19.

2
News from UpToDate | Contact us | About UpToDate | Help


New Search

Patient Info

What's New

Calculators

My Account


Feedback Log Out
SearchAll Topics
endocrinolo

Back to Search Results for "endocrinology parturition"
Abnormal labor: Protraction and arrest disorders
Find Print
Abnormal labor: Protraction and arrest disorders
Authors
Robert M Ehsanipoor, MD
Andrew J Satin, MD, FACOG
Section Editor
Charles J Lockwood, MD
Deputy Editor
Vanessa A Barss, MD
Disclosures
Last literature review version 19.2: May 2011 | This topic last updated: June 8,
2011 (More)
INTRODUCTION Labor refers to uterine contractions resulting in progressive dilation
and effacement of the cervix, accompanied by descent and expulsion of the fetus.
Abnormal labor, dystocia, and failure to progress are imprecise terms that are used to
describe a labor pattern which deviates from that observed in the majority of women
who have spontaneous vaginal deliveries. More useful terminology is to characterize
labor abnormalities as protraction disorders (ie, slower than normal progress) or arrest
disorders (ie, complete cessation of progress).
These disorders are the most common indication for primary cesarean delivery. In one
study of 733 women who had unplanned cesareans, 68 percent of the deliveries were
due to lack of progress in labor [1].
PREVALENCE Protraction and arrest disorders are common. Reported incidences vary
among studies due to differences in the authors definition of dystocia, as well as
differences among study populations (eg, gestational age range, personal
characteristics). About 20 percent of all labors ending in a live birth involve a protraction
and/or arrest disorder [2]. The risk is highest in nulliparous women with term
pregnancies. As an example, a prospective Danish study in low risk nulliparas at term
reported an incidence of 37 percent [3].
NORMAL LABOR Assessing whether labor is progressing normally is a key
component of intrapartum care; however, determining the onset of labor, measuring its
progress, and evaluating the factors that affect its course (power, passenger, pelvis) is
an inexact science.
Definitions
There are three stages of labor:
First stage Time from onset of contractions to complete cervical dilation.
However, the precise time of onset of contractions is difficult to determine
since the uterus normally contracts irregularly.
Second stage Time from complete cervical dilation to expulsion of the fetus.
Third stage Time from expulsion of the fetus to expulsion of the placenta.
There are two phases of labor:
Latent phase The onset of labor begins when the mother perceives regular
contractions, which are typically mild and infrequent. The accompanying
change in cervical dilation and effacement is gradual, less than 1 cm dilation
over a single hour. The concept of a latent phase of labor is controversial, as it
can be difficult to precisely determine the time of onset of contractions and the
time of transition to active phase.
Active phase The active phase is characterized by painful contractions of
increasing frequency, intensity, and duration accompanied by more rapid
cervical change (at least 1 cm/hour), which accelerates as the active phase
progresses.
Friedman's data In the mid-1950s, Emanuel Friedman conducted his now classic
studies attempting to define the spectrum of normal labor [4,5]. He evaluated the course
of labor of 500 primigravidas admitted to the Sloane Hospital for Women in New York.
The Friedman curve and the norms established from his data have historically been
widely accepted as the standard for assessment of normal labor progression.
Friedman divided labor into a first and second stage. The first stage of labor was further
divided into the latent phase, acceleration phase, phase of maximum slope, and a
deceleration phase (figure 1). Based on his data, the transition from the latent phase to
the acceleration phase appeared to occur at 3 to 4 cm cervical dilation and the minimum
rate of acceptable cervical dilation during the active phase of labor was 1.2 cm/hour for
nulliparous patients and 1.5 cm/hour for multiparous patients [6].
The applicability of the Friedman curve and its established norms to contemporary
obstetric practice has recently been challenged. Several studies have evaluated labor
curves and tried to establish contemporary thresholds for normal labor progression [7-
9]. The new thresholds are somewhat different from those cited by Friedman for several
reasons. Clearly, there have been significant changes in patient characteristics,
anesthesia practices, and obstetric practices over the past half century. In addition, a
limitation of Friedmans findings is that his data are based on labors in only 500 women
who were managed at a single institution.
Friedman versus contemporary data
Labor curve Zhang and colleagues determined normal labor patterns by evaluating
contemporary data from the Consortium on Safe Labor, which included information on
62,415 singleton cephalic vaginal deliveries with spontaneous onset of labor and normal
neonatal outcome [8]. The data were collected retrospectively from the electronic
medical records at 19 medical centers in the United States.
The shape of the labor curve generated from Zhangs data (figure 1) is different from
Friedmans (figure 2). The Friedman curve depicts a relatively slow rate of cervical
dilation until approximately 4 cm (ie, latent labor), which is followed by an abrupt
acceleration in the rate of dilation until a deceleration phase at approximately 9 cm.
Zhangs curves also demonstrate an increase in the rate of cervical dilation as labor
progresses, but the increase appears to be more gradual, and greater than 50 percent of
patients do not dilate at a rate of >1 cm/hour until 5 to 6 cm dilation. They did not
observe a deceleration phase at the end of the first stage of labor.
Labor curves have been constructed from other data sets, as well, and the shapes of
these curves generally are different from Friedmans curve [7,9,10]. Specifically, there
does not appear to be an abrupt change in the rate of cervical dilation indicating a clear
transition from latent to active labor and there also does not appear to be a deceleration
phase at the end of the first stage of labor. While the presence of a deceleration phase is
not of major clinical significance, defining a point in labor at which rapid cervical change
is expected (active labor) is clinically relevant.
Other authors contemporary data also suggest that the rate of cervical change between
3 and 6 cm is likely much slower than previously thought [9,11]. It is normal for women
who go on to have normal labors and deliveries to have rates of cervical dilation that are
less than 1 cm per hour prior to 5 to 6 cm (table 1). Both nulliparas and multiparas may
take more than six hours to dilate from 4 to 5 cm and more than three hours to dilate
from 5 to 6 cm [8]. However, beyond a dilation of 6 cm, rates of cervical dilation are
more rapid for multiparous women.
