Expert Review
org
The latent phase of labor
Wayne R. Cohen, MD; Emanuel A. Friedman, MD, Med ScD
Introduction
It is generally obvious to the observer,
and more so to the parturient, that after
labor begins, there is a period during
which uterine contractions may be reg-
ular and painful but are accompanied by
little or no progress in cervical dilatation.
This period, known as the latent phase, is
crucial to the normal evolution of labor.
The term was coined by Friedman in his
seminal 1955 work describing the
normal course of primigravid labor.1 It
was chosen to emphasize that subclinical
events were occurring that were not
apparent to the observer but were paving
the way for the quite evident changes in
cervical dilatation that would soon
occur.
Although the lack of (or negligible)
progressive dilatation suggests relative
quiescence, the latent phase is a period of
intense biochemical and electrome-
chanical activity. It can be viewed func-
tionally as a time during which the cervix
and surrounding tissues are being pre-
pared for the more intense events of
cervical dilatation and fetal descent that
will follow.2e4 The latent phase is
defined as the interval between the onset
of labor and the beginning of active
phase dilatation. It is usually described
by its duration. Precise determination of
latent phase length would require
knowledge of the time at which labor
From the Department of Obstetrics and
Gynecology, The University of Arizona College of
Medicine, Tucson, AZ (Dr Cohen); and
Department of Obstetrics, Gynecology, and
Reproductive Biology, Harvard Medical School,
Boston, MA (Dr Friedman).
Received Jan. 18, 2022; revised April 7, 2022;
accepted April 11, 2022.
The authors report no conflict of interest.
Corresponding author: Wayne R. Cohen, MD.
cohenw@email.arizona.edu
0002-9378/$36.00
ª 2022 Elsevier Inc. All rights reserved.
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ajog.
The latent phase of labor extends from the initiation of labor to the onset of the active
phase. Because neither margin is always precisely identifiable, the duration of the latent
phase often can only be estimated. During this phase, the cervix undergoes a process of
rapid remodeling, which may have begun gradually weeks before. As a consequence of
extensive changes in its collagen and ground substance, the cervix softens, becomes
thinner and dramatically more compliant, and may dilate modestly. All of these changes
prepare the cervix for the more rapid dilatation that will occur during the active phase to
follow. For the clinician, it is important to recognize that the latent phase may normally
extend for many hours. The normal limit for the duration of the latent phase should be
considered to be approximately 20 hours in a nullipara and 14 hours in a multipara.
Factors that have been associated with a prolonged latent phase include deficient
prelabor or intrapartum cervical remodeling, excessive maternal analgesia or anesthesia,
maternal obesity, and chorioamnionitis. Approximately 10% of women with a prolonged
latent phase are actually in false labor, and their contractions eventually abate spon-
taneously. The management of a prolonged latent phase involves either augmenting
uterine activity with oxytocin or providing a sedative-induced period of maternal rest.
Both are equally effective in advancing the labor to active phase dilatation. A very long
latent phase may be a harbinger of other labor dysfunctions.
Key words: cervical remodeling, cervical ripening, collagen, epidural anesthesia, false
labor, initiation of labor, labor, latent phase, morphine, oxytocin, prolonged latent phase,
therapeutic rest
began and the time of onset of the active release of various substances (notably
phase. Neither, especially the former, can the proinflammatory platelet-activating
always be identified with certainty, often factor) that may contribute to a cascade
rendering latent phase duration an of inflammatory events.11 Important in
estimate. this regard is the increased expression of
proinflammatory transcription factors
Initiation of labor that diminish progesterone and its re-
The onset of labor is associated with ceptor activity, thus neutralizing factors
uterine contractions of increasing fre- that helped maintain uterine quiescence
quency and intensity. The cervix be- during most of pregnancy.12 Analysis of
comes more effaced and often begins to the myometrial transcriptome during
dilate. However, attempting to pinpoint labor supports the importance of
the onset of labor using these quotidian inflammation in the parturitional pro-
clinical measures lacks precision.5 As a cess, as gene activity during term labor
consequence, the literature addressing typically differentially expresses loci
this issue, while extensive, is so contra- involved in the inflammatory response
dictory and inconsistent that it is not and related systems.13
especially helpful.6 Some progress in recognizing the
There is strong evidence that labor onset of labor has been made using
begins through an inflammatory electrohysterography (EHG); however,
process,7e9 which may be triggered by although differences in electrical signals
oxidative stress related to senescence of generated between prelabor and true
chorionic and amniotic cells at term.10 labor contractions have been identified,
Further evidence that fetal events this transition seems to occur gradually,
trigger the initiation of labor is that fetal so the value of EHG for determining the
lung maturation is accompanied by the precise time of labor onset or for
MAY 2023 American Journal of Obstetrics & Gynecology S1017
Expert Review
distinguishing true labor from false labor
remains uncertain.14,15 The application
of methods to better characterize the
complex 3-dimensional propagation of
electrical signals within the uterus may
provide valuable insights in this regard.
Despite the recent advances in our
understanding of the control of uterine
activity, no discrete endocrine, chemical,
or biomechanical trigger for the initia-
tion of human labor has been identified,
and therefore, no measurable biomarker
exists to determine whether a woman’s
labor has begun.6 Lacking a more reliable
and predictive tool, clinicians often rely
on contraction frequency to decide
whether a patient is in labor. Most
women at term having at least 12 con-
tractions per hour are in labor, but
approximately 25% of women are not;
similarly, about half with a lower
contraction frequency may be in true
labor or are about to enter labor.16 The
clinician must make an estimate based
on available information from the pa-
tient and her examination. Until more
precise tools become available, we
recommend assuming that labor has
commenced when contractions are
regularly spaced and are occurring 5
minutes apart, while recognizing the
substantial chance of error inherent in
this approach.
