INTRODUCTION

The diagnosis of abnormal labor (dystocia) has four major etiologic categories: (1) the
“passage,” or pelvic architecture; (2) the “passenger,” or fetal size, presentation, and position;
(3) the “powers,” or uterine action and cervical resistance; and (4) the “patient” and
“provider.”

PASSAGE—THE OBSTETRIC PELVIS

During labor, the fetus assumes positions and attitudes that are determined in part by the
configuration of the mother’s pelvis. The “true” pelvis includes the inlet, the midpelvis, and
the outlet. The anterior wall at the pubic symphysis measures approximately 5 cm, and the
posterior wall measures approximately 10 cm.

Pelvic Inlet

The pelvic inlet is bounded laterally by the iliopectineal lines, which can be traced anteriorly
along the pectineal eminence and pubic crest to the symphysis. The posterior boundary is
composed of the sacrum at the level of the iliopectineal lines. The anteroposterior diameter
(obstetric conjugate) is the shortest distance between the sacral promontory and the pubic
symphysis. The inlet usually is considered to be contracted if the obstetric conjugate is less
than 10 cm or the greatest transverse diameter is less than 12 cm. When both diameters are
contracted, the incidence of dystocia is much greater than when only one diameter is
contracted.

Midpelvis

The midpelvis is bounded anteriorly by the posterior aspect of the symphysis and pubis and
posteriorly by the sacrum at the level of S3 or S4. The lateral boundary is the pelvic sidewalls
and ischial spines. The distance between the ischial spines is usually the smallest diameter of
the pelvis, typically measuring 10 cm or more. The anteroposterior diameter of the midpelvis,
which runs from the inferior aspect of the pubic symphysis to the sacral hollow at the level of
the ischial spines, averages 11.5 cm or more. Midpelvic contraction should be suspected
whenever the interspinous diameter is less than 10 cm. When the diameter is less than 9 cm,
the midpelvis is considered definitely contracted. Midpelvic contraction is more common
than inlet contraction.

Pelvic Outlet

The pelvic outlet is composed of two triangular areas that share the same base but are not in
the same plane. The anterior triangle is formed by the pubic arch. The apex of the posterior
triangle is the tip of the sacrum, and the sides are the sacral sciatic ligaments and ischial
tuberosities. The anteroposterior diameter, from the inferior edge of the pubic symphysis to
the tip of the sacrum, usually measures approximately 11.5 cm. The transverse diameter, the
distance between the inner edges of the ischial tuberosities, measures approximately 10 cm. It
is rare to find outlet contraction without midplane contraction.

Contracted Pelvis
Of the four types of pelves, gynecoid, android, anthropoid, and platypelloid, the gynecoid
pelvis is most optimal for normal delivery. Other abnormalities also may affect the bony
pelvis. Kyphosis, if it involves the lumbar area, may be associated with a typically funnel-
shaped pelvis, which leads to late arrest of labor. Scoliosis, which involves the lower region
of the spine, may produce an irregular inlet, leading to obstructed labor. The pelvis usually is
not contracted in cases of unilateral lameness. With bilateral lameness, the pelvis is wide and
short, but most women are able to deliver vaginally. In poliomyelitis, now extremely rare, the
pelvis may be asymmetric, but most patients can deliver vaginally. In dwarfism, cesarean
delivery is generally the rule because of marked fetopelvic disproportion. Cesarean sections
occur more frequently in women with a history of a pelvic fracture, especially bilateral
fracture of the pubic rami, before pregnancy.1 In the aforementioned uncommon pelvic
abnormalities, it may be helpful to assess the pelvis further with imaging pelvimetry.

Soft Tissue Dystocia

Soft tissue abnormalities in the pelvis occasionally can result in dystocia. Uterine myomas are
the most common pelvic masses associated with dystocia. They may obstruct the birth canal
or cause malpresentation of the fetus. Other possible causes of upper genital tract dystocia
include ovarian tumors, bladder distention, a pelvic kidney, excess adipose tissue, uterine
malposition, and cervical stenosis or neoplasm. Lower genital tract dystocia can be caused by
partial vaginal or vulvar atresia, severe edema or inflammation, Bartholin’s or Gartner’s duct
cysts, vaginal septum, large condylomata, hematomas, and neoplasms.

Pelvimetry

Clinical estimation of the adequacy of the pelvis can alert the clinician to the possible risk of
pelvic dystocia. A clinically small pelvis is associated with a 2.5-fold increase in primary
cesarean section.2 The outcome of labor depends more on the actual pelvic diameters than
the shape and type of pelvis. Several pelvic diameters can be assessed clinically, including
the diagonal conjugate (measured from the inferior edge of the pubic symphysis to the sacral
promontory), prominence of the ischial spines, convergence of pelvic sidewalls, angle of the
subpubic arch, and sacral curvature. In general, suspicion of a contracted pelvis is increased
with the conditions listed in Table 1.

Table 1: Clinical indices that increase the suspicion of potential for disproportion during
labor

Pelvic sidewalls are convergent

Ischial spines are prominent
Diagonal conjugate is <11.5 cm
Subpubic arch angle is <90 degrees
Sacrum is flat
No descent of vertex with Valsalva or fundal pressure (Müller-Hillis maneuver)
PASSENGER—THE FETUS

The size, presentation, and position of the fetus are important factors in the conduct of labor.
Pelvic size and configuration and excessive soft tissue may influence the fetal position and
presentation. Although the macrosomic infant is at greater risk for dystocia, most cases of
abnormal labor occur among fetuses weighing less than 4000 g.

The biparietal diameter (BPD), the smallest transverse dimension of the fetal skull, averages
approximately 9.5–9.8 cm among term fetuses. The shortest anteroposterior dimension is the
suboccipitobregmatic diameter, which also averages approximately 9.5 cm. The fetal head
can overcome minor degrees of pelvic contracture by molding. The bones of the skull overlap
at major suture lines, which can decrease the BPD by 0.5 cm without fetal injury. Severe
molding may lead to tentorial tears and intracranial hemorrhage.

Prolonged, severe pressure between the fetus and birth canal may lead to fetal scalp necrosis
or skull fracture. The mother may develop a vesicovaginal, vesicocervical, or rectovaginal
fistula. Other risks of fetopelvic disproportion include cord prolapse, prolonged labor with an
increase in maternal and fetal infections, uterine rupture, postpartum hemorrhage, abnormal
presentation or position, and maternal and neonatal trauma.

Malposition and Malpresentation

Fetal malpresentation may be the result of or the cause of dystocia. Nonvertex presentations
should alert the clinician to the possibility of pelvic dystocia. In compound presentations, a
fetal hand beside the head may be encouraged to withdraw by a gentle pinch. A fetal foot
beside the head is more unusual; vaginal delivery still may be possible if the pelvis is
adequate. Other than cases of extreme prematurity, the delivery of transverse lies require
cesarean delivery.

In a brow presentation, the partially extended head presents with the occipitomental diameter
of 13.5 cm in the average term fetus. Brow presentations are associated with pelvic
contraction, small or large fetuses, and nuchal masses. Two thirds spontaneously convert to
either a face or an occipital presentation. Manual or forceps conversion is no longer
advocated. Cesarean birth is recommended if the brow presentation persists except in cases of
a small fetus.