Duration of the latent phase and the first stage As discussed above, the concept
of a latent phase of labor is controversial, as it can be difficult to pinpoint both the time
of onset of contractions and the transition to the active phase. For these reasons, the
duration of the latent phase and the first stage of labor are also difficult to determine.
Assessment of the active phase and second stage of labor are clinically more useful.
Duration of the active phase According to Friedman, the mean (95th percentile)
duration of the active phase in nulliparous and parous women was 4.6 hours (11.7) and
2.4 hours (5.2), respectively [6].
Most contemporary studies suggest that the upper limit of a normal active phase is
longer [7,10,12-14]. Zhang found that the median (95th percentile) duration of time for
the cervix to dilate from 4 to 10 cm in nulliparas and multiparas was 5.3 hours (16.4)
and 3.8 hours (15.7), respectively [8].
Duration of the second stage Type of analgesia, duration of the first stage, parity,
maternal habitus, birth weight, and station at complete dilation all play a role in
predicting the duration of the second stage [15]. For this reason, the American College
of Obstetricians and Gynecologists (ACOG) recommends that the normal duration of
second stage of labor be based upon parity and presence of regional anesthesia, with no
intervention as long as the fetal heart rate pattern is normal and some degree of
progress is observed [16]. Induction does not affect the duration of the second stage of
labor. (See "Induction of labor", section on 'Failed induction'.).
Friedman defined an abnormally long second stage for nulliparas and multiparas as three
hours and one hour, respectively. This conclusion was derived when many of the
variables described above (eg, maternal habitus, type and use of analgesia) were
different from those in contemporary practice.
Zhang found that the median (95th percentile) duration of the second stage in
nulliparous and parous women with epidural anesthesia was 1.1 hours (3.6) and 0.4
hours (2.0), respectively [8]. Without epidural anesthesia, the median (95th percentile)
was 0.6 hours (2.8) and 0.2 hours (1.3), respectively.
DIAGNOSIS OF LABOR ABNORMALITIES One practical system for diagnosing
labor abnormalities is to classify them as either protracted or arrested labor. Protraction
and arrest can occur anytime during labor. The thresholds are defined according to the
phase or stage of labor when they occur.
Active phase As discussed above, Friedman considered the minimum rate of
acceptable cervical dilation during the active phase of labor to be 1.2 cm/hour for
nulliparous patients and 1.5 cm/hour for multiparous patients [6]. A slower rate of
cervical dilation was diagnostic of protracted labor. A difficulty with this system is the
inability to accurately define when a patient enters active labor.
The following table serves as a better guide for determining whether labor progress is
within the normal range or protracted (table 1). It is based on Zhangs studies showing
that rates of dilation in the first stage slower than those shown in the table are
suggestive of a protraction disorder [8]. These studies demonstrated that labor may take
more than six hours to progress from 4 to 5 cm and more than three hours to progress
from 5 to 6 cm, regardless of parity. Labor accelerates much faster after 6 cm, and is
significantly faster in multiparas compared to nulliparas at this dilation.
An arrest disorder has traditionally been defined as a cervix that ceases to dilate after
reaching 4 cm dilation despite adequate uterine contractions (greater than or equal to
200 Montevideo units for two or more hours) [16]. Zhangs studies suggest that it is
more reasonable to wait until cervical dilation ceases after reaching 5 to 6 cm dilation
before establishing the diagnosis [8].
Second stage In the second stage of labor, protracted labor has traditionally been
defined as a second stage longer than two hours in nulliparas (three hours when regional
analgesia is used), and longer than one hour in multiparas (two hours when regional
analgesia is used) [16].
Zhangs studies suggest that many women will have successful vaginal deliveries with
second stages longer than these times (table 1) [8], thus intervention is not necessarily
indicated as long as labor appears to be progressing and the fetal heart rate pattern is
reassuring. In this system, a protracted second stage in nulliparous women is defined as
over 3.5 hours with epidural anesthesia and over 2.5 to 3 hours without epidural
anesthesia; in multiparous women, these times would be about 2 hours and 1 hour,
respectively.
An arrest of descent can be diagnosed after one hour if there is no descent, despite good
maternal pushing efforts.
Precipitous labor Of note, labor can be abnormally fast, as well as slow. The term
precipitate or precipitous labor has been defined as a labor that lasts no more than three
hours from onset of contractions to delivery.
Partogram Management of labor includes several components: a disciplined
approach to the diagnosis of labor, assessment of maternal and fetal well-being, and
careful monitoring of labor progress. Once active labor is diagnosed, serial cervical
examinations are performed to determine whether progression is adequate [6]. The
results can be noted on a partogram, which is a graphical representation that clearly
shows the patient's labor in comparison to the expected lower limit of "normal progress."
The following figure is a partogram for the slowest 95th percentile in labor progress
based on dilation at the time of admission (graph 1) [8]. Deviation from this curve is
diagnostic of a protraction or arrest disorder.
ETIOLOGY Abnormal labor can be the result of one or more abnormalities of the
cervix, uterus, maternal pelvis, or fetus (ie, power, passenger, or pelvis). As an
example, women with very long cervices in mid-pregnancy are more likely to experience
poor progress during labor and cesarean delivery, which suggests that cervical changes
in preparation for delivery begin as early as the second trimester [17]. Interestingly, a
genetic component has been purported to account for 28 percent of the susceptibility to
prolonged and difficult labor [18]. Risk factors for abnormal labor are shown in the table
(table 2) [16,19].
Hypocontractile uterine activity Hypocontractile uterine activity is the most
common cause of protraction and/or arrest disorders in the first stage of labor. This
entity refers to uterine activity that is either not sufficiently strong or not appropriately
coordinated to dilate the cervix and expel the fetus. It occurs in 3 to 8 percent of
parturients and has been defined as uterine contraction pressures less than 200
Montevideo units.
Normal uterine activity Uterine activity can be monitored by palpation, external
tocodynamometry, or internal uterine pressure catheters. External and intrauterine
monitoring devices appear to perform equally well, although the latter may work better
in obese women [20].