Cervical remodeling
Although the cervix is sometimes
considered a passive mechanical guard-
ian of the uterine contents, it is a com-
plex structure that becomes quite
metabolically active just before and after
the onset of labor.17e19 The cervix is
approximately 80% dense connective
tissue by weight; the remainder is largely
smooth muscle, epithelial, vascular, and
immune cells.
A process of structural remodeling of
the cervix occurs to a variable extent before
the onset of labor and accelerates dramat-
ically during the latent phase. These events
are often referred to by clinicians synony-
mously as maturation or ripening. These
terms generally refer to palpable changes in
the cervix, including shortening, reduced
firmness, increased compliance, and often
a small amount of dilatation. However,
investigators recognize several overlapping
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phases in the structural reorganization of
the cervix.20e22 Softening begins early in
pregnancy, followed later by evidence of
inflammation, alterations in connective
tissue structure and their biomechanical
consequences, dilatation, and then post-
partum repair. Clinical ripening often
progresses with singular urgency during
the latent phase of labor. The cervix can be
felt to become more compliant, softer, and
thinner as labor approaches and as the
latent phase progresses. In addition, these
changes affect the lower uterine segment,
which becomes thinner and stretches to
accommodate the fetal head.23 Why the
cervix of some women becomes maximally
effaced, softened, and even somewhat
dilated before labor and in others remains
thick, closed, and unyielding is not known.
A complex set of biochemical events allows
these physical changes to occur. Differ-
ences in the genes that encode the sub-
stances that participate in these events
probably help determine the course of
cervical remodeling in an individual. Very
little is known about this genetic control of
early labor, but studies of the cervical
transcriptome have begun to identify genes
that are expressed in the cervical remod-
eling process.17,18
Cervical remodeling often occurs
somewhat differently in multiparas than
in women who have not had a previous
vaginal delivery. In some parous women,
the cervix is often 2 or 3 cm dilated
before labor begins. However, in many
multiparas, cervical effacement and
softening do not begin until well into the
first stage of labor.
Both squamous and columnar
epithelial surfaces of the cervix prolifer-
ate during gestation. They serve as an
immunologic barrier and express spe-
cific proteins that contribute to soft-
ening. These include connexins (gap
junction proteins), hyaluronan synthase,
and desmogleins.20e24
The function of cervical smooth
muscle is uncertain.24e27 It is concen-
trated in the upper cervix near the in-
ternal os and is electrically active
throughout labor. This muscle has a
different activity pattern than that of the
uterine corpus, displaying primarily
high-frequency short-duration bursts on
electromyographic recordings.28,29 Of
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interest, cervical contractions may occur
independent of muscular activity in the
corpus.25 It has been suggested that
cervical contractions occur primarily in
the latent phase and influence its
duration.28e30 This observation begs the
question of whether cervical muscle tis-
sue serves to help maintain dilatational
stasis in the latent phase until optimal
conditions for more rapid progress have
been achieved.
Fibrillar collagen is the predominant
cervical protein and contributes heavily
to the tensile strength (compliance) of
the cervix. During pregnancy, the cervi-
cal stroma becomes highly vascularized
and often shows signs of inflammation.
Collagen content increases, and smooth
muscle cells hypertrophy.31 Although
there is some evidence that cervical
remodeling is essentially an inflamma-
tory process, some studies have cast
doubt on this model.21
At term, changes occur in the cervical
collagen structure, and there is degra-
dation of its fibers. In addition,
destruction and apoptosis32 of stromal
fibroblasts and smooth muscle cells
become evident, provoked by the in-
crease in the concentration of lysosomes
and cytophagolysosomes and their
products.31 Locally synthesized nitric
oxide is an important contributor to the
ripening process.33
Cervical collagen structure is affected
by the composition of the extracellular
matrix, particularly its glycosaminogly-
cans (especially hyaluronan) and various
proteoglycans. There is an increase in the
local production of hyaluronan, which
loosens the dense collagen framework.
Concentrations of dermatan sulfate, an
important stabilizer of cervical consis-
tency, diminish. In addition, the release
of interleukins results in leukocyte
migration into the cervix and the release
of various proteases. There are changes
in proteoglycans as well. The conse-
quence of these biochemical changes is a
dramatic degradation and reorganiza-
tion of connective tissue elements in the
cervix, which change its biomechanical
characteristics. Its compliance increases
rapidly, a change that can be appreciated
(but not precisely quantitated) clinically
as the cervix becomes softer, thinner, and
ajog.org
more stretchable. Several sophisticated
techniques aimed at quantifying these
physical changes have been explored in
the hope of identifying a threshold of
cervical elasticity, distensibility,
compressibility, water content, and other
measures that would distinguish the
onset of true labor. Several of these ap-
proaches seem potentially useful, but
none has yet been shown effective in a
clinical trial.34e36
The latent-to-active phase transition
Many clinicians and investigators as-
sume incorrectly that the transition from
the latent phase to the active phase of
labor occurs at a fixed degree of dilata-
tion. Regrettably, there is no uniform
understanding of when in labor this
transition occurs, particularly given the
wide individual variation among partu-
rients. In various studies and clinical
guidelines, a dilatation of 3-, 4-, 5-, or 6-
cm dilatation has been assigned as the
transition point.37e42 This makes little
practical or intellectual sense because the
changeover may normally occur be-
tween 3- and 6-cm dilatation (occa-
sionally, even more or less) and depends
on several factors, including especially
the degree of prelabor cervical matura-
tion. The transition point in an indi-
vidual labor can only be determined in
retrospect by identifying the place on the
dilatation curve at which the rate of
dilatation began to accelerate.42 In 1
study,43 it was found that at 4-cm dila-
tation fewer than half of nulliparous la-
bors had entered active phase dilatation.
By 5 cm, approximately 74% had done
so, but at least 10% were still in the latent
phase at 5-cm dilatation. Therefore, we
feel it is important to emphasize that an
arbitrary choice for designating the cer-
vical dilatation at the endpoint of the
latent phase of labor and the beginning
of the active phase, whether for research
uniformity or clinical application, is
fraught with error. That error includes
both cases still in the latent phase at and
beyond that chosen dilatation and those
already in the active phase beforehand.