The fetal head is completely hyperextended in a face presentation. The incidence is about
1:600 deliveries. Associated factors include anencephaly and brow presentations. If the
mentum (chin) persists posteriorly, cesarean delivery is necessary because the fetal neck
cannot hyperextend further to accommodate the pelvic curve. A vaginal delivery is possible
with mentum anterior presentations. Manual or forceps conversion of face presentations is no
longer advocated.
The fetal occiput presents posteriorly in about 25% of early labors and 10–15% of active
labors. The anthropoid-type pelvis predisposes to this position. Clinical signs of occiput
posterior position include accentuated maternal backache, persistent anterior cervical lip,
ineffective contractions, and a prolonged second stage. Ultrasound is invaluable to confirm an
occiput posterior position when the diagnosis by clinical examination is questionable.
Spontaneous rotation to occiput anterior may be impeded by regional anesthesia and poor
voluntary effort. If the posterior triangle of the pelvic outlet is roomy, the infant can deliver
spontaneously from the occiput posterior position, but an episiotomy may be needed. Other
options include manual or forceps rotation. Kielland forceps, which do not have a pelvic
curve, are ideal. Classic forceps can be used to rotate the vertex by the Scanzoni
maneuver. Forceps rotations are seldom performed in current clinical practice, and require
training and expertise. Persistent occiput posterior position is associated with an increased
risk of cesarean section and operative vaginal deliveries, resulting in a spontaneous vaginal
delivery rate of ~25% for nulliparous women and 57% for multiparous women.1 Peristent
occiput posterior position has also been associated with adverse neonatal outcomes including
a 5-minute Apgar score <7, neonatal acidemia, birth trauma, admission to the intensive care
nursery, and longer neonatal hospitalization.2 An occiput posterior fetus may be manually
rotated to an occiput anterior position, resulting in lower cesarean section rates. The primary
factor associated with success in manual rotation attempts is multiparity.3 An additional
reason to attempt manual rotation from the posterior position is the fact that occiput posterior
position increases risk of severe perineal lacerations, both with and without operative
delivery attempts.4

The occiput transverse position is normally transitory because of the process of internal
rotation. Platypelloid and android pelves have narrow anteroposterior diameters, which may
not allow normal rotation. If the transverse arrest is believed to be due to a contracted pelvis,
cesarean delivery is necessary. If the pelvis is thought to be adequate, a forceps rotation may
be attempted. Oxytocin may be of benefit in causes of transverse arrest, which include uterine
inertia and compromise of the pelvic floor muscles. If the pelvis has a prominent sacral
promontory, asynclitism may develop; the vertex does not orient the sagittal suture in the
midplane of descent. Asynclitism of the fetal head may overcome small degrees of pelvic
inlet contraction. In anterior asynclitism, in which the sagittal suture is nearer the sacrum, the
outcome is more favorable than in posterior asynclitism, in which the sagittal suture is closer
to the pubic symphysis. If the asynclitism does not overcome the contracted anteroposterior
diameter, a deep transverse arrest results.

Fetal Anomalies

With the common use of ultrasound, most anomalies capable of producing disproportion are
diagnosed before the onset of labor. Hydrocephalus is a frequently encountered
developmental abnormality that causes dystocia. A biparietal diameter greater than 120 mm
has been associated with true cephalopelvic disproportion. If the fetus has a lethal condition,
cerebrospinal fluid can be removed to allow a vaginal delivery; this is a rare procedure in
modern obstetrics. Craniosynostosis, premature closure of the cranial sutures, may cause
distortion but rarely leads to dystocia. Encephaloceles, which carry a poor prognosis, are
usually fragile and may rupture during delivery. Potentially viable conjoined twins require
delivery by cesarean section. Abdominal masses causing dystocia include hydrops fetalis,
posterior urethral valves, Wilms’s tumor, polycystic kidneys, ovarian and hepatic tumors, and
ascites. Ascitic fluid and other cystic masses can be drained percutaneously in labor to allow
vaginal delivery. Ascitic fluid can reaccumulate rapidly, however. Meningomyeloceles,
omphaloceles, and gastroschisis usually do not obstruct labor, but the optimal obstetric
management of these conditions is controversial. A sudden inability to deliver the fetus
beyond the abdomen can be due to an undiagnosed sacrococcygeal teratoma. In such cases, it
may be possible to flex and deliver the legs to allow more room for the mass to deliver.
Another option is resuscitation and stabilization of the infant on the perineum then
replacement with cesarean delivery.

Fetal Macrosomia

There is no consistent definition of fetal macrosomia in the literature. The most commonly
cited definition is birth weight greater than 4000 g. The incidence of birth weight greater than
4000 g has been increasing.5 Typically, fetuses weighing more than 4000 g account for
nearly 10% and fetuses weighing 4500 g or more represent approximately 1% of all
deliveries. Macrosomic infants have a threefold increase in morbidity.5, 6 They have an
increased risk for shoulder dystocia, meconium aspiration, asphyxia, brachial plexus injury,
placenta previa, traumatic midforceps, and fetopelvic disproportion. The head is larger than
average but also more calcified, with less potential for molding. Size of the fetal trunk also
may contribute to dystocia and mechanical problems at delivery. Labor abnormalities include
arrest and protraction disorders and shoulder dystocia.

Estimation of Fetal Weight

The accurate estimation of fetal weight (EFW) is an elusive goal. An accurate EFW would be
useful in making clinical decisions in the management of macrosomic fetuses regarding the
prevention of shoulder dystocia, the use of oxytocin augmentation in abnormal labor, and the
use of midforceps. Clinical EFW is by abdominal palpation and measurements of fundal
height. Studies designed to evaluate the accuracy of clinical EFW consistently have reported
a tendency to estimate toward the mean birth weight. Errors at the extremes of birth weight
are especially undesirable because obstetric interventions are often most important among
preterm and macrosomic fetuses. Most investigators also report that the duration of clinical
experience does not improve accuracy in estimating fetal weight and great individual
variability exists among examiners. The application of clinically estimated fetal weight to
individual patients is difficult but may have its greatest utility in selecting cases to obtain an
ultrasonographic EFW.

The use of ultrasound to estimate fetal weight has improved greatly on and supplanted
clinical estimation. Many investigators have published formulas for sonographically
estimating fetal weight. Shepard and colleagues7 published EFW based on BPD and
abdominal circumference. Probably the most commonly used formula was published by
Hadlock and associates,8 which uses femur length and abdominal circumference. Since then,
many studies have been performed using various sophisticated formulas; however, they have
had minimal improvement in the accuracy of sonographic EFW. Similar to the tendency
found in the clinical EFW, ultrasound predictions of birth weight tend to overestimate low-
birth-weight infants and underestimate macrosomic infants. Many mathematical models using
different fetal measurements have been tested to detect the macrosomic fetus. Comparisons
are difficult because the studies use varying fetal parameters, statistics, populations, and
definitions of macrosomia. Even with improvements in technology, ultrasonographic EFW
has a variability of ± 15% and may be ± 20% with EFW greater than 4000 g. The use of
ultrasonographic EFW should be tempered by other clinical parameters.
POWER—UTERINE CONTRACTILITY

The causes of purely dysfunctional dystocia, in which uterine contractility is inadequate in

effecting dilation and descent, are not well understood. The perception of uterine contractions
via abdominal palpation requires a pressure more than 10 mmHg above the resting pressure.
External electronic monitoring consists of a tocodynamometer on the abdomen over the
fundus. It can provide the frequency and an estimate of the duration of contractions but does
not provide information concerning intensity and tone. Internal pressure monitoring is
accomplished by transcervical insertion of an open-ended plastic cannula, which is filled with
fluid and attached to a pressure transducer, or insertion of a disposable pressure transducer
into the amniotic cavity after rupture of membranes. Internal intrauterine pressure monitoring
provides estimates of resting uterine tone and the duration, frequency, and intensity of
contractions. The term estimates is used because, with ruptured membranes, the uterus is not
a closed fluid system; intrauterine pressures also vary according to the position of the patient.

