E l e c t ro n i c F e t a l

Monitoring: Past,
P re s e n t , a n d F u t u re
a, b
Molly J. Stout, MD *, Alison G. Cahill, MD, MSCI

KEYWORDS
 Electronic fetal monitoring  Intrapartum continuous monitoring
 Neonatal outcomes

The use of continuous intrapartum electronic fetal monitoring (EFM) with cardiotocog-
raphy in labor and delivery units has become the rule, not the exception. More than
3 million pregnancies are monitored during labor in the United States annually using
EFM.1 The use of such technology can be easily taken for granted in most labor suites
because physicians and other medical personnel follow continuous paper or elec-
tronic tracings of fetal heart rate (FHR) and contraction patterns and virtually all
patients arrive to labor and delivery expecting the tool to be used in their care. Despite
its now ubiquitous use, continuous electronic monitoring and its associated risks and
benefits are worth considering. To meaningfully evaluate the current use of EFM and
make educated decisions regarding future research goals, it is imperative to analyze
the research and clinical practices of several past decades, which have shaped and
molded what has now become a routine modern obstetric practice.

THE BIRTH OF EFM: 1960S AND 1970S

The goals of intrapartum medical care 50 years ago during the advent of EFM were
not significantly different from modern obstetric goals: to decrease morbidity and
mortality both in the mother and the newborn. The standard of care for intrapartum
fetal assessment before the introduction of EFM was intermittent auscultation of fetal
heart tones and fetal scalp pH sampling. FHR characteristics are, in part, a product
of central nervous system’s sympathetic and parasympathetic outflow.2 If one
accepts the theory that intrapartum hypoxia leads eventually to changes in the fetal
central nervous system that are manifested postnatally in the form of cerebral palsy

Financial disclosure: the authors have nothing to disclose.

a
Department of Obstetrics and Gynecology, Washington University in St Louis, 4911 Barnes
Jewish Hospital, 2nd Floor Maternity Building, St Louis, MO 63110, USA
b
Division of Maternal Fetal Medicine, Washington University in St Louis, 4911 Barnes Jewish
Plaza, Box 8064, St Louis, MO 63110, USA
* Corresponding author.
E-mail address: stoutm@wudosis.wustl.edu

Clin Perinatol 38 (2011) 127–142

doi:10.1016/j.clp.2010.12.002 perinatology.theclinics.com
0095-5108/11/$ – see front matter Ó 2011 Elsevier Inc. All rights reserved.
128 Stout & Cahill

(CP) and other permanent neurologic damage, the goal then becomes to identify
hypoxia during labor via identifiable FHR characteristics in an effort to intervene
before permanent damage occurs. The hope was that continuous EFM would
be the answer—a continuous window into the fetal central nervous system and the
opportunity to prevent permanent neurologic damage and stillbirth.
In 1969, Kubli and colleagues3 published data on the correlation between FHR
patterns and fetal pH. Eighty-five patients underwent continuous EFM and simulta-
neous fetal scalp pH sampling. The pH sample was then correlated with the preceding
20 minutes of FHR findings. If a mixture of findings were present in the tracing, the
most “ominous” finding was used (eg, it would be classified according to a prolonged
late deceleration preferentially over a mild variable deceleration). Their data showed
that moderate variable decelerations are associated with a lower mean pH compared
with tracings with no decelerations, early decelerations, or mild variable decelerations.
Severe variable decelerations and late decelerations were associated with a further
shift toward lower pH. Most (but not all) of the tracings with late decelerations had
a pH less than 7.25.3 They published that their single most important result was the
absence of major alterations in fetal pH in the context of a normal FHR pattern.
Myers and colleagues,4 in 1973, evaluated physiologic oxygenation and pH
changes associated specifically with late decelerations in rhesus monkeys and sug-
gested that there is a direct correlation between depth of late deceleration and blood
oxygen tension. Rhesus monkey fetuses underwent continuous fetal monitoring and
were catheterized in utero to directly examine blood pH. Maternal monkeys had a peri-
aortic loop inserted to manipulate uterine perfusion. The investigators found that
during decreased uterine perfusion, fetal blood oxygen saturation decreases signifi-
cantly with an associated fetal bradycardia, which subsequently resolved as uterine
blood flow was restored. Despite the decrease in oxygen tension and the resultant
bradycardia, pH remained essentially unchanged during the event. It was also noted
that even a well-oxygenated fetus responds with late deceleration if the uterine
contractions are sufficiently prolonged. It was concluded that fetal blood oxygen
tension is the principle determinant of FHR patterns.
Murata and colleagues5 evaluated FHR patterns in rhesus monkeys preceding fetal
death and showed that late decelerations were uniformly present before fetal death.
Fetal monkeys were catheterized for continuous monitoring until fetal death occurred.
At the beginning of the experiment, all blood gas and pH parameters were normal. In
the 9 fetuses observed, accelerations were initially present at the time of appearance
of late decelerations. By the time the late decelerations became repetitive, the fetal
blood oxygen saturation was significantly decreased, but pH and PaCO2 had not
changed significantly. The complete absence of accelerations with persistent late
decelerations characterized the phase immediately preceding fetal death and was
associated with both decreased blood oxygen tension and decreased pH. Late decel-
erations were present in 84% of fetal deaths. Thus, as data mounted linking physio-
logic data to FHR patterns, it was hoped that EFM could provide a window into
fetal well-being and facilitate intervention before permanent damage occurs.
In 1974, Quilligan and Paul6 wrote that although there had not yet been any scien-
tifically proved value of EFM over intermittent auscultation, they speculated, based on
an observed decrease in perinatal mortality at their institution, that EFM could reduce
intrapartum fetal death and improve neonatal survival. In 1976, a prospective cohort
study was published comparing continuous EFM to intermittent auscultation but
was stopped early because of the evidence of what the investigators described as
a clear benefit in the EFM group observed as decreased neonatal intensive care
unit (NICU) admission and decreased neurologic symptoms.7 Subsequently, multiple
 Electronic Fetal Monitoring 129