When a latent phase in which there has
been some dilatational progress transi-
tions to a slowly progressing active phase,
it can be very difficult to recognize the
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change. Moreover, a normal latent phase
exhibiting progressive dilatation is often
mistaken for a protracted active phase. In
such situations, a useful clinical guideline
is that it is unusual (but not unheard of)
for a nulliparous labor to still be in the
latent phase at or beyond 6-cm dilata-
tion. Moreover, it is unlikely for a labor to
still be in the latent phase if the rate of
cervical dilatation exceeds 0.6 cm/h.
Attempts to define the physiological
events that occur in the shift from latent-
to-active phase dilatation have not found
success. Spectral analysis of electromyo-
graphic patterns has provided important
clues in this regard44,45 and is the subject
of considerable ongoing research.46e48
The transition to the active phase
seems to be associated with higher fre-
quencies in the power spectrum density
of the EHG, consistent with energy being
generated at a higher rate. This suggests
that the clinically observable differences
in latent and active phase dilatation
patterns have electrophysiological
correlates.
False labor
Sometimes regular, intense uterine con-
tractions occur, and both the patient and
her obstetrical attendants deduce that
labor has begun. They may be incorrect.
In false labor, such uterine activity may
be transient or may last for many hours
before it abates spontaneously. This
pattern of uterine contractility is not
generally associated with changes in
cervical dilatation or effacement.
Approximately 5% to 10% of women
found to have an abnormally long latent
phase are actually in false labor.42 Dis-
tinguishing false labor from a normal or
prolonged latent phase by clinical
criteria is often impossible, particularly
on a prospective basis.49 This is unfor-
tunate because managing false labor can
be expensive, wasteful (because of over-
crowding of labor facilities), inconve-
nient for the patient, and frustrating for
her and her caretakers.50 Moreover, false
labor can be associated with iatrogenic
morbidity, often related to the unnec-
essary use of oxytocin, such as fetal
hypoxemia and operative delivery.51,52
Clinicians should be alert to the fact
that when true labor eventually develops
MAY 2023 American Journal of Obstetrics & Gynecology
Expert Review
in a woman previously diagnosed with an
episode of false labor, some,49,51 but not
all,52,53 studies suggested that there is an
elevated risk of dysfunctional labor pat-
terns and the potentially hazardous use
of oxytocin and instrumental delivery.
This raises the question of whether false
labor is a premonitory manifestation of
some failure in the normal latent phase
mechanism and, as such, is sometimes a
bellwether for subsequent dystocia.
Efforts to distinguish the onset of true
labor from the presence of false labor on
clinical grounds are of little avail, and
using modern diagnostic methods has
not thus far been helpful either. An
ultrasonographically determined cervi-
cal length of 1.5 cm was shown in 1
study to have an 83% positive predictive
value for identifying true labor54;
another study found it to be only 14%.55
Combining cervical length and utero-
cervical angle improved predictive per-
formance in the latter study, but it
remains unclear whether these or other
sonographic measurements will provide
sufficient sensitivity and specificity to
guide clinical decision-making when the
presence of true labor must be verified.
Latent phase duration
Determining the normal length of the
latent phase accurately would require
precise information about the time of
labor onset and the beginning of the
active phase of dilatation in a large
cohort of women. As noted above,
neither can always be determined with
certainty. Nevertheless, it is important to
adopt a uniform standard for use in
clinical care. The data from Friedman
indicated that the 95th percentile for the
length of the latent phase is 20 hours in
nulliparas and 14 hours in multiparas,
and we recommend these limits as
practical guidelines for clinical use.3,42
Other investigators have found values
that are similar to, shorter, or longer
than these.38,56e58 The differences were
attributable to variations in the way la-
bor onset and the initiation of the active
phase were defined. Studies and clinical
experience suggest that the latent phase
is considerably longer in nulliparas than
in multiparas, but this has not been a
universal investigative finding.37
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Expert Review
Peisner and Rosen56 studied the in-
fluence of easily measured variables on
the duration of the latent phase. They
found that cervical dilatation at the onset
of labor accounted for approximately
10% of the variance in duration. Parity
contributed only 1.4% and station <1%.
These observations suggested that clini-
cally unmeasurable or unmeasured fac-
tors have a major influence on the length
of the latent phase.
Prolonged latent phase
A “prolonged latent phase” is defined as
one that exceeds the 95th percentile limits
described above. The specific cause of a
long latent phase has not been deter-
mined, but it may well reside in some
genetic or acquired impediment to
normal cervical and uterine remodeling59
or, we speculate, to insufficient or disor-
dered myometrial contractility. This same
dysfunction may predispose to episodes
of false labor. The prolonged latent phase
has been associated with several clinical
features (Table), some of which, such as
maternal obesity, also can cause active
phase abnormalities.42,57,60 The less
mature the cervix is at labor onset, the
longer the latent phase tends to be.61 A
recent evaluation of women with a long
latent phase57 suggested chorioamnionitis
and fetal malposition to be risk factors.
The reasons for these associations have
never been elucidated. Certainly, uterine
infection can inhibit labor progress, and
this is likely the explanation for the effects
of chorioamnionitis.62e65
Knowing the exact length of the latent
phase is less crucial than the simple
TABLE
Prolonged latent phase
Clinical associations
Deficient prelabor cervical remodeling
Excessive sedation, analgesia, or
anesthesia
Maternal obesity
Malposition
Chorioamnionitis
Postterm labor
Cohen. The latent phase. Am J Obstet Gynecol 2023.
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recognition of the fact that the latent
phase may normally be quite long. Fail-
ure to recognize the upper boundaries of
the normal course of this portion of la-
bor sometimes leads to unnecessary use
of oxytocin or even cesarean delivery,
under the erroneous assumption that
continuous progress should be expected
in all parts of labor or that very long la-
bors are always abnormal. Patients with a
prolonged latent phase are often quite
exhausted and emotionally discouraged.