In early labor, contractions occur approximately every 3–5 minutes with a pressure of 20–30
mmHg above resting tone. In active labor, contractions are usually every 2–4 minutes with
pressures 30–50 mmHg above resting tone. With pushing, the pressures may rise to 100–150
mmHg. The resting pressure increases from 5 to 10 mmHg in early labor to 12–14 mmHg
later. In addition to increased frequency and tone, the duration of contractions lengthens from
30 to 60 seconds in early labor to 60–90 seconds in later labor. The minimal effective uterine
contractility has been characterized as being a minimum of contractions occurring more
frequently than every 5 minutes and developing greater than 25 mmHg pressure.9

Information about the intensity and strength of uterine activity is most accurately provided by
direct monitoring obtained with an intrauterine pressure catheter. Most commercially
available systems include a stiff catheter guide that is inserted just beyond the fetal presenting
part and no further. The pressure catheter is advanced into the uterine cavity, and the catheter
guide is removed. The appropriate depth of insertion can be determined by a mark on the
catheter that should be at the level of the introitus after insertion. The catheter should be
inserted posterior to the fetal presenting part. If the presenting part is well engaged in the
pelvis, posterior insertion may be impossible, and anterior insertion may be attempted.
Lateral insertion is discouraged because lateral perforation may precipitate uterine artery
compromise with its attendant complications, including broad-ligament hematoma. Currently
available catheters interface with the fetal monitor via a manufacturer-specific reusable cable.
The set-up and calibration process are straightforward, and most systems incorporate a lumen
into the catheter to permit simultaneous monitoring of intrauterine pressure as well as
amnioinfusion. Various commercial models of intrauterine pressure catheter are available,
including the Intran™ from Utah Medical Products10 and the Koala™ from Clinical
Innovations.11 Because the equipment for using the IUPCs is generally not transferable from
one brand to another, labor and delivery units will usually purchase only one brand of
intrauterine pressure catheters. When changing brands, introducing the new equipment to
nurses, physicians and other patient care providers is vital. There are no head-to-head trials
suggesting any brand of intrauterine pressure catheter is better than any other brand.

Many investigators have developed objective measurements of uterine contractility; however,

none have had wide clinical usage. The simplest estimate of uterine work is the Montevideo
unit. Developed by Caldeyro-Barcia,12 the Montevideo unit is the peak intensity above resting
pressure multiplied by the number of contractions in a 10-minute time interval. Normal labor
encompasses a wide range of uterine work – 95–395 Montevideo units.13 The Alexandria
unit is the Montevideo unit multiplied by the average duration per contraction in a 10-minute
interval.

Work by investigators including Seitchik and Chatkoff14 and Steer and coworkers15 has
shown that the progress of labor is not related solely to uterine work, especially in cases of
dysfunctional labor. The total uterine work required to achieve dilation and descent reflects
the amount of resistance that must be overcome. This resistance varies greatly among
individuals, although dilation in multiparas requires less work than nulliparas. Although it is
of interest, the objective quantitation of uterine activity at present has limited ability to aid in
the management of labor. The same quality and quantity of contractions in a normal labor
also may be seen with an abnormal labor in a different patient.

Functional dystocia has been associated with two different types of abnormal contraction
patterns. A hypertonic pattern typically has elevated resting pressures, increased contraction
frequency, and decreased coordination, as well as a delayed fall to baseline uterine tone.16
This pattern is seen more often with fetal malpresentation and uterine overdistention.
Oxytocin generally has not been recommended but occasionally has been shown to convert
this pattern to effective labor. Hypotonic uterine dysfunction is more common and frequently
responds to oxytocin. The contractions are synchronous but weak or infrequent or both. With
primary dysfunction, it is hypothesized that contractions were never normally established.
With secondary dysfunction, it is suggested that contractions were once adequate and became
weaker as labor progressed, usually after 4 cm dilation.

PROVIDER/PATIENT

Absolute fetopelvic disproportion is uncommon, but the performance of cesarean delivery for
that indication is common. It is assumed that the physician factor is significant in the
diagnosis of dystocia. Physicians may be influenced by the patient’s attitude, the time of day,
anesthesia support, the medicolegal climate, and their own training and experience. The
patient’s level of anxiety and pain tolerance also may influence the character and duration of
labor.

Medications given during labor may alter uterine contractility. β-Mimetics, calcium channel
blockers, magnesium sulfate, and antiprostaglandins have been used to inhibit labor. Ethanol
has a direct depressant effect on smooth muscle and inhibits oxytocin release. Theophylline
and caffeine may lead to longer labors. The effects of barbiturates are dose-related.
Pentobarbital and thiopental in anesthetic doses may stop labor, whereas phenobarbital has
little effect. Atropine and scopolamine relax the lower uterine segment and decrease the
frequency of contractions. Tranquilizers have variable effects; usually, large doses delay
labor. Cocaine has been “marketed” as a drug that reduces the duration of labor. Although
there is accumulating evidence that cocaine abuse is associated with an increased incidence
of prematurity, it does not significantly shorten the total duration of labor.15 There is evidence
that propranolol, when given in low doses in conjunction with oxytocin for augmentation in
patients with dysfunctional labor can safely reduce the need for cesarean section. The
mechanism is thought to have to do with the β-blockade produced by propranolol.17
Epidural anesthesia may cause a transient decrease in contractility for 10–30 minutes. This
effect is much more pronounced if anesthesia is given in the latent phase or with fetopelvic
disproportion or malposition. The action of voluntary muscles in correction of malposition
may be impaired. Because epidural anesthesia is associated with a prolongation of the second
stage of labor, intervention is not recommended unless the duration of the second stage
exceeds 3 hours with a regional anesthetic in a nulliparous or 2 hours in a parous parturient.18
An increase in malpresentations and instrumental deliveries has been reported with epidural
anesthesia. In 1989, Thorp and colleagues19 reported a significantly increased frequency of
oxytocin augmentation and incidence of cesarean section for dystocia among patients
receiving epidural anesthesia compared with controls. The increased rate of cesarean delivery
for dystocia was not explained by other potentially confounding variables, including
gestational age, cervical dilation, use of oxytocin, and birth weight. Other randomized trials
investigating early and late administration of epidural anesthesia have not shown an increase
in the rate of cesarean delivery.20, 21, 22, 23, 24.

The latent phase of labor is particularly sensitive to narcotics. Although active labor is
considerably less sensitive than in the latent phase, heavy sedation may slow dilation and
increase the chance of protraction and arrest of dilation. Inhalation agents also have a wide
range of effects that are dose dependent. Nitrous oxide has no effect on contractions, but
halothane and other halogenated agents are strongly inhibitory. Intravenous nitroglycerin (in
increments of 50 μg) results in rapid and profound uterine relaxation. Halothane and
nitroglycerin can be used to relax the uterus to facilitate internal podalic version of a second
twin, delivery of entrapped breech head, or manual removal of the placenta. The use of these
agents can be associated with postpartum hemorrhage, however.

There is a close relationship between the cervical score and onset of spontaneous labor. The
state of the cervix may reflect myometrial sensitivity to oxytocin. It is possible that the
promotion of cervical ripening may increase myometrial sensitivity and soften the cervix.
Many agents have been investigated and found to induce cervical ripening with varying
success, including estradiol and relaxin gels, Foley catheters, Laminaria tents, and
prostaglandin E2 and F2α by various routes. Other newer induction agents, such as
misoprostol, a prostaglandin E1 analogue, may cause cervical ripening and labor induction
and stimulation.