randomized trials comparing EFM to intermittent auscultation were performed

(Table 1).
In 1976, Haverkamp and colleagues8 published findings from a randomized
controlled trial comparing 242 low-risk obstetric patients undergoing continuous
EFM to 241 patients undergoing intermittent auscultation. They reported an increased
risk of cesarean delivery in the EFM group but no difference in Apgar scores and no
difference in cord blood gas values between the groups. There were no intrapartum
deaths but 3 perinatal deaths; 2 in the EFM group, 1 in the intermittent auscultation
group. The 2 deaths were because of congenital anomalies, and the 1 death was
thought to be due to meconium aspiration. This study was followed by another study
of a low-risk obstetric population in England of 254 women undergoing continuous
EFM compared with 251 women undergoing intermittent auscultation.9 Again, they
reported increased cesarean delivery rates, with no difference in Apgar scores, in
the incidence of a depressed infant at delivery, in admission to special care nursery,
or in blood gas parameters.
Given these findings, raising questions as to whether EFM improved neonatal
outcomes, investigators wondered whether continuous EFM may be more appropri-
ately applied to high-risk obstetric situations. Haverkamp and colleagues,10 having
previously found no improved outcomes in an unselected patient population, pub-
lished a study in 1979 of 690 high-risk women in labor. Women were assigned to either
intermittent auscultation alone, continuous EFM alone, or continuous EFM with pH
sampling. Women in the continuous EFM group were more likely to undergo cesarean
delivery, independent of whether pH sampling was performed or not. No differences in
Apgar score or acid-base parameters were found. They summarized: “Two primary
conclusions emerge from this investigation on the differential effects of fetal moni-
toring: (1) electronic fetal monitoring with or without scalp sampling did not improve
perinatal outcomes over that achieved by intermittent auscultation alone; (2) the
cesarean section rate was much higher among electronically monitored patients.”
Concerns with interpretation of this early data are that the populations were rela-
tively small and no comment was made regarding power calculations. Thus, it was
unclear whether there truly was no improvement in neonatal outcomes with EFM or
whether the outcomes of neonatal morbidity and mortality were so rare that the
studies were not powered appropriately to detect a difference. In 1985, the Dublin
randomized controlled trial of intrapartum FHR monitoring was published. The study
included more than 12,000 women (as compared with prior studies of 400–600
women) and a power calculation that dictated that 10,000 women in each group would
yield a sufficient sample size.11 Contrary to the prior studies, there was no increased
rate of cesarean delivery in the EFM group. The investigators present that in the
neonates who survived, there was a significant decrease in the incidence of neonatal
seizures in the EFM group. However, despite the difference noted in the incidence of
neonatal seizures, in the 1-year follow-up, equal number in each group was found to
have severe disabilities, suggesting that neonatal seizures by their definition were not
a reasonable surrogate marker for the clinically important outcome of long-term
central nervous system disabilities into childhood.
Subsequently in 1993, Vintzileos and colleagues,12 with attention to an appropriately
powered study, published outcomes of 1428 low-risk and high-risk pregnancies. This
prospective randomized study, conducted at 2 university hospitals in Greece, included
all singleton pregnancies at greater than 26 weeks of gestation; patients were random-
ized by a coin toss to either continuous EFM or intermittent auscultation. In the pres-
ence of nonreassuring FHR patterns, both groups were managed with conservative
intrauterine resuscitation (maternal oxygen and intravenous fluids, maternal position
 130
Stout & Cahill
Table 1
Summary of studies comparing continuous EFM to intermittent auscultation