If there is a compelling reason not to
lengthen the labor of a woman with a
long latent phase, such as the presence of
preeclampsia, prolonged rupture of
membranes, or chorioamnionitis,
oxytocin stimulation is appropriate.
Unfortunately, there is no way to deter-
mine clinically when a prolonged latent
phase is the consequence of a pathologic
process or simply a necessary physio-
logical component of a long labor. Pa-
thology is more likely present if the
latent phase is prolonged in the presence
of a ripe cervix (ie, dilated, soft, and
effaced, which tends to rule out false la-
bor) or a small or distorted pelvis (sug-
gesting cephalopelvic disproportion).
Whether having a long latent phase
predisposes to later problems during
labor or beyond is uncertain. Early data
suggested that such adverse effects were
unlikely, that the risk of cesarean or
subsequent dysfunctional labor in the
active phase was not increased, and that a
very long latent phase contributed
minimally to the risk of an abnormal
long-term outcome.42,66 More recent
data suggest that a prolonged latent
phase may predispose to several com-
plications, including an increase in the
rate of cesarean delivery for dystocia. In a
study that compared labors with a latent
phase >18 hours to controls with a
shorter latent phase, the study group was
more likely to experience amniotomy,
oxytocin, instrumental delivery, and
emergency cesarean delivery.67 Other
observational studies have reached
similar conclusions.42,68,69 It is difficult
to interpret these studies because they
used different definitions of prolonged
latent phase and did not confine clinical
decision-making to a standard protocol.
Thus, the staff ’s preferences and biases
ajog.org
about managing labor could have influ-
enced the results. We can conclude that a
prolonged latent phase may be a
harbinger of further complications of
labor. It is not itself an indication for
urgent delivery but should sensitize the
healthcare team to be especially vigilant
in further assessment of the labor. At the
same time, they should be alert to the
need to avoid unnecessary interventions.
The treatment of a prolonged latent
phase generally involves either oxytocin
stimulation of contractility or so-called
therapeutic rest (Figure). Both have
similar success rates, defined as the labor
entering active phase dilatation, of about
85%.3,42 The precise mechanisms
through which these treatments work
have never been evaluated. Presumably,
it is the increased uterine contractile
activity provided by oxytocin that is of
benefit. Rest may be salutary by reducing
anxiety and general fatigue or perhaps
allowing a self-regulatory mechanism
that is postulated but unexplored to be
reset. The notion of therapeutic rest in-
volves giving the mother a dose of
morphine sulfate sufficient to cause her
to sleep for several hours. Approximately
10 mg intramuscularly has generally
been used, but this must be adjusted
according to the patient’s body mass and
the use of other medications that might
potentiate the side effects of the opioid.
When she awakens, the cervix is often
dilating more rapidly. This approach
seems to be safe for the fetus and mother,
although there have been concerns
raised about the possibility of occasional
maternal or fetal deoxygenation, so
maternal and fetal monitoring should
continue during the rest period.69e71
In most cases, oxytocin is used, but the
choice of therapy should depend heavily
on the patient’s desires, her emotional
state, and her level of fatigue. If rest fails
to result in the initiation of the active
phase yet intense contractions persist or
return, she likely has a true labor disor-
der; if contractions stop, it may be
assumed that she had been in false labor.
However, if oxytocin has been used
instead, the continuation of intense
contractions without active phase dila-
tation cannot be interpreted reliably.
Stopping the uterotonic stimulation on a
ajog.org Expert Review

trial basis should be considered. If con-

FIGURE
tractions cease, false labor can be diag-
nosed; if they continue and remain
Management of a prolonged latent phase of labor
strong, a dysfunctional labor is probably
present. Although logical, this advice has
not ever been objectively tested.
Amniotomy is often used during a
long latent phase to stimulate progress. It
may be helpful in a small number of
cases, but its overall benefit is probably
minimal42 and may superimpose the
infection risks of ruptured membranes.
However, when oxytocin is used for the
treatment of a prolonged latent phase,
concomitant amniotomy should be
considered if there is no clinical contra-
indication. It may reduce the time to
achieve the active phase.72 Other ap-
proaches to a prolonged latent phase that
have been suggested include ambulation,
hot tub immersion, and hypnosis. None
has been subjected to a proper clinical
trial. Similarly, the efficacy and safety of
drugs that might speed the remodeling
process, such as mifepristone, miso-
prostol, or collagenases, have not been
studied.
In a randomized trial of the manage-
ment of nulliparous women with a pro-
longed latent phase after therapeutic rest
with zolpidem, Bräne et al73 found that
prompt initiation of oxytocin did not
significantly alter the cesarean delivery
rate or the patients’ perception of their
experience in labor compared with a
group managed more conservatively.
Several clinical observations regarding
the latent phase are important. The most
obvious is that its duration is inversely A, Time the latent phase from the onset of regular uterine contractions to the upswing of the labor
proportional to the degree of prelabor curve at the beginning of active phase dilatation. If the latent phase of labor exceeds 20 hours in a
cervical remodeling. Supporting this nullipara or 14 hours in a multipara, diagnose prolonged latent phase. B, Prolonged latent phase is
thesis is the finding of a clear relationship not by itself an indication for active intervention. Evaluate to determine if there is any need for haste in
between prelabor dilatation and dura- achieving delivery. C, If an indication exists for prompt delivery, augment labor with oxytocin, pro-
tion of the latent phase, that is, the less vided there is no contraindication to its use. D, If there is no urgency to deliver, evaluate for any
the cervix is dilated before labor begins, remediable cause, such as dense conduction anesthesia or heavy narcotic analgesia. Allow them to
the longer the latent phase will be.61 The abate or counter their effect with oxytocin. If no cause is discernible, 2 options are available:
latent phase may be prolonged by heavy augmentation with oxytocin or therapeutic rest with narcotic analgesia. An important consideration in
sedation, whereas light sedation may choosing between these options is the patient’s preference. E, Uterotonic stimulation is usually
have no effect or even shorten it.42,74 The effective in propelling the labor into the active phase. F and G, After awakening from the narcotic
duration of the latent phase has little analgesic, most women will be in the active phase of dilatation. H, If uterine contractions fail to
relationship to uterine contractility. resume after she awakens, it becomes clear by hindsight that the long period of contractions did not
Some women with relatively mild, represent true labor at all. I, In a few women (approximately 5%) who have been managed with
infrequent contractions may have a short therapeutic rest, effective uterine contractions fail to resume when the drug wears off. Oxytocin is
latent phase; conversely, others may have required at this point to effect the transition to the active phase of labor. Adapted from Cohen et al.3
very intense frequent contractions for Cohen. The latent phase. Am J Obstet Gynecol 2023.