Obesity

With the increasing rates of obesity in the United States and the developed world, obesity is
likely to become an increasingly important cause of labor dystocia. There is substantial
evidence that obesity predisposes to dystocia. Excess prepregnancy weight has been shown
to increase the cesarean section rate in nulliparous women giving birth to singletons at term,
particularly in very obese women.25, 26 Additional research has shown that increases in the
BMI between the first two pregnancies from the normal range to the obese range (as in when
a parturient fails to loose the weight gained with the first pregnancy before conceiving the
second pregnancy) increased their risk of primary cesarean section significantly. In the case
of women who went from normal weight to obese, the OR was 1.96 (95% CI 1.71–
2.26). The magnitude of increased risk was even greater for women who went from
underweight to obese. Importantly, women who went from obese to normal weight also had
an increased risk of cesarean section of 1.51.27

Advancing Maternal Age

As the parturient population ages, it is important to acknowledge that older women have a
higher risk of cesarean section. The mechanism of this increased risk is not entirely clear,
however older women appear to have both longer labors and higher primary cesarean section
rates for elective and non-elective (i.e., breech and myomectomy) indications.28, 29

In this age of personalized medicine, we may soon enter the age of personalized labor
curves. As we learn more about the fact that older and obese women have different and
longer labors, it is also interesting and helpful to know that labor curves may also vary by
ethnic group, with African Americans tending to have a shorter length of the second stage
than other groups.30

Oxytocin

Oxytocin is an octapeptide that is synthesized in the hypothalamus and transported to axonal

terminals in the posterior pituitary gland. Wide variability exists regarding reported maternal
plasma concentrations of oxytocin during pregnancy and spontaneous labor. In addition to a
tonic baseline release, oxytocin is released in pulses occurring at 3- to 5-minute intervals
during normal labor, and fetal transfer of oxytocin to the maternal side may be an important
physiologic source.31 Most investigators report a gradual rise in plasma oxytocin levels
throughout gestation with a peak during the second stage of labor. Human myometrial
oxytocin receptors, which peak in early spontaneous labor, seem to contribute to the initiation
of uterine contractions. Receptor concentration is probably the major determinant controlling
uterine response to either endogenous or exogenous oxytocin.

Oxytocin is a potent uterotonic agent that can be safe and efficacious when used
appropriately. Friedman32 advocated the use of oxytocin with a secondary arrest of labor or
failure of descent when there is no suspicion of cephalopelvic disproportion. Many
physicians also use oxytocin for prolonged latent phase or protracted active phase disorders.
There is some evidence that preventing prolonged labor by the use of oxytocin results in a
better fetal and maternal outcome. This improved outcome seems to apply even if
cephalopelvic disproportion is clinically suspected because the diagnosis may be arrived at
sooner. In general, when dysfunctional labor is present and vaginal delivery is deemed
possible by the enhancement of uterine contractions, augmentation of labor may be
indicated.33

In vivo studies determined that the interval to reach a steady-state concentration of oxytocin
in plasma (and maximal response) is 40–60 minutes after initiating or altering the infusion.
The in vivo half-life of oxytocin is approximately 10–15 minutes. Studies of plasma oxytocin
levels during continuous intravenous infusion show first-order saturation kinetics, with a
progressive, linear, stepwise increase with each increase in the infusion rate. Pharmacologic
data suggest that the infusion rate of oxytocin should start low (0.5–2 mU/min) with an
increase arithmetically by 1–2 mU/min every 40–60 minutes. Because of varied response
ranges in individuals secondary to differences in clearance rates and sensitivities, however,
this rate of increase is inefficient in a significant portion of patients. Clinically, this variation
resulted in an unacceptable delay in reaching an effective maintenance dose of oxytocin in
31% of patients who required greater than 4 mU/min. Seitchik and Castillo34, 35, 36 proposed,
as a compromise, an increase in the infusion rate every 30 minutes with cautious observation
for hyperstimulation. This proposal was tested in term nulliparas and multiparas with
dysfunctional labor. When the oxytocin infusion rate was increased at less than 30-minute
intervals, there was a twofold increase in the frequency of discontinuing or decreasing the
oxytocin infusion because of hyperstimulation or fetal distress. A short (less than 30 minutes)
interval of rate increase also was shown to be the most important factor resulting in a higher
maximum dose of oxytocin and an actual delay in delivery by an average of 3 hours.

The preterm uterus is usually less sensitive to oxytocin than the term uterus and may require
larger doses. Theobald and coworkers37 reported that a 2 mU/min infusion of oxytocin at 32
weeks’ gestation induced small contractions, but just before, during, or after spontaneous
labor, regardless of gestational age, the uterus responded to 0.5 mU/min. At term, an oxytocin
infusion rate of 2–8 mU/min is usually sufficient for the successful induction of
labor.38 Doses of 5 mU/min or less have been found to improve vaginal delivery rates,
improve 1-minute Apgar scores, and cause no hyperstimulation. A dose greater than 20
mU/min at term is rarely necessary. The higher the dose required to produce effective
contractions, the less likely is success. Seitchik and Castillo34, 35, 36 found in oxytocin
augmentation of labor that with an initial dose of 1 mU/min and an increase of 1 mU/min
every 30 minutes until a dilation rate of 1 cm/h was reached, more than 90% of multiparas
and 85% of nulliparas required less than 4 mU/min.

Oxytocic effects on the myometrium include increased strength, velocity, and frequency of
contractions and increased intrauterine resting pressure. After maximum efficiency is
reached, further increases in oxytocin may result in excessive contraction frequency and
increased baseline tone, resulting in decreased effectiveness of the contractions and the
development of fetal distress. If the contraction pattern seems adequate (one every 3–4
minutes), but cervical dilation is inadequate, clinical experience indicates that occasionally a
decrease in the oxytocin dose may improve efficacy. The uterine contractile pattern may
provide an initial evaluation of response, but the quantitation of uterine activity is far from
perfect in identifying hypocontractile labor, identifying excessive stimulation, or guiding
oxytocin therapy. Because normal labor has wide variability in uterine activity within and
between individuals, other criteria for titrating oxytocin also are recommended. Melmed and
Evans39 reported that if the initial cervical dilation rate was at least 1 cm/h among
spontaneously laboring nulliparas, 93% had a spontaneous vaginal delivery. In contrast, 67%
required forceps or vacuum delivery or cesarean section if the cervical dilation rate was less
than 1 cm/h.

Proponents of “active management of labor” use a cervical dilation rate of 1 cm/h among
nulliparas to guide their use of oxytocin. As described by O’Driscoll and associates,40 active
management of labor included early routine amniotomy and oxytocin infusions starting at 6
mU/min with increases every 15 minutes up to 40 mU/min, for dilation rates less than 1 cm/h,
provided that there was no fetal distress. Among 3106 nulliparas, the cesarean section rate for
the diagnosis of dystocia was only 1.4%. Although some claim that this policy for oxytocin
use might result in too many patients receiving oxytocin, evidence from clinical studies
suggests that a 1 cm/h rate of dilation may serve as a useful guide to determine the most
effective dose of oxytocin in induction or augmentation in nulliparous women. In the United
States, this active management approach resulted in a shorter duration of labor but did not
result in a decreased cesarean section rate.