Ninety-five percent of women in active labor will have three to five contractions per 10
minutes. Although numerous methods for quantifying uterine activity have been
reported, Montevideo units (ie, the peak strength of contractions in mmHg measured by
an internal monitor multiplied by their frequency per 10 minutes) are most often
employed. In a retrospective report, 91 percent of women in spontaneous active labor
achieved contractile activity greater than 200 Montevideo units and 40 percent reached
300 Montevideo units [21].
Intrauterine pressure catheter Clinically, an intrauterine pressure catheter (IUPC)
can be helpful, but is not mandatory, in diagnosis and management of hypocontractile
uterine activity, particularly in patients in whom it is difficult to monitor contractions
externally [16,22,23]. A large randomized trial showed there was no reduction in the
rate of operative delivery (cesarean or instrumental vaginal) or improvement in perinatal
outcome attributable to use of intrauterine catheters for measuring uterine activity [24].
(See "Insertion of intrauterine pressure catheters".)
Neuraxial anesthesia The potential impact of neuraxial anesthesia on uterine
activity, fetal malposition, and, ultimately arrest disorders, has received much attention
as a possible source of increasing rates of cesarean delivery. A Cochrane review of
randomized trials concluded that neuraxial anesthesia compared to non-neuraxial
anesthesia or no analgesia is not associated with a significant increase in duration of the
first of labor (weighted mean difference [WMD] 23.8 minutes; 95% CI -18.9 to 66.51) or
cesarean delivery (RR 1.07; 95% CI 0.93-1.23) [25]. There were small but statistically
significant increases in the second stage of labor (WMD 15.6 minutes; 95% CI 7.5-23.6)
and use of oxytocin (RR 1.18 95% CI 1.03-1.34), but these findings are of questionable
clinical significance. Women receiving neuraxial anesthesia were more likely to undergo
operative vaginal delivery (RR 1.38; 95% CI 1.24 to 1.53).
It is possible that recent changes in neuraxial technique or drugs (eg, use of narcotics or
low-dose anesthetics) could affect these findings. The consequences of withdrawing the
block before the second stage of labor, appropriate use of oxytocin, delayed pushing in
the second stage, and timing of administration also need to be considered.
(See "Adverse effects of neuraxial analgesia and anesthesia for obstetrics", section on
'Effect of neuraxial analgesia on labor and delivery'.)
ACOG has stated that the decision to place a neuraxial anesthetic should depend upon
the patient's wishes with consideration of factors, such as parity, also taken into account
[26]. In particular, women should not be required to reach an arbitrary cervical dilation,
such as 4 to 5 cm, before receiving neuraxial anesthesia.
Cephalopelvic disproportion (CPD) A disproportion in the size of the fetus relative
to the mother can result in dystocia. The term CPD was originally used to describe
disparity between the size of the fetus and maternal pelvis. In contemporary practice,
this diagnosis is often based upon observation of protracted or arrested labor during the
active phase. In this circumstance, it is often due to fetal malposition (eg, extended or
asynclitic fetal head) or malpresentation (mentum posterior, brow) rather than a true
disparity between fetal size and maternal pelvic dimensions.
Antepartum, the clinician's ability to predict maternal pelvis-fetal size discordance
leading to arrest of labor requiring cesarean delivery has been disappointing. Clinical and
radiologic assessment of the maternal pelvis and fetal size are inexact with poor
predictive value [27,28].
Intrapartum, both abnormal progress of labor and certain physical findings support the
diagnosis of CPD. The soft bones and open sutures of the fetal skull allow it to change in
shape (ie, mold) and thus adapt to the maternal pelvis during descent. Some overlap of
the parietal and occipital bones at the lambdoid sutures and overlap of the parietal and
frontal bones at the coronal sutures are common in normal labor (figure 3) [28].
However, protracted or arrested descent with increased molding, especially overlap of
the parietal bones at the sagittal suture, is suggestive of CPD.
Malpositions and malpresentations are discussed in detail separately. (See individual
topic reviews).
Bandl's ring An hourglass constriction ring of the uterus, called Bandl's ring, is a rare
pregnancy complication associated with obstructed labor [29-31]. The constriction forms
between the upper contractile portion of the uterus and the lower uterine segment. It is
not clear if it is the cause or the result of the associated dystocia. It may also occur
between delivery of the first and second twin. Diagnosis is typically made at cesarean
delivery. At the time of laparotomy, a transverse thickened muscular band can be
observed separating the upper and lower segment of the uterus.
Occiput posterior (OP) position Persistent OP position is associated with longer
duration of active labor and the second stage, as well as a higher risk of arrest of
descent requiring operative delivery [32-34]. The length of the second stage appears to
correlate with the degree of rotation away from occiput anterior (OA). Among nulliparous
women under neuraxial anesthesia who began pushing at full dilation, the mean duration
of the second stage for OA, occiput transverse (OT), and OP positions was 2.2, 2.5, and
3.0 hours, respectively, and the cesarean delivery rates were 3.4, 6.9, and 15.2 percent,
respectively [35]. (See "Management of the fetus in occiput posterior position", section
on 'Risk factors and consequences'.)
MANAGEMENT Management of protraction and arrest disorders depends on the
etiology and stage/phase of labor.
Patients with protracted latent phase Some women do not transition to the active
phase despite many hours of contractions. As discussed above, the concept of a latent
phase of labor is controversial, as it can be difficult to precisely determine the time of
onset of contractions, the time of transition to active phase, and the cervical dilation
when this transition should occur. The diagnosis and management of latent phase of
labor abnormalities are reviewed separately. (See "Latent phase of labor".)
Patients with protracted active phase The optimal management of poor labor
progression in the active phase is to confirm that the patient is in the active phase
(cervix is at least 5 to 6 cm), administer oxytocin, and wait four hours. The evidence for
this recommendation is described in the following sections.
A meta-analysis of randomized trials found that early initiation of oxytocin as soon as
progress was slower than predefined criteria rather than conservative measures (eg,
oxytocin deferred for 4 hours, ambulation) appeared to modestly improve the
probability of spontaneous vaginal delivery (RR 1.09. 95% CI 1.03-1.17) and reduce
antibiotic use (RR 0.45. 95%CI 0.21-0.99) [36]. In these trials, oxytocin was initiated
without consideration of baseline uterine activity and membrane status was the same in
both groups.