Power
Author Year Study Type; Population N Calculation Rate of Cesarean Delivery Apgar Score Neonatal Outcomes
Renou et al7 1976 Prospective cohort; 440 None No difference No difference Increased NICU admission and
high risk other symptoms in
Cases, continuous EFM intermittent auscultation
Controls, no EFM, no fetal group. Study stopped early.
scalp sample
Haverkamp et al8 1976 Prospective randomized 483 None Increased in EFM group No difference No difference in NICU
EFM vs intermittent admission, pH, intubations,
auscultation; high risk or seizures
Kelso et al9 1978 Prospective randomized 504 None Increased in EFM group No difference No difference in NICU
EFM vs intermittent admission or pH
auscultation;
normal risk
Haverkamp et al10 1979 Prospective randomized 690 None Increased in EFM groups No difference No difference in pH or NICU
EFM 1 pH vs EFM alone admission
vs intermittent
auscultation; unselected
Wood et al40 1981 Prospective randomized 504 None Increased in EFM group No difference No difference in neurologic
EFM vs intermittent symptoms
auscultation;
normal risk
MacDonald et al11 1985 Prospective randomized 12,964 Yes No difference No difference Decreased neonatal seizures
EFM vs intermittent with EFM. 1-year follow-up
auscultation; mixed no difference in severe
high and normal risk disabilities between groups
Vintzileos et al12 1993 Prospective randomized 1428 Yes Increased in EFM group No difference No difference in NICU
EFM vs intermittent admission or neonatal
auscultation; mixed seizures. Decreased perinatal
high and normal risk death
 Electronic Fetal Monitoring 131

change, discontinuation of oxytocin administration) followed by operative vaginal

delivery or cesarean delivery if the nonreassuring pattern persisted for more than
20 minutes. No crossover between groups occurred (eg, no patients undergoing inter-
mittent auscultation were transitioned to continuous monitoring because of identified
abnormal auscultation), and no pH sampling was undertaken to confirm or reject
FHR findings. Similar to previous studies, it was found that the incidence of cesarean
delivery for nonreassuring FHR patterns was increased in the EFM group. All neonatal
complications (such as NICU admission, assisted ventilation, hypoxic-ischemic
encephalopathy [HIE], seizures) were not significantly different between EFM and inter-
mittent auscultation groups. However, the researchers commented that their data
support the use of EFM because the perinatal death rate was significantly decreased
in the EFM group. Despite an a priori power calculation being performed for this study,
the sample size was not met because the study was stopped due to ethical concerns
regarding a trend for decreased perinatal death in the EFM group.