Especially in the nulliparous patient, fetal heart rate response provides a further, and perhaps
more appropriate, basis for titration of oxytocin than does uterine contractility. Placental
venous outflow has been shown to stop during contractions, but adequate exchange follows
with good relaxation. Arterial inflow continues until pressures of 30–70 mmHg, then may
stop completely. The fetus continues to extract oxygen from the intervillous blood but
eventually may resort to anaerobic metabolism until oxygen is restored after the contraction.
Uterine blood flow varies indirectly with resting pressure, frequency, intensity, and duration
of contractions. There are wide variations in fetal reserve, but excessive uterine tone and
frequency of contractions may lead to acidosis, distress, and fetal death, even in the normal
fetus. If the intensity and frequency of contractions must be kept low to protect a fetus with
“decreased reserve,” more contractions are needed, but it is possible that this patient still may
deliver vaginally with careful titration of the oxytocin dose.

If, during oxytocin induction or augmentation, excess uterine activity or fetal distress occurs,
it may not be a pathologic state requiring immediate cesarean delivery. When a patient moves
to the supine position, contractions may become more frequent but less intense. This position
also may result in increased risk of fetal hypoxemia and less progress in cervical dilation.
Placing the patient in a left lateral position may be the only corrective measure necessary for
hyperstimulation and fetal distress. Additional measures include starting oxygen and
decreasing or stopping the infusion of oxytocin. Decreasing the oxytocin dose, rather than
stopping it, may correct the abnormal pattern and prevent an unwarranted delay in delivery.
When restarting the oxytocin, we suggest decreasing the previous rate by at least half.

It may be possible to decrease the dose of oxytocin when labor has been established.
Continuation of oxytocin throughout delivery may decrease the risk for postpartum uterine
atony. Monitoring of the fetal heart rate and uterine activity should begin before and continue
throughout oxytocin induction or augmentation. This monitoring is vital in the current
medicolegal climate and may assist in determining the most efficient dose of oxytocin.
Accurate documentation of fetal heart tones, frequency and duration of contractions, and
oxytocin rate also is recommended.

DYSTOCIA—FUNCTIONAL DEFINITION OF LABOR ABNORMALITY

In the preceding sections, the limitations of pelvimetry, EFW, and uterine contractility to
predict dystocia were discussed. For clinical purposes, other means must be employed to
identify dystocia.

Labor Graph

From a functional perspective, the only essential features of labor are cervical dilation and
fetal descent. The assessment of labor on a functional rather than on an anatomic/physiologic
basis was pioneered by Caldeyro-Barcia,12 who evaluated the number of uterine contractions
necessary to effect delivery, and Friedman,32 who emphasized that the arbiter of labor
progress was cervical dilation and fetal descent as a function of time. The process of normal
labor was dissected and defined (Table 2). Specific abnormal labor patterns were related to
causative factors, and specific management decisions based on the type of abnormality were
proposed.

Table 2: Diagnostic criteria for abnormal labor patterns

Labor pattern Nulliparous Parous

Protraction disorders
Dilation <1.2 cm/h <1.5 cm/h
Descent <1.2 cm/h <1.5 cm/h
Arrest disorders
Dilation >2 h >2 h
Descent >1 h >1 h

Adapted from Dystocia and the augmentation of labor. ACOG Technical Bulletin No. 218,
December 1995 (replaces no. 137, December 1989, and no. 157, July 1991). American
College of Obstetricians and Gynecologists. Int J Gynaecol Obstet 53:73, 1996.

In the 1950s, Friedman introduced the “graphico/statistical” method of labor analysis; it was
recommended that the clinician make a graph of dilation of the uterine cervix and station of
the fetal presenting part versus time.32 An idealized labor is presented in Fig.1. Dilation
extends from 0 to 10 cm, and station extends from either −3 to +3 finger breadths or −5 to +5
cm, depending on the method used for station. We recommend the −5 to +5 cm system for
station.18 A graphical presentation of labor greatly facilitates the diagnosis of arrest and
protraction disorders (Fig. 2). At the time of each examination, the physician or nurse in
attendance should record the time, dilation, and station on the labor graph. Constructing the
graph after labor has been completed is not helpful.

Fig 1: An idealized labor pattern. The normal patterns of cervical

dilation (solid line) and descent (broken line) as they are traced
against elapsed time in labor. The distinctive phases of the first stage
are shown. The active phase comprises the interval from the onset of
the acceleration phase to the beginning of the second stage.

Fig 2: Graphic representation of disorders of the functional divisions of

labor. Cervical dilation and fetal station as the ordinate and time as the
abscissa. At the top, the normal dilation curve is compared with the
preparatory division abnormality of prolonged latent phase (1). The middle
group presents the protraction disorders of the dilational division—
protracted active-phase dilation (2) and protracted descent (3). At the
bottom are the pathologic states of the pelvic division, including prolonged
deceleration phase (4), secondary arrest of dilation (5), arrest of descent
(6), and failure of descent (7). The broken portions of the curves represent mean normal
patterns; the unbroken portions represent abnormal patterns.

Onset of labor is considered 0 time on the labor graph and is defined as the time of onset of
regular uterine contractions. Because the patient is generally at home at the beginning of
contractions, the onset of labor (latent phase) is based on her estimate. At the beginning of
labor for nulliparas and multiparas, the usual cervical dilation is approximately 2 cm,
although with premature rupture of the membranes, sometimes the cervix may be closed.
Some multiparas may begin labor, however, with cervical dilations of 4–5 cm. The station of
the fetal presenting part tends to be lower in the pelvis in nulliparas than in multiparas.
Although it often is said that nulliparas should have an engaged fetal head at the onset of
labor, this is frequently not the case. On average, the presenting part can be expected to be a
−1 station in the nullipara at labor onset compared with −1 to −2, or even slightly higher, in
the multipara.

When the patient has been admitted in labor, the question arises as to the appropriate interval
for subsequent examinations. This is a controversial subject. Some authorities believe that
repeated vaginal examination increases the risk for postpartum endometritis.41 Other
authorities, using multivariate analyses, have suggested that the problem is not repeated
examination but rather prolonged labor, which in turn leads to more examinations.42 We
recommend examinations approximately every 2 hours during latent phase, with
examinations each hour later in active phase.40 This general approach, with appropriate
documentation of the examinations, helps ensure that developing labor abnormalities are
neither missed nor neglected. An increased risk for infection has not been documented over
many thousands of deliveries managed with this approach.

In our experience, clinicians often resist making labor graphs during the labor progress,
despite service policy. In response to this resistance, an approach has been developed that
allows a similar decision process without the necessity of making a labor graph. All that is
necessary is that the clinician determines whether labor is latent or active and remembers
some simple numeric rules. If the cervix is less than 4 cm, and dilation is greater than l cm/h
in the nullipara and 1.5 cm/h in the multipara, the patient should be considered to be in latent
phase. The average slope of dilation in latent phase is less than 0.6 cm/h. The patient is in
active phase if cervical dilation is greater than 5 cm or the cervix is dilating at a rate of at
least 1 cm/hr in the nullipara and 1.5 cm/h in the multipara. The two definitions for latent and
active phases are mutually exclusive but are not exhaustive. Intermediate dilations (i.e., from
4 to 5 cm) and slopes yield an unclear picture as to the phase of labor. Often these patients are
entering active from latent phase (i.e., they are in acceleration phase).

The acceleration phase is followed by the phase of maximum slope, in which there is rapid
cervical dilation. Finally, a dilation of 9–10 cm (full dilation) is considered the deceleration
phase. The descent of the fetal presenting part may remain latent until 9 cm of dilation has
been attained, when descent should be proceeding actively (i.e., the deceleration phase is an
acceleration phase in terms of descent). The second stage of labor begins on complete
dilation.