Oxytocin augmentation Oxytocin is the only medication approved by the US Food
and Drug Administration (FDA) for labor stimulation in the active phase. It is typically
dosed to effect, as predicting a women's response to a particular dose is not possible
[37]. Numerous oxytocin protocols that vary in initial dose, incremental dose increase,
and time interval between doses have been studied (table 3). These oxytocin protocols
may be used in both nulliparas and multiparas [22,38,39]. We do not alter our
management based on parity with one important exception: we do not use a high dose
regimen in women with a previous cesarean [38].
High dose regimens have been associated with a high incidence of uterine tachysystole
(>5 contractions in 10 minutes, averaged over a 30-minute window). Low dose regimens
were developed, in part, to avoid uterine tachysystole and are based upon the
observation that it takes 40 to 60 minutes to reach steady state oxytocin levels in
maternal serum [40]. A systematic review of randomized trials of high versus low dose
oxytocin for augmentation of women in spontaneous labor (10 trials, n = 5423 women)
found that high dose oxytocin:
Decreased the cesarean delivery rate (RR 0.85, 95% CI 0.75-0.97) and increased
the rate of spontaneous vaginal delivery (RR 1.07, 95% CI 1.02-1.12)
Decreased the total duration of labor (mean difference -1.54 hours, 95% CI -2.44
to -0.64 hours)
Increased the frequency of tachysystole (RR 1.91, 95% CI 1.49-2.45)
Resulted in similar maternal and neonatal morbidities
The decision to use a high versus a low dose oxytocin regimen poses a risk benefit
dilemma: higher dose regimens are associated with shorter labor and fewer cesareans,
but more tachysystole. The value placed on each of these outcomes and the ability to
respond to tachysystole may vary among labor and delivery units. Thus, either a high or
low dose oxytocin regimen is acceptable.
Assessing progress after initiating oxytocin Traditionally, active phase arrest has
been diagnosed when slow cervical dilation is not corrected by oxytocin therapy that
achieves 200 Montevideo units for two hours; cesarean delivery is often performed at
this point. However, the two-hour threshold is not highly predictive that the patient will
fail to deliver vaginally. A better threshold is a minimum change in cervical dilation of 2
cm over four hours [23,41].
This was illustrated in a prospective trial of 542 women with slow labors in which the
obstetrician waited four to six hours (instead of two) before performing intervening
surgically [22]. Among women with persistent slow progress despite two hours of
oxytocin administration, vaginal deliveries occurred in 91 percent of multiparas and 74
percent of nulliparas. Among women with persistent slow progress despite four hours of
oxytocin administration, vaginal deliveries occurred in 88 percent of multiparas and 56
percent of nulliparas. These findings suggested that extending the minimum period of
oxytocin augmentation for active phase labor arrest from two hours to at least four
hours was safe and increased the rate of vaginal delivery.
The same investigators subsequently used a standardized protocol to manage 501
consecutive, term, spontaneously laboring women with slow progress in labor [23]. The
protocol involved administration of oxytocin to achieve at least 200 Montevideo units for
four hours before considering cesarean delivery. Vaginal delivery occurred in about 80
percent of nulliparous women and 95 percent of multiparous women, whether or not
they were able to achieve and/or maintain the Montevideo unit goal. Mean (5th
percentile) rates of cervical dilation in nulliparas and multiparas were 1.4 cm/h (0.5) and
1.8 cm/h (0.5), respectively. This study confirmed that oxytocin augmentation of a
protraction disorder for at least four hours is both safe and effective for achieving vaginal
delivery. It also showed that success was often possible despite levels of uterine activity
and rates of cervical dilation that were below the normal range considered effective.
Other approaches
Amniotomy There is evidence from randomized trials that routine amniotomy
does not accelerate spontaneous labor [42], but no trials have compared
amniotomy with no intervention for management of women with intact
membranes and established labor abnormalities.
Prostaglandins Prostaglandins are typically used for cervical ripening and labor
induction; there are sparse data on their safety and efficacy for treatment of
protraction disorders. A single trial randomly assigned 332 term nulliparas with
protracted active phase of labor (defined as <2 cm dilation over four hours) to
receive a single dose of one of three vaginal gels: prostaglandin E2 (1 mg),
prostaglandin E2 (2 mg), or placebo [43]. The mean cervical dilation at
randomization was 2.8 cm and all cervices were <5 cm. Compared to the
placebo group, the prostaglandin groups had a higher proportion of patients
achieving a fast rate of cervical dilation (50 versus 30 percent) and the time
from randomization to delivery was shorter (11 versus 13 hours).

However, the proportion of patients whose dystocia resolved was similar to that
seen in patients treated with early assisted rupture of membranes and
oxytocin. In addition, there was no improvement in the overall rate of vaginal
delivery in women receiving prostaglandins versus placebo. Cesarean delivery
rates in the first stage of labor were equal in all three groups, but there was a
significant increase in cesareans in the second stage in women receiving
prostaglandins. Given these findings, we prefer oxytocin over prostaglandins
for treatment of protraction disorders.
Ambulation [44] and continuous labor support [45] may increase the comfort of
the parturient, but there is no evidence that they are clinically effective for
treatment of established protraction or arrest disorders [16].
Poor progression in the second stage A prolonged second stage of labor (table 1)
warrants clinical reassessment of the mother, fetus, and expulsive forces. A variety of
factors should be considered when determining when and how to intervene for slow
descent in the second stage of labor. These factors include the degree to which
macrosomia is suspected, adequacy of the pelvis, the fetal heart rate tracing, and
maternal pushing efforts.
Prompt use of an appropriate method of operative intervention is indicated for those
fetuses with nonreassuring fetal heart rate tracings. An appropriate method of operative
intervention is also indicated when cephalopelvic disproportion is likely because of
macrosomia, malposition, or a clinically small maternal pelvis. Radiographic pelvimetry is
of no value and is not recommended [27]. (See "Occiput transverse
position" and "Management of the fetus in occiput posterior position" and "Fetal
macrosomia" and "Timing and route of delivery in pregnancies at risk of shoulder
dystocia".)