THE 1980S: DISCREPANCY BETWEEN DATA AND EXPECTATIONS

After nearly 20 years of data had been amassed, with conflicting results and no
demonstrable benefit, the question remained as to whether continuous EFM was
more appropriately applied in specific pregnancies at higher risk of intrapartum and
neonatal death. Leveno and colleagues13 published a study in 1986 on 34,995 preg-
nancies using either universal EFM or selective monitoring. The standard of care at
that time at the investigators’ institution was to “selectively” monitor pregnancies
with a high-risk condition using continuous EFM and use intermittent EFM if none of
the high-risk criteria were met. The definition of high risk as used by the investigators
was extremely broad: induction or augmentation of labor with oxytocin, dysfunctional
labor, abnormal FHR, meconium in the amniotic fluid, hypertension, vaginal bleeding,
prolonged pregnancy, diabetes, twins, breech presentation, or preterm labor. They
found that universal monitoring had no significant improvement in stillbirth, Apgar
scores, assisted ventilation at birth, NICU admission, or seizures compared with
selective monitoring. Luthy and colleagues14 studied 246 pregnancies with preterm
labor at 26 to 32 weeks with estimated fetal weight of 700 to 1750 g randomized to
either EFM or intermittent auscultation. There was no difference in the rate of cesarean
delivery between the 2 groups. Fetal acidosis, neonatal seizures, respiratory distress
syndrome, and intracranial hemorrhage did not differ between the 2 groups. Similarly,
monitoring technique was not associated with any difference in the rate of neonatal
mortality. They concluded: “additional data from continuous electronic monitoring
does not improve clinical management of premature labor enough to reduce intrapar-
tum acidosis, perinatal morbidity, or perinatal mortality.” A team of physical therapists,
psychologists, and developmental pediatricians evaluated the surviving 212 infants
aged 18 months.15 Neurologic development at 18 months was not improved in the
group that had been monitored with EFM compared with the intermittent auscultation
group. An unexpected finding was an increased diagnosis of CP in the EFM group
(20%) compared with the intermittent auscultation group (8%). They speculated that
perhaps knowing the high rate of false-positive results with abnormal FHR tracings,
clinicians were falsely reassured by other parameters in the continuous monitoring.

THE 1990S: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT

DEFINITIONS AND NEW RESEARCH GOALS

Despite a tepid indication in the above-mentioned studies that continuous EFM

provides early recognition of fetal hypoxia to facilitate intervention and improve
132 Stout & Cahill

outcomes as was promised at its inception, the use of EFM had already become wide-
spread. In 1997, the Eunice Kennedy Shriver National Institute of Child Health and
Human Development (NICHD) proposed that 1 roadblock to a useful interpretation
of research on EFM was lack of agreement in definitions and patterns on EFM
tracings.16 A consensus workshop put forth standardized interpretations for FHR
patterns, facilitating a common language for researchers and caregivers to communi-
cate. The components of FHR patterns identified by the expert panel are baseline rate,
baseline variability, presence of accelerations, presence of decelerations, and types of
decelerations. These components are reviewed in the following sections.

Baseline Rate
The baseline rate is the mean FHR rounded to 5 beats per minute and increments
during a 10-minute segment. The normal baseline rate is from 110 to 160 beats per
minute. Fetal bradycardia is a baseline FHR of less than 110 beats per minute, and
fetal tachycardia is a baseline FHR of greater than 160 beats per minute.

Baseline Variability
Variability is seen as fluctuations in FHR, which are typically irregular in amplitude and
frequency (Fig. 1). Variability amplitude is visually quantified as absent, amplitude
range undetectable; minimal, amplitude range of 5 beats per minute or less; moderate,
amplitude range of 6 to 25 beats per minute; or marked, amplitude range of more than
25 beats per minute. The sinusoidal pattern is not to be confused with variability and is
instead defined as a wavelike pattern with regular frequency and amplitude.

Acceleration
Acceleration is a visibly apparent abrupt increase (onset to peak in <30 seconds) in
FHR above the baseline. At greater than 32 weeks of gestation, the peak of the accel-
eration must reach 15 beats per minute above the baseline and must last for
15 seconds from start to finish (it is not required to remain at the peak throughout
the 15 seconds). At less than 32 weeks’ gestation, an increase of 10 beats per minute
above the baseline lasting for 10 seconds is appropriate. Prolonged accelerations are

Fig. 1. FHR tracing demonstrating a normal baseline of 130 beats per minute with moderate
variability.
 Electronic Fetal Monitoring 133

defined as lasting from 2 to 10 minutes. Any acceleration lasting more than 10 minutes
is considered a change in baseline.