many hours with a minimal effect on

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Expert Review
cervical characteristics. Pajntar et al29
found that the Bishop score, fetal head
circumference, and uterine and cervical
contractility explained 64% of the vari-
ance in latent phase duration. A longer
latent phase was related to a rigid cervix
and higher intensity cervical muscle
contractions. However, the frequency,
intensity, and duration of uterine con-
tractions did not contribute significantly
to latent phase duration.
The question of whether it is necessary
to wait a full 20 hours in a nullipara
before initiating treatment for a long (if
not officially prolonged) latent phase is
often raised. It is not necessary; however,
decisions about early intervention, usu-
ally with oxytocin infusion, should be
based on the individual clinical situation.
This includes a thorough evaluation of
fetal oxygenation, the cervix, the uterine
contractile pattern, the woman’s prefer-
ence, and her willingness to tolerate an
abrupt increase in contractility and
discomfort. Moreover, it requires un-
derstanding that some of these patients
would have turned out to be in false la-
bor and that one would be in essence
doing an induction of labor with an
unfavorable cervix, which raises the
specter of failure and other complica-
tions. That caveat notwithstanding, in
treating a prolonged latent phase, ob-
stetricians today tend to eschew thera-
peutic rest in favor of labor
augmentation. This trend is supported
by the results of a randomized trial of
nulliparas with a latent phase longer
than 8 hours. Women received labor
augmentation (dinoprostone, amniot-
omy, or oxytocin) or expectant man-
agement for 24 hours.75 As expected, the
length of labor was shorter in the
augmented group, but there was no dif-
ference between the groups in the ce-
sarean or instrumental delivery rates or
measures of immediate neonatal
outcome.
Epidural block
An investigation from several decades
ago indicated that the latent phase could
be prolonged by the initiation of
epidural analgesia early in the labor.42 As
a consequence, such analgesia was often
withheld until the active phase began.
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Since then, neuraxial anesthetic agents
and techniques have changed substan-
tially. Several recent studies indicated
that the early administration of an
epidural block, using agents with negli-
gible motor blockade, has little adverse
effect on the overall duration of labor or
the likelihood of operative delivery.76e82
The available studies, except for Wang
et al,82 who found no effect, did not
address the influence of a neuraxial block
on the length of the latent phase per se,
so whether modern neuraxial methods
can prolong the latent phase is uncertain.
Shiro et al77 found early epidural block
prolonged the first stage of labor but did
not specify whether the effect was on the
latent or active phase or both. Never-
theless, the clinician should not hesitate
to administer this kind of anesthesia
early in labor if the patient requires pain
relief during that time or if there is a
medical indication for epidural
blockade.
The mechanism by which epidural
drugs may alter the latent phase is not
known. It may have to do with altered
contractility but might also be influ-
enced by the autonomic blockade pro-
vided by the neuraxial block. The
reduction in maternal anxiety conse-
quent to pain relief could even have a
positive effect.
Induction of labor
Induction of labor has become an
increasingly common approach and is
used in >20% of labors in the United
States. The propriety of this trend is a
matter of some debate, which we will
not address here. However, for pur-
poses of interpreting the latent phase,
the issue has considerable practical
importance. Most inductions involve
the use of synthetic oxytocin infusions.
These can shorten the latent phase
considerably, rendering the standards
for latent phase duration derived from
spontaneous labors inapplicable.
Moreover, the common use of cervical
ripening agents before oxytocin infu-
sion will tend to shorten the latent
phase relative to its expected duration
when labor begins with a thick and
unyielding cervix. The use of oxytocin
will shorten the latent phase on
ajog.org
average by approximately 2 hours, but
that information is of little practical
use. When the latent phase is pro-
gressing very slowly during an induc-
tion of labor, and especially if the
cervix has not responded to attempts
at ripening, consideration should be
given to discontinuing oxytocin and
allowing the mother to rest for several
hours, assuming that this is consistent
with maternal and fetal well-being.
Often when the infusion is restarted,
the transition to the active phase will
occur
Psychosocial issues
The latent phase can be emotionally
challenging for women, particularly when
it is prolonged. Long hours of discomfort
can be frustrating and disheartening.83
For nulliparas, it may be their first expo-
sure to the pain and anxiety inevitably
associated with parturition, and its effect
should never be trivialized.83,84 Good
supportive care during a long latent phase
can help engender trust between patient
and provider, serving both well in the
more arduous task ahead.3 If the provider
has established a good relationship with
the patient during prenatal care, particu-
larly if she has been prepared for the
possibility of a long latent phase, their
presence during labor can provide essen-
tial comfort. Under any circumstances,
the importance of providing necessary
emotional support and encouragement
by the entire obstetrical team cannot be
underestimated. Doing so will provide
important dividends for both patient and
staff.
Research questions
Several clinically relevant questions
about the latent phase of labor should be
addressed by appropriate research:
1. What makes the latent phase of labor
especially sensitive to inhibition by
sedatives, analgesics, and anesthetics?