Pregnancies with reassuring fetal heart rate patterns can be managed expectantly if
progress is being made. Hypocontractile uterine activity should be treated with oxytocin.
A prolonged second stage does not appear to be an independent risk factor for neonatal
morbidity, with the possible exception of brachial plexus injury [16,46,47]. A relationship
between a prolonged second stage and shoulder dystocia has been reported, but
inconsistently.
On the other hand, a prolonged second stage has been associated with increased
maternal risks (chorioamnionitis, postpartum hemorrhage, operative vaginal delivery,
third/fourth degree perineal lacerations [19,47-51]). For example, in one study of
women with second stages less than and more than three hours, the rate of
chorioamnionitis was 3.1 and 12.5 percent, respectively and uterine atony was 3.5 and
7.8 percent, respectively [50]. These complications may not have been the result of a
prolonged second stage of labor, but rather additional consequences of the underlying
cause of the labor abnormality [52]. Although maternal morbidity increases with
increasing duration of the second stage, the duration of the second stage alone does not
mandate intervention by operative delivery.
Ineffective interventions
Lessening neuraxial blockade Dense motor blocks from neuraxial analgesia
may impair a woman's ability to push. For this reason, some experts have
advocated turning down the neuraxial anesthetic to facilitate progress during a
prolonged second stage. A meta-analysis including five randomized trials of
epidurals discontinued late in labor compared with continuation of the same
epidural protocol until birth concluded there is insufficient evidence to support
the hypothesis that discontinuing epidural analgesia late in labor reduces the
rate of instrumental delivery [53]. (See "Adverse effects of neuraxial analgesia
and anesthesia for obstetrics" and "Adverse effects of neuraxial analgesia and
anesthesia for obstetrics", section on 'Effect of neuraxial analgesia on labor and
delivery'.)
There is no strong evidence that a change in maternal position (eg, upright posture,
lateral, or hands and knees position instead of supine) is useful in treatment of second
stage arrest [54-56]. Women should be encouraged to give birth in the position they find
most comfortable.
OUTCOME Contemporary data on the outcome of protracted labor are limited, but
generally show good neonatal outcomes.
A retrospective cohort study of nulliparous women in spontaneous labor found
that women with a prolonged first stage of labor (over 30 hours) were at
increased risk of chorioamnionitis and cesarean delivery, but their infants were
not at significantly increased risk of adverse outcome [57].
A prospective study including 2810 low risk nulliparous Danish women in
spontaneous labor at term compared the outcomes of women with dystocia
who received augmentation with the outcomes of a control group of women
with no dystocia and no augmentation [3]. Importantly, in this report, a
majority of women with dystocia (61 percent) were diagnosed in the second
stage because of lack of descent over two hours (three hours with an epidural
in place), or a lack of expulsion defined as no progress in the second stage for
one hour despite good pushing.
Compared to controls, women with dystocia and augmentation had fewer spontaneous
deliveries (59 versus 92 percent), a higher rate of heavily meconium stained amniotic
fluid (13 versus 8 percent), a higher rate of postpartum hemorrhage 1000 mLs (4.2
versus 2.5 percent), and more infants with birth weights 4000 g (19 versus 14
percent).
PREVENTION There is no strong evidence that any intervention will prevent
protracted labor. The best evidence is for the combination of early initiation of oxytocin
and amniotomy.
Oxytocin and amniotomy A systematic review of randomized trials found that
prophylactic use of both early amniotomy and oxytocin significantly shortened the first
stage of labor (WMD -1.57 hours; 95% CI -2.15 to -1.00), but was not effective as a
treatment of women with established delay in labor progress [58].
Active management of labor Most randomized trials of the active management of
labor approach have reported a reduction in protracted labors, but have not
demonstrated a significant decrease in cesarean birth [59-62]. How active management
affects the course of labor and the components of this approach that are most important
(strict criteria for diagnosis of labor, oxytocin initiation and dose, one-on-one labor
support, early amniotomy, etc) are unclear.
Avoidance of occiput posterior Pregnant women are often advised to perform
exercises to facilitate anterior rotation of the fetus, but there is no good evidence that
these maneuvers are effective. The lack of benefit was best illustrated by a large,
multicenter, randomized trial that assigned 2547 women at 36 to 37 weeks of gestation
to one of two exercise programs [63]. Group 1 was told to take a daily walk and Group 2
was asked to assume a hands and knees position with slow pelvic rocking for 10 minutes
twice a day until labor began. The incidence of persistent occiput posterior position at
birth or before instrumental rotation was similar in both groups (about 8 percent).
Pelvic floor muscle exercises Training the muscles of the pelvic floor may prevent
some cases of prolonged second stage. One trial randomly assigned 301 healthy
nulliparous women to an antepartum pelvic floor muscle training program or usual care
from 20 to 36 weeks of gestation [64]. Women in the intervention group trained with a
physiotherapist for one hour per week and were encouraged to perform 8 to 12 intensive
pelvic floor muscle contractions twice daily. Women in the exercise group were less likely
to have a second stage over 60 minutes than controls (21 versus 34 percent), but the
overall duration of the second stage was similar for both groups (40 and 45 minutes,
respectively), as was the rate of instrumental delivery (15 and 17 percent, respectively).
Volume replacement Myometrial function may be suboptimal in women who are not
adequately hydrated. Physiologists have shown that hydration improves skeletal muscle
performance during prolonged exercise; however, the effects of hydration on smooth
muscle are less clear [65,66]. Two small randomized trials in laboring women observed
that nulliparous women in labor given intravenous fluids at 250 mL/hour had a lower
frequency of prolonged labor and possibly less need for oxytocin than those who
received the traditional 125 mL/hour [67,68]. Similarly, another randomized trial showed
that nulliparous women receiving intravenous fluids with dextrose were less likely to
have a prolonged labor and, in particular, there was a significant reduction in the second
stage of labor [69].