Deceleration
Decelerations are categorized into 4 types: late, variable, early, and prolonged. All
decelerations should be described with the duration and the depth of the nadir.
They are classified as recurrent if they occur with more than 50% of the contractions
over a 20-minute period.
Prolonged decelerations are defined as lasting from 2 to 10 minutes (Fig. 2). Any
deceleration lasting more than 10 minutes is classified as a change in baseline.
Late decelerations are typically a gradual descent from the baseline, with onset to
nadir of 30 seconds or more (Fig. 3). The depth of the deceleration is calculated
from the baseline to the nadir. It is termed late relative to the contraction because
the nadir of the deceleration occurs after the peak of the contraction. Late decelera-
tions are thought to occur because of a decrease in uterine blood flow with the uterine
contraction. The relatively deoxygenated blood is sensed by chemoreceptors in the
fetus, causing vagal stimulation, and thus there is a decrease in the FHR. A second
mechanism for late deceleration involves the relatively deoxygenated blood from
the placenta during the contraction, causing direct hypoxic depression of the
myocardium.2
Variable decelerations are termed as such because they can occur in any location
with respect to the contraction. They are typically abrupt decreases from the baseline
(onset to nadir of deceleration, <30 seconds) often with abrupt recovery back to base-
line (Fig. 4). Variable decelerations are commonly associated with umbilical cord
compression.2
Early decelerations are a visibly apparent gradual decrease (onset to nadir, 30
seconds) and return to baseline that occurs with uterine contraction (Fig. 5). The
beginning, nadir, and recovery are coincident with the beginning, peak, and release
of the uterine contraction and are thought to be mediated by fetal head compression.2
The 1996 U S Preventive Services Task Force recommendation was that EFM
should not be used in low-risk pregnancies and there is insufficient evidence to recom-
mend its use in high-risk pregnancies.17 Despite this recommendation, EFM was
being used in more than 70% of all live births, making it the most common obstetric
procedure.18 Among members of the 1997 NICHD consensus meeting, there was

Fig. 2. FHR tracing demonstrating prolonged deceleration.

134 Stout & Cahill

Fig. 3. FHR tracing demonstrating late decelerations. MSpO2, maternal serum partial pres-
sure of oxygen.

Fig. 4. FHR tracing demonstrating variable decelerations. MSpO2, maternal serum partial
pressure of oxygen.

Fig. 5. FHR tracing demonstrating early decelerations. MSpO2, maternal serum partial pres-
sure of oxygen.
 Electronic Fetal Monitoring 135

good agreement that a normal tracing confers a very high prediction of a normally
oxygenated fetus at delivery. Similarly, members agreed that certain patterns such
as recurrent late decelerations with absent variability and prolonged or significant
bradycardia are almost uniformly nonreassuring. However, the intermediate group,
those tracings not belonging to either end of the spectrum of normalcy, lacked uniform
consensus on evidence-based management. The planning workshop put forth several
research goals regarding EFM, including studying the correlation between specific
FHR patterns and immediate outcome measures, such as Apgar scores, blood gases,
and neonatal death, as well as long-term outcome measures of neurodevelopment.16
One study retrospectively evaluated more than 2000 FHR tracings at 3 different time
points during labor: early labor, active labor 1 hour before complete dilation, and
throughout the entire second stage of labor in 30-minute segments. It was concluded
that variability alone cannot be a single predictor for fetal well-being because most of
the cases with adverse fetal outcomes demonstrated normal variability.19 A case-
control study reviewing FHR tracings of cases of known neonatal encephalopathy
compared with controls without encephalopathy was performed in 1997. The study
reported that most cases of neonatal encephalopathy were preceded by an abnormal
FHR tracing but that 52% of normal controls also had an abnormal FHR tracing before
delivery.20
Another case-control study of 71 term infants with metabolic acidosis (base
deficit >16 mmol/L) and a control group of 71 term infants without metabolic acidosis
evaluated the FHR tracings in the 4-hour period before delivery.21 Spontaneous accel-
erations occurred significantly more frequently in the control group. Absent or minimal
variability in the 1-hour period before delivery occurred in 68% of the cases
with acidosis, but 40% of the control group also had periods of absent variability. In
the acidosis group, 4 infants had no FHR tracing findings suggestive of asphyxia,
and accelerations did occur in the tracings of some fetuses ultimately found to be
acidemic. Sameshima and Ikenoue22 retrospectively reviewed FHR tracings of more
than 5000 low-risk pregnancies and correlated FHR patterns with umbilical blood
gas and CP diagnosis. They reported that decreasing variability in tracings with late
or prolonged decelerations was associated with decreasing pH. The false-positive
rate of recurrent late decelerations or prolonged deceleration was 89%. Notably,
6 of the 9 cases of CP had nonreassuring FHR tracings before the initiation of fetal
monitoring on admission.
Williams and Galerneau23 retrospectively evaluated 186 term patients who had
a bradycardia in the last 2 hours before delivery. The tracings were grouped according
to the 2 factors variability and recovery of bradycardia as follows: group 1, normal
variability, recovery of bradycardia; group 2, normal variability, no recovery of
bradycardia; group 3, decreased variability, recovery of bradycardia; and group 4,
decreased variability, no recovery of bradycardia. The findings of both decreased vari-
ability and no recovery of bradycardia were significantly associated with pathologic
acidosis. Specifically, the presence of decreased variability before bradycardia, irre-
spective of whether the bradycardia recovered, was associated with a 44% incidence
of fetal acidosis.