2. How does oxytocin work to shorten
the latent phase? Is it through more
uterine contractions or cervical con-
tractions, or does it have some effect
on cervical connective tissue or a
combination of these and other
factors?
ajog.org
3. Are there other potentially effective
treatments for the prolonged latent
phase of labor, such as a beta-blocker,
prostaglandin, or misoprostol?
4. Can electrohysterogram bursts be
analyzed in a manner that will reli-
ably distinguish true labor from false
labor and identify the latent-to-active
phase transition? - molecular basis for sonographic cervical short-
REFERENCES
1. Friedman EA. Primigravid labor; a graph-
icostatistical analysis. Obstet Gynecol 1955;6:
567–89.
2. Friedman EA. The functional divisions of la-
bor. Am J Obstet Gynecol 1971;109:274–80.
3. Cohen WR, Friedman EA. Labor and delivery
care: a practical guide. Oxford, England: Wiley-
Blackwell; 2011.
4. Cohen WR, Friedman EA. The assessment of
labor: an evidence- and experience-based
approach. J Perinat Med 2020;34:263–71.
5. Ragusa A, Mansur M, Zanini A, Musicco M,
Maccario L, Borsellino G. Diagnosis of labor: a
prospective study. MedGenMed 2004;7:61.
6. Hanley GE, Munro S, Greyson D, et al.
Diagnosing onset of labor: a systematic review of
definitions in the research literature. BMC Preg-
nancy Childbirth 2016;16:71.
7. Vidaeff AC, Ramin SM. Potential biochemical
events associated with initiation of labor. Curr
Med Chem 2008;15:614–9.
8. Garfield RE, Bytautiene E, Vedernikov YP,
Marshall JS, Romero R. Modulation of rat
uterine contractility by mast cells and their
mediators. Am J Obstet Gynecol 2000;183:
118–25.
9. Sivarajasingam SP, Imami N, Johnson MR.
Myometrial cytokines and their role in the onset
of labour. J Endocrinol 2016;231:R101–19.
10. Menon R. Initiation of human parturition:
signaling from senescent fetal tissues via extra-
cellular vesicle mediated paracrine mechanism.
Obstet Gynecol Sci 2019;62:199–211.
11. Mendelson CR, Montalbano AP, Gao L.
Fetal-to-maternal signaling in the timing of birth.
J Steroid Biochem Mol Biol 2017;170:19–27.
12. Mendelson CR, Gao L, Montalbano AP.
Multifactorial regulation of myometrial contrac-
tility during pregnancy and parturition. Front
Endocrinol (Lausanne) 2019;10:714.
13. Mittal P, Romero R, Tarca AL, et al. Char-
acterization of the myometrial transcriptome and
biological pathways of spontaneous human la-
bor at term. J Perinat Med 2010;38:617–43.
14. Lucovnik M, Kuon RJ, Chambliss LR, et al.
Use of uterine electromyography to diagnose
term and preterm labor. Acta Obstet Gynecol
Scand 2011;90:150–7.
15. Lucovnik M, Kuon RJ, Garfield RE. Assess-
ment of parturition with cervical light-induced
fluorescence and uterine electromyography.
Comput Math Methods Med 2013;2013:
165913.
Downloaded for Anonymous User (n/a) at University of Indonesia from ClinicalKey.com by Elsevier on July 02, 2023.
For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved.
16. Pates JA, McIntire DD, Leveno KJ. Uterine
contractions preceding labor. Obstet Gynecol
2007;110:566–9.
17. Hassan SS, Romero R, Tarca AL, et al. The
transcriptome of cervical ripening in human
pregnancy before the onset of labor at term:
identification of novel molecular functions
involved in this process. J Matern Fetal Neonatal
Med 2009;22:1183–93.
18. Hassan SS, Romero R, Tarca AL, et al. The
ening at term: identification of differentially
expressed genes and the epithelial-
mesenchymal transition as a function of cervi-
cal length. Am J Obstet Gynecol 2010;203:472.
e1–14.
19. Stjernholm Y, Sahlin L, Åkerberg S, et al.
Cervical ripening in humans: potential roles of
estrogen, progesterone, and insulin-like growth
factor-I. Am J Obstet Gynecol 1996;174:
1065–71.
20. Timmons BC, Mahendroo M. Processes
regulating cervical ripening differ from cervical
dilation and postpartum repair: insights from
gene expression studies. Reprod Sci
2007;14(Suppl 8):53–62.
21. Timmons B, Akins M, Mahendroo M. Cer-
vical remodeling during pregnancy and parturi-
tion. Trends Endocrinol Metab 2010;21:353–61.
22. House M, Kaplan DL, Socrate S. Relation-
ships between mechanical properties and
extracellular matrix constituents of the cervical
stroma during pregnancy. Semin Perinatol
2009;33:300–7.
23. Winkler M, Oberpichler A, Tschesche H,
Ruck P, Fischer DC, Rath W. Collagenolysis in
the lower uterine segment during parturition at
term: correlations with stage of cervical dilatation
and duration of labor. Am J Obstet Gynecol
1999;181:153–8.
24. Akgul Y, Word RA, Ensign LM, et al. Hya-
luronan in cervical epithelia protects against
infection-mediated preterm birth. J Clin Invest
2014;124:5481–9.
25. Oláh KS. Changes in cervical electromyo-
graphic activity and their correlation with the
cervical response to myometrial activity during
labour. Eur J Obstet Gynecol Reprod Biol
1994;57:157–9.
26. Vedernikov YP, Mayes M, Moore E, Gei A,
Saade GR, Garfield RE. The effects of preg-
nancy and smooth muscle contractility on cer-
vical distensibility in the rat. Am J Obstet Gynecol
2000;182:905–8.
27. Bryman I, Norström A, Lindblom B. Has
cervical smooth muscle any physiological role in
the human? Acta Physiol Hung 1985;65:
327–30.