Delayed pushing Pooled data from seven randomized trials (n = 2827 women)
indicated that passive descent significantly increased a woman's chance of having a
spontaneous vaginal birth, decreased her risk of having an instrument-assisted delivery,
and decreased pushing time, but had no significant effect on rates of cesarean birth,
laceration, or episiotomy [70]. This analysis was dominated by a randomized multicenter
trial (n = 1862) that showed delayed pushing was an effective means of reducing
difficult deliveries in nulliparous women (relative risk 0.79; 95% CI 0.66-0.95) [71].
Delayed pushing predictably increased the duration of the second stage (by 54 minutes),
and resulted in lower umbilical cord blood pH, but no difference was detected in overall
neonatal morbidity. Maternal position and technique do not appear to affect the length of
the second stage. (See "Management of normal labor and delivery", section on
'Pushing'.)
SUMMARY AND RECOMMENDATIONS
The Friedman curve (figure 1) and the norms established from Friedmans data
have historically been widely accepted as the standard for assessment of
normal labor progression. Contemporary thresholds are somewhat different
from those cited by Friedman because there have been significant changes in
patient characteristics, anesthesia practices, and obstetric practices over the
past half century, and Friedmans findings were based on labors in only 500
women who were managed at a single institution. (See 'Friedman's
data' above.)
Contemporary studies do not show an abrupt change in the rate of cervical
dilation indicating a clear transition from latent to active labor; over 50 percent
of women do not dilate at a rate of >1 cm/hour until 5 to 6 cm dilation.
(See 'Friedman versus contemporary data' above.)
In contemporary studies of the active phase, the median (95th percentile)
duration of time for the cervix to dilate from 4 to 10 cm in nulliparas and
multiparas is 5.3 hours (16.4) and 3.8 hours (15.7), respectively.
(See 'Duration of the active phase' above.)
In contemporary studies of the second stage, the median (95th percentile)
duration in nulliparous and parous women with epidural anesthesia was 1.1
hours (3.6) and 0.4 hours (2.0), respectively. Without epidural anesthesia, the
median (95th percentile) was 0.6 hours (2.8) and 0.2 hours (1.3), respectively.
(See 'Duration of the second stage' above.)
The following table (table 1) is a reasonable guide for determining when the
progress of labor is protracted in the active phase and can be used with a
partogram (graph 1). These data show that labor may take more than six
hours to progress from 4 to 5 cm and more than three hours to progress from
5 to 6 cm, regardless of parity. (See 'Active phase' above
and 'Partogram' above.)
Hypocontractile uterine activity is the most common cause of protraction and/or
arrest disorders in the first stage of labor. This entity refers to uterine activity
that is either not sufficiently strong or not appropriately coordinated to dilate
the cervix and expel the fetus, and has been defined as uterine contraction
pressures less than 200 Montevideo units. (See 'Hypocontractile uterine
activity' above.)
For women with poor labor progression after reaching 5 to 6 cm dilation, we
recommend administering oxytocin (Grade 1B) and monitoring another four
hours with adequate uterine contractions (>200 Montevideo units), or six hours
if unable to achieve this contraction pattern, before resorting to operative
delivery. (See 'Oxytocin augmentation' above.)
Criteria for average and protracted second stage are shown in the table (table 1).
Intervention is not indicated as long as labor appears to be progressing and the
fetal heart rate pattern is reassuring. (See 'Second stage' above and 'Poor
progression in the second stage' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. Gifford DS, Morton SC, Fiske M, et al. Lack of progress in labor as a reason for
cesarean. Obstet Gynecol 2000; 95:589.
2. Zhu BP, Grigorescu V, Le T, et al. Labor dystocia and its association with
interpregnancy interval. Am J Obstet Gynecol 2006; 195:121.
3. Kjaergaard H, Olsen J, Ottesen B, Dykes AK. Incidence and outcomes of dystocia in
the active phase of labor in term nulliparous women with spontaneous labor onset.
Acta Obstet Gynecol Scand 2009; 88:402.
4. FRIEDMAN E. The graphic analysis of labor. Am J Obstet Gynecol 1954; 68:1568.
5. FRIEDMAN EA. Primigravid labor; a graphicostatistical analysis. Obstet Gynecol 1955;
6:567.
6. Friedman, EA, ed. Labor clinical evaluation and management. 2nd ed New York.
Appleton-Century Crofts, 1978.
7. Zhang J, Troendle J, Mikolajczyk R, et al. The natural history of the normal first stage
of labor. Obstet Gynecol 2010; 115:705.
8. Zhang J, Landy HJ, Branch DW, et al. Contemporary patterns of spontaneous labor
with normal neonatal outcomes. Obstet Gynecol 2010; 116:1281.
9. Suzuki R, Horiuchi S, Ohtsu H. Evaluation of the labor curve in nulliparous Japanese
women. Am J Obstet Gynecol 2010; 203:226.e1.
10. Zhang J, Troendle JF, Yancey MK. Reassessing the labor curve in nulliparous women.
Am J Obstet Gynecol 2002; 187:824.
11. Peisner DB, Rosen MG. Transition from latent to active labor. Obstet Gynecol 1986;
68:448.
12. Albers LL. The duration of labor in healthy women. J Perinatol 1999; 19:114.
13. Kilpatrick SJ, Laros RK Jr. Characteristics of normal labor. Obstet Gynecol 1989;
74:85.
14. Neal JL, Lowe NK, Ahijevych KL, et al. "Active labor" duration and dilation rates among
low-risk, nulliparous women with spontaneous labor onset: a systematic review. J
Midwifery Womens Health 2010; 55:308.
15. Piper JM, Bolling DR, Newton ER. The second stage of labor: factors influencing
duration. Am J Obstet Gynecol 1991; 165:976.
16. American College of Obstetrics and Gynecology Committee on Practice Bulletins-
Obstetrics. ACOG Practice Bulletin Number 49, December 2003: Dystocia and
augmentation of labor. Obstet Gynecol 2003; 102:1445.
17. Smith GC, Celik E, To M, et al. Cervical length at mid-pregnancy and the risk of
primary cesarean delivery. N Engl J Med 2008; 358:1346.
18. Algovik M, Nilsson E, Cnattingius S, et al. Genetic influence on dystocia. Acta Obstet
Gynecol Scand 2004; 83:832.