REVISITING THE LINK BETWEEN INTRAPARTUM HYPOXIA AND CP

The original intention of EFM—to reduce intrapartum stillbirth and improve

neonatal outcomes—is revisited in this section. In the 1970s, Quilligan and Paul6
suggested that brain damage is “merely an intermediate point on the pathway
to death,” and therefore, they speculated that early recognition of fetal distress
136 Stout & Cahill

could reduce mental retardation by half. Despite the now 40 years of EFM, no
decrease in the incidence of CP has been noted.24 HIE is a small subset of the
broader category of neonatal encephalopathy. Even within the category of HIE,
only a small subset progress to CP.25
In a matched case-control study of 107 cases with an arterial pH less than 7.0 and
base excess of 12 mmol/L or more, 13 cases had neurologic complications
(8 neonates with seizures, 1 with bilateral grade 3 intraventricular hemorrhage, and
4 died).26 There was no difference in total, late, or prolonged decelerations in the
neurologically injured group when compared with the noninjured group. However,
neurologically injured infants were more likely to have a positive result in blood culture
in the neonatal period. The researchers concluded that although late decelerations
were more common in the presence of metabolic acidosis, they were unable to identify
the presence of HIE (the precursor diagnosis to CP).
Nelson and colleagues27 published a case-control study comparing 78 children with
CP who had survived to age 3 years with controls without CP. The prevalence of CP
was 1.1 per 1000 patients. The finding of multiple late decelerations was associated
with a quadrupling of the risk for CP and that of decreased variability with a tripling
risk for CP. However, 73% of the children with CP did not have multiple late deceler-
ations. Extrapolation of the data from this study suggests that in an imaginary popu-
lation of 100,000 children born at term and weighing 2500 g or more, 9.3% (study
incidence of abnormal tracing) or 9300 children would have abnormal tracings with
multiple late decelerations or decreased variability. Of those with abnormal tracings,
18 will be diagnosed with CP (0.19% study incidence of CP after an abnormal tracing).
Assuming that 20% of CP might be related to asphyxia during delivery and an inter-
vention that could prevent asphyxia-related CP could be applied, approximately
4 of the 9300 children would benefit from this intervention, leaving 9296 pregnancies
intervened on without benefit or 2324 nonbeneficial interventions for each case of CP
prevented.
In 1998, 2 case-control studies from Australia evaluated both antepartum and intra-
partum risk factors for newborn encephalopathy.28,29 Only 4% of the cases had
evidence of intrapartum hypoxia without any preconception or antepartum abnormal-
ities that put them at risk for newborn encephalopathy. Similarly, more than two-thirds
of neonates with encephalopathy had only antepartum risk factors (and no intrapartum
risk factors). Thus, the investigators suggested that most cases of newborn enceph-
alopathy may be mediated more by antepartum risk factors (such as maternal thyroid
disease, preeclampsia, growth restriction, and family history of neurologic disease)
than by intrapartum hypoxia.
In a cohort of 139 pregnancies complicated by confirmed bacterial chorioamnionitis
(a well-accepted risk factor for CP), FHR tracings were reviewed to determine if there
was any association between nonreassuring FHR patterns and subsequent CP
diagnosis.30 The incidence of nonreassuring FHR patterns was increased overall rela-
tive to a population not affected with chorioamnionitis; however, there were no
specific heart rate patterns predictive of CP development.
In 2003, a Task Force on Neonatal Encephalopathy and Cerebral Palsy was
convened in an effort to review both historical and current data and to outline
specific definitions for neonatal encephalopathy and acute intrapartum hypoxia.
Conclusions from the task force suggest that intrapartum hypoxia is rarely the
sole cause of neonatal encephalopathy or CP. Neonatal encephalopathy is defined
clinically from several abnormal neurologic findings in a term or a near-term
neonate, including abnormal consciousness, tone, reflexes, feeding, respirations,
or seizures. Not all neonatal encephalopathy results in permanent neurologic
 Electronic Fetal Monitoring 137

