 cm) does not increase the rate of cesarean delivery or prolong the duration of labor.

Effective neuraxial analgesia likely results in a modest prolongation of the second stage of labor.

Controversy exists as to whether there is a cause-and-effect relationship between neuraxial labor analgesia and risk for instrumental vaginal delivery. Dense neuroblockade (e.g., presence of significant motor blockade) and complete analgesia during the second stage of labor probably increase the rate of instrumental vaginal delivery. Use of a dilute solution of local anesthetic and opioid is less likely to adversely affect the progress of labor.

Maternal-fetal factors and obstetric management—not the use of neuraxial analgesia—are the most important determinants of the cesarean delivery rate.

Intrapartum History

The time from the onset of labor to delivery is the period of greatest vulnerability of the fetus to infection and asphyxia. However, the results of the Collaborative Perinatal Study as reported by Nelson and collaborators in a series of papers highlighted the difficulty in relating specific events during labor and delivery and outcome. An established association does not exist between specific obstetrical complication and a bad neurological outcome in term newborns. Cerebral palsy occurs in only 2% of surviving newborns whose fetal heart rate had been less than 60 per minute. In a prospective study of almost 3000 labors and deliveries, the incidence of meconium staining of the amniotic fluid was 22%. However, only 0.4% of term newborns with meconium-stained amniotic fluid later showed cerebral palsy.

Onset and Events of Labor

The timing of the onset of labor and the events that occur around it are important. Examples are an automobile accident, premature rupture of membranes, and sharp, near-continuous low back pain with vaginal bleeding. Indications for risk of acute infections in the fetus should be sought. Has the mother had a recent infection? Did she have a fever around the time of delivery? The diagnosis of maternal chorioamnionitis has been associated with a high risk of neonatal encephalopathy and cerebral palsy. Has the mother received antibiotics? How long did labor last, and how long were the membranes ruptured before delivery?

The fetal heart rate in conjunction with uterine contractions is the best signal during labor of the condition of the fetus (see Chapter 13). Adjuncts include the use of fetal scalp pH monitoring.

The presentation of the fetus in the birth canal and the route of delivery are of obvious importance. Breech position occurs in 8% of women in labor. In approximately 25% of breech deliveries, conditions such as placenta previa, malformations of the fetus or uterus, twinning, and premature labor may coexist. Risks of vaginal delivery for the fetus in the breech position include prolapse of the cord, trapping of the head at the level of the cervix, asphyxia, trauma, and congenital hip dysplasia.

A. Antenatal Prevention

Altered vaginal microflora before the onset of labor (e.g., BV; heavy vaginal colonization by Streptococcus agalactiae, Streptococcus pyogenes, or E. coli) has been associated with greater rates of endometritis.2 In one cohort study with 924 patients enrolled, the risk for postpartum endometritis was tripled among women with BV in early pregnancy (RR, 3.26).10 However, no trials to date have demonstrated that screening for and treating BV reduces infectious complications.11

A Cochrane analysis that examined 6 RCTs, involving 2184 women, concluded that in high-risk patients, defined as those with a previous preterm birth, antibiotic prophylaxis in the second and third trimester results in a reduced risk for postpartum endometritis (odds ratio [OR], 0.46; 95% confidence interval, 0.24-0.89).12 These studies used various antibiotics and delivery units. Thus, the ideal prophylactic regimen remains uncertain.

Premature rupture of membranes

Amniotic sac rupture before the onset of labor (premature rupture of membranes, PROM) before 37 weeks gestation occurs in about 3% of pregnancies in the United States [57]. At term, PROM occurs in approximately 8% of pregnancies and is generally followed by spontaneous labor and delivery. Regardless of term, the greatest maternal risk is intrauterine infection. In preterm PROM, the risks to the fetus (in addition to intraamniotic infection) are generally complications associated with premature birth, and treatment is accordingly focused on extending gestation to the extent possible. While there are many risk factors, including smoking, low body mass index, history of PROM, and intraamniotic infection, PROM often occurs in individuals with no risk factors.