19. Myles TD, Santolaya J. Maternal and neonatal outcomes in patients with a prolonged
second stage of labor. Obstet Gynecol 2003; 102:52.
20. Chua S, Kurup A, Arulkumaran S, Ratnam SS. Augmentation of labor: does internal
tocography result in better obstetric outcome than external tocography? Obstet
Gynecol 1990; 76:164.
21. Hauth JC, Hankins GD, Gilstrap LC 3rd, et al. Uterine contraction pressures with
oxytocin induction/augmentation. Obstet Gynecol 1986; 68:305.
22. Rouse DJ, Owen J, Hauth JC. Active-phase labor arrest: oxytocin augmentation for at
least 4 hours. Obstet Gynecol 1999; 93:323.
23. Rouse DJ, Owen J, Savage KG, Hauth JC. Active phase labor arrest: revisiting the 2-
hour minimum. Obstet Gynecol 2001; 98:550.
24. Bakker JJ, Verhoeven CJ, Janssen PF, et al. Outcomes after internal versus external
tocodynamometry for monitoring labor. N Engl J Med 2010; 362:306.
25. Anim-Somuah M, Smyth R, Howell C. Epidural versus non-epidural or no analgesia in
labour. Cochrane Database Syst Rev 2005; :CD000331.
26. American College of Obstetricians and Gynecologists. Obstetric analgesia and
anesthesia. ACOG practice bulletin #36. Obstet Gynecol 2002; 100;177.
27. Pattinson RC. Pelvimetry for fetal cephalic presentations at term. Cochrane Database
Syst Rev 2000; :CD000161.
28. Maharaj D. Assessing cephalopelvic disproportion: back to the basics. Obstet Gynecol
Surv 2010; 65:387.
29. Turrentine MA, Andres RL. Modern analysis of pathologic uterine rings. South Med J
1997; 90:40.
30. Turrentine MA, Andres RL. Recurrent Bandl's ring as an etiology for failed vaginal birth
after cesarean section. Am J Perinatol 1994; 11:65.
31. Lauria MR, Barthold JC, Zimmerman RA, Turrentine MA. Pathologic uterine ring
associated with fetal head trauma and subsequent cerebral palsy. Obstet Gynecol
2007; 109:495.
32. Gardberg M, Tuppurainen M. Persistent occiput posterior presentation--a clinical
problem. Acta Obstet Gynecol Scand 1994; 73:45.
33. Ponkey SE, Cohen AP, Heffner LJ, Lieberman E. Persistent fetal occiput posterior
position: obstetric outcomes. Obstet Gynecol 2003; 101:915.
34. Sizer AR, Nirmal DM. Occipitoposterior position: associated factors and obstetric
outcome in nulliparas. Obstet Gynecol 2000; 96:749.
35. Sencal J, Xiong X, Fraser WD, Pushing Early Or Pushing Late with Epidural study
group. Effect of fetal position on second-stage duration and labor outcome. Obstet
Gynecol 2005; 105:763.
36. Wei SQ, Luo ZC, Xu H, Fraser WD. The effect of early oxytocin augmentation in labor:
a meta-analysis. Obstet Gynecol 2009; 114:641.
37. Satin AJ, Leveno KJ, Sherman ML, McIntire DD. Factors affecting the dose response to
oxytocin for labor stimulation. Am J Obstet Gynecol 1992; 166:1260.
38. Satin AJ, Leveno KJ, Sherman ML, et al. High- versus low-dose oxytocin for labor
stimulation. Obstet Gynecol 1992; 80:111.
39. Satin AJ, Leveno KJ, Sherman ML, McIntire D. High-dose oxytocin: 20- versus 40-
minute dosage interval. Obstet Gynecol 1994; 83:234.
40. Seitchik J, Amico J, Robinson AG, Castillo M. Oxytocin augmentation of dysfunctional
labor. IV. Oxytocin pharmacokinetics. Am J Obstet Gynecol 1984; 150:225.
41. Kenyon S, Ullman R, Mori R, Whittle M. Care of healthy women and their babies during
childbirth: summary of NICE guidance. BMJ 2007; 335:667.
42. Smyth RM, Alldred SK, Markham C. Amniotomy for shortening spontaneous labour.
Cochrane Database Syst Rev 2007; :CD006167.
43. Oppenheimer LW, Labrecque M, Wells G, et al. Prostaglandin E vaginal gel to treat
dystocia in spontaneous labour: a multicentre randomised placebo-controlled trial.
BJOG 2005; 112:612.
44. Bloom SL, McIntire DD, Kelly MA, et al. Lack of effect of walking on labor and delivery.
N Engl J Med 1998; 339:76.
45. Hodnett ED, Gates S, Hofmeyr GJ, et al. Continuous support for women during
childbirth. Cochrane Database Syst Rev 2011; 2:CD003766.
46. Cohen WR. Influence of the duration of second stage labor on perinatal outcome and
puerperal morbidity. Obstet Gynecol 1977; 49:266.
47. Cheng YW, Hopkins LM, Caughey AB. How long is too long: Does a prolonged second
stage of labor in nulliparous women affect maternal and neonatal outcomes? Am J
Obstet Gynecol 2004; 191:933.
48. Cheng YW, Hopkins LM, Laros RK Jr, Caughey AB. Duration of the second stage of
labor in multiparous women: maternal and neonatal outcomes. Am J Obstet Gynecol
2007; 196:585.e1.
49. Allen VM, Baskett TF, O'Connell CM, et al. Maternal and perinatal outcomes with
increasing duration of the second stage of labor. Obstet Gynecol 2009; 113:1248.
50. Rouse DJ, Weiner SJ, Bloom SL, et al. Second-stage labor duration in nulliparous
women: relationship to maternal and perinatal outcomes. Am J Obstet Gynecol 2009;
201:357.e1.
51. Le Ray C, Audibert F, Goffinet F, Fraser W. When to stop pushing: effects of duration
of second-stage expulsion efforts on maternal and neonatal outcomes in nulliparous
women with epidural analgesia. Am J Obstet Gynecol 2009; 201:361.e1.