Classically, six dysfunctional labor patterns are defined, including (1) prolonged latent phase,
(2) protracted active phase dilation, (3) secondary arrest of dilation, (4) prolonged
deceleration phase, (5) protracted descent, and (6) arrest of descent (see Fig. 2). Some
authorities would add to this list the additional diagnoses of prolonged acceleration phase and
failure to descend as an abnormality separate from arrest of descent. Precipitous labor also
sometimes is added to the list, the usual definition being a total labor duration of less than 3
hours. From a functional perspective, however, there are only two ways in which labor can be
abnormal: Dilation and descent may be either protracted or arrested.
FIRST STAGE OF LABOR

Prolonged Latent Phase

Latent phase begins with regular contractions that efface and dilate the cervix and ends with
the onset of active labor. The length of latent phase is a function of several factors. Generally,
latent phase is inversely related to cervical dilation at the time of onset of labor. Similarly the
lower in the pelvis the fetal presenting part is at the onset of labor, the shorter the latent
phase. A potential for producing prolonged latent phase with sedation must be remembered.
In most sedated patients, labor resumes when sedation has worn off.

Based on standard criteria, prolonged latent phase is diagnosed after 21 hours in the nullipara
or 14 hours in the multipara.32 This disorder is relatively rare, occurring in 3–4% of labors.43,
44
In the absence of sedation and analgesia, such long intervals tend to be unacceptable to
patients and can result in maternal exhaustion. One approach is to evaluate the patient
carefully as 12 hours in latent phase approaches. If there has been interval cervical
effacement and dilation or fetal descent (indicating that the patient is not in false labor), a
reasonable approach is to begin oxytocin augmentation. In such cases, we recommend
starting at a low dose (1–2 mU/min), with increases of 1–2 mU/min every 30 minutes. An
oxytocin infusion of 16 mU/min or less is successful in bringing the patient into active labor
in approximately 9 out of 10 cases. Typically an oxytocin infusion of 4–6 mU/min is usually
sufficient.

When studied epidemiologically, prolonged latent phase seems to be a relatively benign labor
disorder. It is associated with a 2.5-fold increase in risk for primary cesarean section,
however.45 It previously was reported that the fetus tolerates prolonged latent phase well,
without an increase in morbidity or mortality.

ACTIVE PHASE

Protracted Active Phase Dilation

For nulliparas, protracted active phase dilation should be diagnosed when the dilation rate is
less than 1 cm/h. For the multipara, the lower limit of normal is 1.5 cm/h. Based on
Friedman’s original definition,32 a limit for nulliparas of 1.2 cm/h might be used, but in our
experience, such a limit may be overly sensitive and is more difficult to remember than the 1
cm/h limit. In addition, the 1 cm/hr limit has been validated by Philpott and Castle,46 who
proposed an alternative and simple method of graphing labor progress (Fig. 3). A common
error is diagnosing protracted active phase when the patient is really in the latent phase of
labor. Because of the changes in the increased use of epidural anesthesia and its “slowing
effect,” Rouse and colleagues47 reported that the fifth percentile rate may be lower for
nulliparas and parous women (0.5 cm/h). Another potential reason for lower rate of dilation
was that Friedman reported on patients with “normal labor” who did not require oxytocin,
whereas Rouse described patients with “abnormal labor” who required augmentation.
 Fig 3: Cervicograph for evaluating the active phase of labor. Zone 1
represents normal labor (>1 cm/h). Zone 2 indicates the possibility of
dysfunctional labor. Zone 3 indicates a need for intervention. (Adapted
from Philpott RH, Castle WM: Cervicographs in the management of
labour in primigravidae. J Obstet Gynaecol Br Commonw 79: 592,
1972)

Protracted active phase dilation is a common dysfunctional labor pattern. It seems to be

associated with mild cephalopelvic disproportion. Clinical experience with intrauterine
pressure catheters suggests that many cases of protracted active phase dilation might have
been termed primary uterine inertia or hypertonic uterine inertia previously, suggesting some
type of uterine dysfunction. There also may be an iatrogenic contribution to this labor
abnormality, with the possibility that supine position may decrease uterine contractility,
leading to slowed cervical dilation. Also, although active labor is relatively insensitive to
analgesia, the use of narcotics may be associated in some cases with precipitating slow
dilation in active phase. Early epidural anesthesia, particularly if the station of the presenting
part is higher than −1, also is associated with an increased risk for this labor abnormality.
Sharma and coworkers48 compared labor progress between patients with epidural anesthesia
and patients with intravenous narcotics and noted a 1-hour increase in the duration of the first
stage of labor.

The occurrence of protracted active phase dilation should also be considered an important
risk for later labor dysfunction. The risk for subsequent arrest of dilation or descent,
prolonged deceleration phase, and protracted descent may be increased 2.5-fold to 8-fold in
nulliparas and multiparas. As a clinical rule of thumb, later problems should be anticipated
when active labor begins more slowly than normal.

Despite its relatively common occurrence, there are limited data for the use of oxytocin in
treating protracted dilation. There is substantial evidence, however, that the “active
management of labor” constitutes an efficacious and safe approach. In a 1988 study by
Akoury and colleagues,49 552 nulliparas with singleton pregnancies who had established
labor and amniotomy were compared with 533 previously delivered similar patients. The
study group received amniotomy and oxytocin augmentation, up to 40 mU/min for dilation
rates less than 1 cm/h. Results of this historically controlled study indicated that in the
actively managed group, the frequency of labor lasting greater than 12 hours was reduced
almost threefold from 20% to 7%. The cesarean birth rate was decreased to one-third of the
previous rate, from 13% to 4.3%. Forceps operations were decreased from 29% to 19.4%.
These differences in operative delivery rates were not associated with any increase in
perinatal morbidity or mortality in the study group.

Although the cause of protraction is unclear, a reasonable approach includes early detection
of abnormal labor progress in active phase, institution of fetal monitoring, lateral positioning,
and careful use of oxytocin. Just as causative factors for protracted active phase dilation are
unclear, so is the most appropriate management. Considering that there may be some
association between mild disproportion and malposition (i.e., occiput posterior and occiput
transverse), this can be a trying situation for the patient and the physician. A conservative
approach is to avoid unnecessary sedation and anesthesia.

Secondary Arrest of Dilation

Secondary arrest of dilation is diagnosed when there has been no change in cervical dilation
for at least 2 hours. This time criterion is the same for nulliparas and multiparas and is based
in part on the certainty with which cervical dilation can be determined on digital examination.
Secondary arrest, which occurs in 5–10% of labors in most series, is more frequent with term
than preterm and with larger than smaller fetuses. This abnormality occurs more frequently
than prolonged latent phase but less frequently than protracted active-phase dilation. It has
been recognized as being the most severe of dilation abnormalities because of its association
with increased fetal morbidity and mortality and with a considerably increased risk of
cesarean birth.

There is a well-recognized relationship of secondary arrest with fetopelvic disproportion. It

has been suggested that the diagnosis not be made unless labor is active, the cervix is dilated
greater than 4 cm, and there has been 2 hours of no cervical change with 200 Montevideo
units or more per 10-minute interval.13 The development of secondary arrest is associated
statistically with the occurrence of persistent malposition (i.e., persistent occiput posterior
and persistent occiput transverse). It is unclear, however, whether the associated malposition
is a result or cause of the arrest disorder.