Often PROM is confirmed visually by direct observation of amniotic fluid pooling in the vaginal canal but in less clear cases, laboratory testing may be required to determine whether a rupture has occurred. Fetal fibronectin, described earlier, is an effective rule-out as a negative result strongly suggests intact membranes. Fern tests, in which dried vaginal fluids are observed microscopically for a characteristic arborization or “ferning” indicative of amniotic fluid, are simple to perform and suggestive of PROM. Vaginal pH testing with nitrazine pH paper is a similarly simple test and normal vaginal secretions are in the pH range of 4.5–6.0, while amniotic fluid has a typical range of 7.1–7.3. However, false positives can occur due to the presence of blood or semen, vaginal infection, or use of alkaline antiseptics, and in extreme cases of prolonged membrane rupture, there may not be sufficient amniotic fluid remaining to influence the pH.

Tests for amniotic proteins are also available. The most widely utilized of these is for placental alpha-microglobulin-1, which is present in 40–5000-fold greater concentrations in amniotic fluid than in maternal blood [58]. However, while their sensitivity is reported to be quite high, false-positive rates of 19%–30% have been observed clinically, and the ACOG recommends that they be used as ancillary diagnostics alongside the standard methods outlined above.

Epidemiology of Preterm Birth

PTL is defined as the onset of labor before 37 completed weeks of gestation. It accounts for 6% to 10% of all births in Western countries and more than 75% of all perinatal deaths. PTL, spontaneous or induced, or a planned cesarean section due to maternal or fetal complications can result in preterm birth.1 It is estimated that up to 30% to 40% of all cases are induced or elective and the remaining 60% to 70% occur spontaneously.2 Epidemiologic studies of PTL vary in terms of categorization, but generally labor at less than 23 to 24 weeks is considered previable, less than 28 weeks is extremely preterm, 28 to 31 weeks very preterm, and 32 to 36 weeks mildly preterm.3 Preterm delivery is a major cause of neonatal morbidity and mortality, accounting for 65% of neonatal deaths and 50% of childhood neurologic disabilities. Prematurity is the biggest single cause of death within the first year of life. Survival rates are determined by gestation and birth weight.4 Intraventricular hemorrhages occur in 25% to 30% of very low-birth-weight neonates,5 compared with 3% to 4% of term babies. Many of these preterm infants develop cerebral palsy, hydrocephalus, and seizures.6 The risks of major long-term morbidities following preterm birth after 34 weeks are considered to be comparable to those after 37 weeks' gestation, although a significant risk of minor morbidities remains.5,7 Although not identifiable in a significant proportion of women with PTL, risk factors include primigravida pregnancy, cervical incompetence or insufficiency, uterine distension (multiple pregnancy or polyhydramnios), infection, uterine and placental abnormalities, a previous history of preterm birth or second-trimester pregnancy loss, age, race, socioeconomic status, and body mass index (BMI).1 In the United Kingdom, the risk of preterm birth is 6% in white Europeans but 10% in Africans or Afro-Caribbeans.8 Similarly, African-American women are overrepresented in rates of preterm birth in the United States. A poorer socioeconomic status in such groups and other minority groups adds environmental causes to probable genetic causes of preterm birth (i.e., polymorphisms in tumor necrosis factor [TNF]-α, a proinflammatory cytokine).9 Other environmental factors include nutrition, smoking, substance abuse, and psychosocial factors.1

There are strong associations with preterm birth in women with diabetes, a low BMI, poor weight gain or excess weight gain, diabetes, and obesity.10,11 Alcohol consumption, smoking, and cocaine use all increase the risk of preterm birth. Dose-response effects have been described in alcohol consumption in various European studies, as well as increased risks from low to moderate and heavy smoking.12-14 Maternal stress is considered to increase the risk of preterm birth via a neuroendocrine pathway that activates the maternal-placental-fetal endocrine systems that promote parturition via immune and/or inflammatory pathway activation.15