28. Oláh KS, Gee H, Brown JS. Cervical con-
tractions: the response of the cervix to oxytocic
stimulation in the latent phase of labour. Br J
Obstet Gynaecol 1993;100:635–40.
29. Rudel D, Pajntar M. Active contractions of
the cervix in the latent phase of labour. Br J
Obstet Gynaecol 1999;106:446–52.
30. Pajntar M, Leskosek B, Rudel D, Verdenik I.
Contribution of cervical smooth muscle activity
MAY 2023 American Journal of Obstetrics & Gynecology
Expert Review
to the duration of latent and active phases of
labour. BJOG 2001;108:533–8.
31. Ferenczy A. Ultrastructure of the uterine
cervix. In: Huszar G, ed. The physiology and
biochemistry of the uterus in pregnancy and la-
bor. Boca Raton, FL: CRC Press; 1986. p.
239–60.
32. Allaire AD, D’Andrea N, Truong P,
McMahon MJ, Lessey BA. Cervical stroma
apoptosis in pregnancy. Obstet Gynecol
2001;97:399–403.
33. Väisänen-Tommiska MR. Nitric oxide in the
human uterine cervix: endogenous ripening
factor. Ann Med 2008;40:45–55.
34. Hee L. Overview of the methods available for
biomechanical testing of the uterine cervix
in vivo. Acta Obstet Gynecol Scand 2014;93:
1219–37.
35. Mazza E, Parra-Saavedra M, Bajka M,
Gratacos E, Nicolaides K, Deprest J. In vivo
assessment of the biomechanical properties of
the uterine cervix in pregnancy. Prenat Diagn
2014;34:33–41.
36. Feltovich H, Carlson L. New techniques in
evaluation of the cervix. Semin Perinatol
2017;41:477–84.
37. World Health Organization. Preventing pro-
longed labour: a practical guide: the partograph.
1994. Available at: https://apps.who.int/iris/handle/
10665/58903. Accessed May 10, 2022.
38. Zhang J, Troendle JF, Yancey MK. Reas-
sessing the labor curve in nulliparous women.
Am J Obstet Gynecol 2002;187:824–8.
39. American College of Obstetrics and Gy-
necology Committee on Practice Bulletins-
Obstetrics. ACOG Practice Bulletin Number
49, December 2003: dystocia and augmen-
tation of labor. Obstet Gynecol 2003;102:
1445–54.
40. Wiafe YA, Whitehead B, Venables H,
Dassah ET, Eggebø TM. Intrapartum ultrasound
assessment of cervical dilatation and its value in
detecting active labor. J Ultrasound 2018;21:
233–9.
41. Boylan PC, Parisi VM. Effect of active man-
agement on latent phase labor. Am J Perinatol
1990;7:363–5.
42. Friedman EA. Labor: clinical evaluation and
management, 2nd ed. New York, NY: Appleton-
Century-Crofts; 1978.
43. Peisner DB, Rosen MG. Transition from
latent to active labor. Obstet Gynecol 1986;68:
448–51.
44. Cohen WR, Pacheco C, Verdiales M,
Karumanchi R, Rosenberg E. Uterine electro-
myography in latent and active phase labor.
J Soc Gynecol Investig 2004;11. Abstract
950318.
45. Trojner Bregar A, Lucovnik M, Verdenik I,
Jager F, Gersak K, Garfield RE. Uterine elec-
tromyography during active phase compared
with latent phase of labor at term. Acta Obstet
Gynecol Scand 2016;95:197–202.
46. Nagarajan R, Eswaran H, Wilson JD,
Murphy P, Lowery C, Preissl H. Analysis of
uterine contractions: a dynamical approach.
J Matern Fetal Neonatal Med 2003;14:8–21.
S1023
Expert Review
47. Li P, Wang L, Qian X, Morse A, Garfield RE,
Liu H. A study of uterine inertia on the sponta-
neous of labor using uterine electromyography.
Taiwan J Obstet Gynecol 2021;60:449–53.
48. Esgalhado F, Batista AG, Mouriño H, et al.
Uterine contractions clustering based on elec-
trohysterography. Comput Biol Med 2020;123:
103897.
49. Schauberger CW. False labor. Obstet
Gynecol 1986;68:770–2.
50. Eganhouse DJ. A comparative study of
variables differentiating false labor from early la-
bor. J Perinatol 1991;11:249–57.
51. Arulkumaran S, Michelsen J, Ingemarsson I,
Ratnam SS. Obstetric outcome of patients with
a previous episode of spurious labor. Am J
Obstet Gynecol 1987;157:17–20.
52. Rozeboom DE, Varner MW. Relationship of
admissions for false labor to perinatal outcome.
J Reprod Med 1989;34:285–8.
53. Nelson DB, McIntire DD, Leveno KJ.
False labor at term in singleton pregnancies:
discharge after a standardized assessment and
perinatal outcomes. Obstet Gynecol 2017;130:
139–45.
54. Kunzier NB, Kinzler WL, Chavez MR,
Adams TM, Brand DA, Vintzileos AM. The use of
cervical sonography to differentiate true from
false labor in term patients presenting for labor
check. Am J Obstet Gynecol 2016;215. 372.
e1e5.
55. Bouzid A, Kehila M, Trabelsi H, Abouda HS,
Ben Hmid R, Chanoufi MB. Sonographic land-
marks to differentiate “false labor” and “early true
labor” as a possible new application of ultra-
sound in labor ward. J Gynecol Obstet Hum
Reprod 2017;46:363–6.
56. Peisner DB, Rosen MG. Latent phase of
labor in normal patients: a reassessment. Obstet
Gynecol 1985;66:644–8.
57. Tilden EL, Phillippi JC, Ahlberg M, et al.
Describing latent phase duration and associated
characteristics among 1281 low-risk women in
spontaneous labor. Birth 2019;46:592–601.
58. Kilpatrick SJ, Laros RK Jr. Characteristics of
normal labor. Obstet Gynecol 1989;74:85–7.