There is a fivefold increase in the risk for secondary arrest of dilation in nulliparous labors
complicated by protracted active phase dilation, with the eightfold increase seen in such
multiparous labors. This increase suggests a possible causative role for “uterine inertia.” This
situation has not been well studied, however, either electrophysiologically or mechanically.
Compared with the available information concerning cause, there are many studies with well-
defined results concerning the appropriate treatment of secondary arrest of dilation. This
secondary arrest of dilation is the classic indication for “trial of labor”; this includes diagnosis
of failure to progress and oxytocin augmentation of labor for patients with an arrest but
without evidence of disproportion.

Friedman32 reported a primary section rate of approximately 40% after secondary arrest of
dilation. He suggested that given appropriate management, this rate might be lowered, an
observation that has been validated by subsequent studies. In a study of 255 primary cesarean
and 2362 vaginal deliveries, Sokol and colleagues45 reported a primary cesarean section rate
of 25.5% after secondary arrest of dilation. This rate represented a 2.6-fold increase. Bottoms
and associates50 studied 4573 singleton, vertex, spontaneous labors. In this study, arrest
disorders occurred in 593 (11%) labors. Patients with arrest disorders were managed by a
“conservative” medical protocol including ambulation, amniotomy, and oxytocin. It was
found that approximately 50% of the arrests resolved spontaneously, with the other 50%
requiring oxytocin stimulation. Overall, 83% of the women delivered spontaneously or with
low forceps. The midforceps rate was increased fivefold to approximately 4%. The cesarean
rate also was increased fivefold to approximately 13%. In this series, there was no perinatal
mortality and no increase in low Apgar scores at 5 minutes (1.5%). Neonatal morbidity was
similar among cases treated conservatively compared with neonates delivered via cesarean
section. It was concluded that conservative management with oxytocin augmentation was
capable of producing maternal and infant outcomes with an increased, but still low, cesarean
birth rate.

During active labor, patients should have cervical examinations at least every 2 hours to
facilitate the diagnosis of secondary arrest as promptly as possible. Examination closer to
every hour may be warranted to detect incipient arrest.43 Electronic monitoring for
evaluation of uterine contractions and fetal heart rate is warranted in cases of secondary arrest
disorders. Oxytocin augmentation, starting at 1–2 mU/min with increasing infusion rate every
30 minutes, is begun with a goal of mimicking normal uterine contractility during the active
phase. Maternal/fetal status should be monitored closely. In the first hour of augmentation,
little cervical dilation may occur, although in some cases cervical dilation resumes rapidly,
typically producing spontaneous vaginal delivery without further incident. More often,
however, there is fetal descent during the first hour, with cervical dilation resuming
thereafter. In patients receiving oxytocin labor augmentation, more than 90% achieve greater
than 200 Montevideo units, and 40% have greater than 300 Montevideo units. It had been
suggested previously that to diagnose labor arrest in active labor, a patient must have a
uterine contraction pattern with greater than 200 Montevideo units for at least 2 hours.
Approximately 60% of women who experience 2 hours of labor arrest with greater than 200
Montevideo units eventually have a vaginal delivery if oxytocin is continued. Studies indicate
that it is safe and effective to extend this period to 4 hours to reduce further the number of
patients with active labor arrest.47, 48, 49, 50, 51

If there is evidence of fetal distress, the fetus may be evaluated biochemically, but often
cesarean delivery is necessary. If labor is not progressing normally within 2–3 hours after the
beginning of the oxytocin augmentation, cesarean section may be indicated. The need for
cesarean delivery is relatively infrequent, however. Studies by Rouse et al.51 have suggested
that the likelihood of vaginal delivery can be improved by waiting for up to 4 hours of
adequate contractions with the administration of oxytocin. In his studies, more than 60% of
patients with arrest of active phase for more than 2 hours eventually achieved a vaginal
delivery. In his studies, however, there was an increased risk of shoulder dystocia, but none
were accompanied by brachial plexus palsies.24, 47, 51 The clinician may expect at least three
of four patients with this complication to have a successful vaginal delivery. It seems that
immediate cesarean delivery for secondary arrest is unwarranted. Good outcomes can be
obtained by way of conservative (medical) management.

Prolonged Deceleration Phase

The deceleration phase is the third phase of active labor, after the phase of maximum slope.
The onset of deceleration phase begins at 9 cm for nulliparous and multiparous labor. Active
descent should start by the beginning of deceleration phase, although in many labors active
descent begins earlier in active labor. Engagement that does not occur by the beginning of
deceleration phase (i.e., 9 cm) in nulliparas and by the end of deceleration phase in multiparas
is abnormal. Prolonged deceleration phase requires at least 3 hours for diagnosis in
nulliparous labor and 1 hour for diagnosis in multiparous labor. Because descent should be
active by this time in normal labor and because the intervals for diagnosis of descent
abnormalities are shorter than those necessary for the diagnosis of prolonged deceleration
phase, the clinician’s attention should focus more on descent than on dilation at this time in
labor.

If engagement has not occurred by 9 cm of dilation, the likelihood of a second-stage

abnormality is increased. Prolonged deceleration phase is strongly associated with descent
disorders. Typically, prolonged deceleration phase as a labor abnormality seems most closely
related to secondary arrest. Careful augmentation of labor with oxytocin, as per the protocol
described earlier, is often warranted. Prolonged deceleration phase is relatively rare,
occurring in only 1–3% of labors. Clinical experience suggests such cases are associated
frequently with persistent occiput transverse or posterior or some pelvic abnormality
frequently detectable on clinical pelvimetry. Patients with this abnormality sometimes
develop cervical edema with considerable molding of the fetal skull. Fetal heart rate
decelerations occur with increased frequency in this situation, leading to a temptation to
apply forceps through an almost but still incompletely dilated cervix. This impulse must be
resisted because there is a substantial chance of severe fetal and maternal trauma.

SECOND STAGE OF LABOR

Onset of the second stage of labor occurs with full dilation of the cervix. On average, the
median duration of the unintervened second stage of labor is estimated to last 1 hour in
nulliparas and 15 minutes in multiparas. “Clinical limits” for second-stage durations at which
time the clinician should become concerned and anticipate problems with delivery have been
proposed. For nulliparas, this clinical limit is 2 hours, and for multiparas, it is 1 hour, but the
clinician should become concerned when the second stage exceeds 45 minutes. These limits
are not intended to indicate that delivery must be achieved by these times. Before the
availability of electronic fetal monitoring, it was believed by many clinicians that a maximum
of 2 hours of the second stage was safe for the fetus. This belief was based on epidemiologic
evidence that fetal morbidity and mortality in nulliparas was increased when the second stage
was at least 2.5 hours.

An overview of the literature strongly suggests that the simple use of time limits for second
stage no longer constitutes an appropriate approach to management of the second stage of
labor. More detailed maternal/fetal assessment with carefully considered intervention seems
optimal. This assessment may include fetal scalp blood sampling, which is usually technically
easiest to perform during the second stage of labor. Close observation, carefully considered
intervention, and technically competent execution of the chosen intervention (i.e., electronic
fetal monitoring, fetal scalp blood sampling, forceps, vacuum extraction, or cesarean
delivery) are necessary to ensure the best maternal/fetal outcome possible in the face of
abnormalities that may develop during the second stage of labor.

Protracted Descent

Protracted descent should be diagnosed in nulliparous labor when descent is proceeding at

less than l cm/h and in multiparous labor when descent is proceeding at less than 2 cm/h.
Although it is true that station of the fetal presenting part is more difficult to estimate reliably
than is dilation, it is possible to make this diagnosis within 1 hour for the nullipara and within
0.5 hour for the multipara. A careful balance should be sought between overdiagnosis and
failure to diagnose protracted descent as promptly as possible because treatment may entail
substantial intervention. The cause of protracted descent often includes malposition and
relatively mild degrees of fetopelvic disproportion; absolute fetopelvic disproportion is
unusual. Slow descent frequently is associated with the use of epidural anesthesia.