52. Caughey AB. Is there an upper time limit for the management of the second stage of
labor? Am J Obstet Gynecol 2009; 201:337.
53. Torvaldsen S, Roberts CL, Bell JC, Raynes-Greenow CH. Discontinuation of epidural
analgesia late in labour for reducing the adverse delivery outcomes associated with
epidural analgesia. Cochrane Database Syst Rev 2004; :CD004457.
54. Hofmeyr GJ, Kulier R. Hands/knees posture in late pregnancy or labour for fetal
malposition (lateral or posterior). Cochrane Database Syst Rev 2000; :CD001063.
55. Gupta JK, Hofmeyr GJ. Position for women during second stage of labour. Cochrane
Database Syst Rev 2004; :CD002006.
56. Roberts CL, Algert CS, Cameron CA, Torvaldsen S. A meta-analysis of upright
positions in the second stage to reduce instrumental deliveries in women with epidural
analgesia. Acta Obstet Gynecol Scand 2005; 84:794.
57. Cheng YW, Shaffer BL, Bryant AS, Caughey AB. Length of the first stage of labor and
associated perinatal outcomes in nulliparous women. Obstet Gynecol 2010; 116:1127.
58. Wei S, Wo BL, Xu H, et al. Early amniotomy and early oxytocin for prevention of, or
therapy for, delay in first stage spontaneous labour compared with routine care.
Cochrane Database Syst Rev 2009; :CD006794.
59. Sadler LC, Davison T, McCowan LM. A randomised controlled trial and meta-analysis of
active management of labour. BJOG 2000; 107:909.
60. Lpez-Zeno JA, Peaceman AM, Adashek JA, Socol ML. A controlled trial of a program
for the active management of labor. N Engl J Med 1992; 326:450.
61. Frigoletto FD Jr, Lieberman E, Lang JM, et al. A clinical trial of active management of
labor. N Engl J Med 1995; 333:745.
62. Rogers R, Gilson GJ, Miller AC, et al. Active management of labor: does it make a
difference? Am J Obstet Gynecol 1997; 177:599.
63. Kariminia A, Chamberlain ME, Keogh J, Shea A. Randomised controlled trial of effect of
hands and knees posturing on incidence of occiput posterior position at birth. BMJ
2004; 328:490.
64. Salvesen KA, Mrkved S. Randomised controlled trial of pelvic floor muscle training
during pregnancy. BMJ 2004; 329:378.
65. Maughan RJ, Bethell LR, Leiper JB. Effects of ingested fluids on exercise capacity and
on cardiovascular and metabolic responses to prolonged exercise in man. Exp Physiol
1996; 81:847.
66. Montain SJ, Coyle EF. Influence of graded dehydration on hyperthermia and
cardiovascular drift during exercise. J Appl Physiol 1992; 73:1340.
67. Garite TJ, Weeks J, Peters-Phair K, et al. A randomized controlled trial of the effect of
increased intravenous hydration on the course of labor in nulliparous women. Am J
Obstet Gynecol 2000; 183:1544.
68. Eslamian L, Marsoosi V, Pakneeyat Y. Increased intravenous fluid intake and the
course of labor in nulliparous women. Int J Gynaecol Obstet 2006; 93:102.
69. Shrivastava VK, Garite TJ, Jenkins SM, et al. A randomized, double-blinded, controlled
trial comparing parenteral normal saline with and without dextrose on the course of
labor in nulliparas. Am J Obstet Gynecol 2009; 200:379.e1.
70. Brancato RM, Church S, Stone PW. A meta-analysis of passive descent versus
immediate pushing in nulliparous women with epidural analgesia in the second stage
of labor. J Obstet Gynecol Neonatal Nurs 2008; 37:4.
71. Fraser WD, Marcoux S, Krauss I, et al. Multicenter, randomized, controlled trial of
delayed pushing for nulliparous women in the second stage of labor with continuous
epidural analgesia. The PEOPLE (Pushing Early or Pushing Late with Epidural) Study
Group. Am J Obstet Gynecol 2000; 182:1165.
2011 UpToDate, Inc. All rights reserved. | Subscription and License Agreement |Support Tag:
[ecapp1104p.utd.com-112.215.66.109-026D026A78-2579.14-178373735]
Licensed to: UpToDate Guest Pass - zul fadi

TOPIC OUTLINE
INTRODUCTION
PREVALENCE
NORMAL LABOR
Definitions
Friedman's data
Friedman versus contemporary data
- Labor curve
- Duration of the latent phase and the first stage
- Duration of the active phase
- Duration of the second stage
DIAGNOSIS OF LABOR ABNORMALITIES
Active phase
Second stage
Precipitous labor
Partogram
ETIOLOGY
Hypocontractile uterine activity
- Normal uterine activity
- Intrauterine pressure catheter
Neuraxial anesthesia
Cephalopelvic disproportion (CPD)
Bandl's ring
Occiput posterior (OP) position
MANAGEMENT
Patients with protracted latent phase
Patients with protracted active phase
- Oxytocin augmentation
Assessing progress after initiating oxytocin
- Other approaches
Poor progression in the second stage
- Ineffective interventions
OUTCOME
PREVENTION
Oxytocin and amniotomy
Active management of labor
Avoidance of occiput posterior
Pelvic floor muscle exercises
Volume replacement
Delayed pushing
SUMMARY AND RECOMMENDATIONS
REFERENCES
GRAPHICSView All
FIGURES
Labor curve
Average labor curve by parity
Fontanelles and suture lines
GRAPHS
Duration of labor by dilation at admission
TABLES
Duration of labor by parity
Risk factors for dystocia
Oxytocin infusion protocols
RELATED TOPICS
Adverse effects of neuraxial analgesia and anesthesia for obstetrics
Fetal macrosomia
Induction of labor
Insertion of intrauterine pressure catheters
Latent phase of labor
Management of normal labor and delivery
Management of the fetus in occiput posterior position
Occiput transverse position
Timing and route of delivery in pregnancies at risk of shoulder dystocia
Help improve UpToDate. Did UpToDate answer your question?
Yes No