59. Granström L, Ekman G, Malmström A.
Insufficient remodeling of the uterine connective
tissue in women with protracted labor. Br J
Obstet Gynaecol 1991;98:1212–6.
60. Polónia Valente R, Santos P, Ferraz T,
Montenegro N, Rodrigues T. Effect of obesity on
labor duration among nulliparous women with
epidural analgesia. J Matern Fetal Neonatal Med
2020;33:2195–201.
S1024 American Journal of Obstetrics & Gynecology MAY 2023
Downloaded for Anonymous User (n/a) at University of Indonesia from ClinicalKey.com by Elsevier on July 02, 2023.
For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved.
61. Friedman EA, Sachtleben MR. Determinant
role of initial cervical dilatation on the course of
labor. Am J Obstet Gynecol 1962;84:930–5.
62. Duff P, Sanders R, Gibbs RS. The course of
labor in term patients with chorioamnionitis. Am
J Obstet Gynecol 1983;147:391–5.
63. Satin AJ, Maberry MC, Leveno KJ,
Sherman ML, Kline DM. Chorioamnionitis: a
harbinger of dystocia. Obstet Gynecol 1992;79:
913–5.
64. Rottenstreich A, Levin G, Tsur A, Shai D,
Meyer R. Chorioamnionitis at latent phase more
than doubles the risk for cesarean delivery
compared to chorioamnionitis at active phase.
Arch Gynecol Obstet 2021;303:905–10.
65. Silver RK, Gibbs RS, Castillo M. Effect of
amniotic fluid bacteria on the course of labor in
nulliparous women at term. Obstet Gynecol
1986;68:587–92.
66. Friedman EA, Neff RK. Labor and delivery:
impact on offspring. Littleton, MA: Publishing
Solutions Group; 1987.
67. Ängeby K, Wilde-Larsson B, Hildingsson I,
Sandin-Böjo AK. Prevalence of prolonged latent
phase and labor outcomes: review of birth re-
cords in a Swedish population. J Midwifery
Womens Health 2018;63:33–44.
68. Chelmow D, Kilpatrick SJ, Laros RK Jr.
Maternal and neonatal outcomes after pro-
longed latent phase. Obstet Gynecol 1993;81:
486–91.
69. Maghoma J, Buchmann EJ. Maternal and
fetal risks associated with prolonged latent
phase of labour. J Obstet Gynaecol 2002;22:
16–9.
70. Mackeen AD, Fehnel E, Berghella V, Klein T.
Morphine sleep in pregnancy. Am J Perinatol
2014;31:85–90.
71. Baxi LV, Petrie RH, James LS. Human fetal
oxygenation (tcPo2), heart rate variability and
uterine activity following maternal administration
of meperidine. J Perinat Med 1988;16:23–30.
72. Nachum Z, Garmi G, Kadan Y, Zafran N,
Shalev E, Salim R. Comparison between
amniotomy, oxytocin or both for augmentation
of labor in prolonged latent phase: a randomized
controlled trial. Reprod Biol Endocrinol 2010;8:
136.
73. Bräne E, Olsson A, Andolf E. A randomized
controlled trial on early induction compared to
expectant management of nulliparous women
with prolonged latent phases. Acta Obstet
Gynecol Scand 2014;93:1042–9.
74. Chazotte C, Cohen WR. Drug use in latent
phase labor. In: Petrie RH, ed. Perinatal
ajog.org
pharmacology. Oradell, NJ: Medical Economics
Publishing; 1989. p.;335–43.
75. Sargunam PN, Bak LLM, Tan PC, et al.
Induction of labor compared to expectant
management in term nulliparas with a latent
phase of labor of more than 8 hours: a ran-
domized trial. BMC Pregnancy Childbirth
2019;19:493.
76. Sng BL, Leong WL, Zeng Y, et al. Early
versus late initiation of epidural analgesia for la-
bour. Cochrane Database Syst Rev 2014:
CD007238.
77. Shiro M, Nakahata K, Minami S,
Kawamata T, Ino K. Perinatal outcome of vaginal
delivery with epidural analgesia initiated at the
early or late phase of labor period: a retrospec-
tive cohort study in the Japanese population.
J Obstet Gynaecol Res 2018;44:1415–23.
78. Ohel G, Gonen R, Vaida S, Barak S,
Gaitini L. Early versus late initiation of epidural
analgesia in labor: does it increase the risk of
cesarean section? A randomized trial. Am J
Obstet Gynecol 2006;194:600–5.
79. Vahratian A, Zhang J, Hasling J,
Troendle JF, Klebanoff MA, Thorp JM Jr. The
effect of early epidural versus early intravenous
analgesia use on labor progression: a natural
experiment. Am J Obstet Gynecol 2004;191:
259–65.
80. Wong CA, McCarthy RJ, Sullivan JT,
Scavone BM, Gerber SE, Yaghmour EA. Early
compared with late neuraxial analgesia in
nulliparous labor induction: a randomized
controlled trial. Obstet Gynecol 2009;113:
1066–74.
81. Wong CA, Scavone BM, Peaceman AM,
et al. The risk of cesarean delivery with neuraxial
analgesia given early versus late in labor. N Engl
J Med 2005;352:655–65.
82. Wang F, Shen X, Guo X, Peng Y, Gu X;
Labor Analgesia Examining Group. Epidural
analgesia in the latent phase of labor and the risk
of cesarean delivery: a five-year randomized
controlled trial. Anesthesiology 2009;111:
871–80.
83. Carlsson IM, Hallberg LR, Odberg
Pettersson K. Swedish women’s experiences of
seeking care and being admitted during the
latent phase of labour: a grounded theory study.
Midwifery 2009;25:172–80.
84. Ängeby K, Wilde-Larsson B,
Hildingsson I, Sandin-Bojö AK. Primiparous
women’s preferences for care during a pro-
longed latent phase of labour. Sex Reprod
Healthc 2015;6:145–50.