Protracted descent requires skillful and attentive management. It frequently is preceded by

other dysfunctional labor patterns, which may constitute evidence of substantial disproportion
or uterine dysfunction or both. Under such circumstances, whether or not it is reasonable to
attempt oxytocin stimulation is an open question. The answer must be rendered on a case-by-
case basis. It is not unreasonable to suggest that if protracted descent occurs in a labor already
complicated by preceding dysfunctional labor patterns in the presence of oxytocin
augmentation, perhaps it would be best to proceed with cesarean delivery.
If the patient also has an epidural anesthetic or voluntary pushing appears inadequate,
effective coaching and allowing more time may be successful. Although controversial, many
clinicians decrease or discontinue the epidural anesthetic to increase the effectiveness of the
parturient’s pushing. Other clinicians believe that having the patient in an upright position
allows the most effective voluntary pushing and has the benefit of gravity. However, the
literature and clinical experience are inconsistent on these points.

Appropriate management for protracted descent, which has been associated with worsened
infant outcome, includes institution of electronic fetal monitoring. Fetal monitoring often is
discontinued when the patient is moved from the labor to the delivery room. Because fetal
monitoring just before delivery relates most closely to neonatal status, the generation of a
paper tracing in the delivery room for documentation is important. If protracted descent
occurs in a labor that has been otherwise normal, it is probably reasonable to augment with
oxytocin. In the nullipara, if full cervical dilation has not been achieved and there is a
persistent anterior cervical lip that becomes edematous, the chance of atraumatic vaginal
delivery is markedly reduced. In the multipara, it is sometimes possible to support the
anterior lip and have the patient bear down, allowing the achievement of full dilation and
significant descent. This latter approach seems particularly effective if preceding labor has
been normal and there is a good response to oxytocin stimulation.

Protracted descent frequently is associated with the presence of a persistent occiput posterior.
Previously the management of occiput posterior commonly included forceps rotation. Direct
occiput posterior delivery and manual rotation constitute appropriate and potentially less
traumatic approaches, however. Normal spontaneous vaginal delivery and low forceps
procedures occur in approximately half of cases complicated by protracted descent.

Arrest of Descent

The diagnosis of arrest of descent should be made when descent has stopped entirely for at
least 1 hour in the nullipara and 0.5 hour in the multipara. It frequently is preceded by and has
the same causative factors as protracted descent. When arrest of descent has not been
preceded by other dysfunctional labor patterns, experience suggests that, similar to secondary
arrest of dilation, it is extremely sensitive to oxytocin augmentation. Low-dose intravenous
oxytocin frequently is associated with spontaneous vaginal delivery. As with the case of
augmentation for other labor abnormalities, electronic monitoring is appropriate.

When arrest of descent is preceded by other dysfunctional labor patterns, the situation is
similar to that regarding protracted descent. If the patient already is receiving oxytocin
augmentation or full dilation has not been attained, proceeding to cesarean section is probably
the best approach. Sometimes vaginal birth may be attained, but great care must be taken
when attempting delivery by midforceps or vacuum extraction under these circumstances.
Before undertaking an operative vaginal delivery, it is crucial to evaluate the maternal outlet
carefully, particularly in terms of the angle of the pubic arch and the distance between the
ischial tuberosities. Also, the possibility of macrosomia and shoulder dystocia should be
entertained. The situation in which the vertex is below +1 cm, but descent has ceased is not
rare. The delivery of such a deeply engaged fetal head at cesarean section commonly results
in lacerations of the cervix and lower uterus. The possibility of operative vaginal delivery
continues to warrant consideration in such cases.
THIRD STAGE OF LABOR

Most studies of the third stage of labor have been confounded by manual removal of the
placenta. In a study of 45,852 gravidas, Dombrowski and coworkers52 used life-tablele
analysis to control for the confounding effects of manual placenta removal. This analysis
revealed that manual removal of placentas shortened the apparent duration of third stage of
labor, especially among preterm deliveries (Table 3). Premature delivery was a significant
risk factor for complications of the third stage of labor, such as retained placenta (undelivered
greater than 30 minutes), manual removal, and hemorrhage (estimated blood loss greater than
500 mL).

Table 3: Life-tablele analysis with censoring of manual placenta removal: predicted third-
stage duration in minutes and predicted incidence of retained placenta

Percentiles Undelivered at 30 minutes

Gestational age (wk) 10th 50th 90th % N
20 2 19 180 42.5 17
21 4 25 180 47.1 32
22 3 19 180 37.7 34
23 3 17 240 40.7 44
24 4 16 80 32.2 38
25 3 11 60 24.7 23
26 3 8 40 11.5 12
27 3 6 19 6.8 6
28 3 8 25 7.4 9
29 3 6 24 8.2 12
30 3 6 21 5.9 13
31 3 6 17 3.8 10
32 3 6 19 6.4 26
33 3 6 20 6.2 36
34 3 6 17 3.5 28
35 3 6 16 3.7 42
36 3 6 17 3.8 72
37 3 6 15 3.2 112
38 3 6 14 2.4 142
39 3 6 14 2.1 183
40 3 6 14 2.1 280
 41 3 6 14 2.1 115
42 3 6 14 1.6 35
43 3 5 15 1.3 4

Adapted from Dombrowski MP, Bottoms SF, Saleh AAA, et al: Third stage of labor:
Analysis of duration and clinical practice. Am J Obstet Gynecol 172:1281, 1995

The management of the third stage of labor (i.e., when placentas should be removed manually
or managed expectantly) is controversial. Life-tablele analysis estimated that 90% of term
placentas spontaneously deliver by 15 minutes, and only 2.2% would be undelivered at 30
minutes (i.e., a “retained placenta”).52 A 30-minute threshold would result in a low
intervention rate in term gestations. The current management of third stage of labor is a
function of several factors, including a perceived standard of care that term placentas should
be delivered by 30 minutes and fear of hemorrhage with a prolonged third stage. Although
the most important factor is a desire to reduce maternal hemorrhage and need for
transfusion,53 physician and patient anxiety also play a role. The incidence of hemorrhage has
been decreased by the institution of prophylactic oxytocin, controlled cord traction, fundal
massage, and early cord clamping to facilitate delivery of the placenta.54, 55

The frequency of hemorrhage peaks by 40 minutes regardless of gestational age. This peak
may be because manual placental removal was accomplished for patients with active uterine
bleeding, although manual removal per se may increase blood loss in some cases. On the
basis of these data, it would be difficult to justify routine manual removal of the placenta
before 10 minutes for any gestational age. We believe that manual removal of the placenta
must be balanced against the risk for increased maternal trauma and hemorrhage. It is
unknown whether the risk of hemorrhage or the amount of blood loss can be decreased by
manual placental removal; the optimal time for intervention can be determined only by a
prospective clinical trial.

CONCLUSION

There is no known test that can differentiate normal from abnormal labor. The diagnosis and
optimal management of abnormal labor combine science and art. The management of
abnormal labor taxes one’s clinical skills under the best of circumstances. Such cases are
complicated by patients who demand and expect a painless and fast delivery resulting in a
perfect infant. The possibility of malpractice litigation further complicates the issues—a
thorough documentation of events, especially in the face of maloccurrence, cannot be stressed
enough. A key to the optimal management of abnormal labor remains intensive observation
with conservative, well-chosen, and carefully executed interventions.