damage. However, the progression from an acute intrapartum hypoxic event to the
development of spastic CP must pass through neonatal encephalopathy. The
criteria of an acute intrapartum hypoxic event sufficient to cause CP as defined
by the task force are as follows:
1. Evidence of metabolic acidosis in umbilical cord arterial blood (pH <7.0 and base
deficit 12 mmol/L)
2. Early onset of moderate or severe neonatal encephalopathy in infants born at or
after 34 weeks of gestation
3. CP of the spastic or dyskinetic type
4. Exclusion of other identifiable causes (trauma, infection, genetic, coagulation).
Criteria to suggest (but are not specific for) intrapartum timing include
1. A sentinel hypoxic event occurring immediately before or during labor
2. A sudden or sustained fetal bradycardia in the absence of FHR variability in the
presence of persistent, late, or variable decelerations, usually after a sentinel
hypoxic event when the pattern was previously normal
3. Apgar score of 0 to 3 beyond 5 minutes
4. Onset of multiorgan involvement within 72 hours of delivery
5. Early imaging showing evidence of acute nonfocal cerebral abnormality.
Understanding the link between intrapartum acute hypoxic events, neonatal
encephalopathy, and CP requires understanding the idea of attributable risk. The
attributable fraction is the proportion of cases that is attributable to a specific expo-
sure (in this case, acute intrapartum hypoxia) and similarly the proportion of cases
of disease that could be eliminated in a population if the available intervention elimi-
nated the exposure while other risk factors remain constant. The task force suggested
that the best available evidence indicated that the incidence of neonatal encephalop-
athy with intrapartum hypoxia in the absence of other antepartum abnormalities is
approximately 1.6 per 10,000 births. Approximately 70% of neonatal encephalopathy
is thought to be secondary to events arising before labor.31

WHERE ARE WE NOW?

In 2005 and again in 2009, the American College of Obstetricians and Gynecologists
(ACOG) put forth practice bulletin guidelines, regarding interpretation and manage-
ment of intrapartum FHR monitoring.32,33 The 2009 and 2005 practice bulletins
acknowledge that available data suggest that EFM increases cesarean delivery rate,
increases operative vaginal deliveries, and does not reduce overall perinatal mortality
(although comments regarding the rarity of the outcomes and relatively small sample
sizes are noted). The practice bulletins also attempt to debunk the idea that a nonreas-
suring FHR tracing is predictive of CP and indicate that in fetuses weighing more than
2500 g, the positive predictive value is 0.14% (or only approximately 1 or 1000 fetuses
with an abnormal tracing will progress to CP). ACOG suggests that either EFM or
intermittent auscultation is an acceptable form of monitoring but that continuous
monitoring should be used for women in labor with high-risk conditions (eg,
preeclampsia, fetal growth restriction, or type 1 diabetes). If intermittent auscultation
is being used in the absence of risk factors, there are no data to suggest the optimal
frequency at which intermittent auscultation should be performed. The 2009 level A
recommendations and conclusions were as follows: (1) the false-positive rate of
EFM for predicting CP is high (>99%); (2) the use of EFM is associated with increased
operative vaginal deliveries and cesarean deliveries; (3) when FHR tracing has
138 Stout & Cahill

repetitive variable decelerations, amnioinfusion should be considered; (4) pulse oxi-

metry has not been demonstrated to be a useful test in evaluating fetal status. The
level B conclusions of the 2009 recommendation are that there is high interobserver
and intraobserver variability in FHR interpretation and re-interpretation, especially in
the context of knowing neonatal outcome, may not be reliable. Lastly, the use of
EFM does not result in the reduction of CP.
According to a Cochrane review published in 2008, possible advantages of contin-
uous EFM include measurable parameters of FHR patterns and a physical record,
which can be reevaluated at any time during or after labor. The review’s comments
on possible disadvantages of EFM are difficult standardization of the complexity of
FHR patterns, prevents full mobility and other pain-coping strategies during labor,
and may foster a belief that all perinatal mortality and neurologic injury can be pre-
vented. The investigators commented that a trial powered adequately to measure
the effect on perinatal death (given an incidence of 0.1%) would require 50,000 women
to be randomized.34
In 2008, a joint meeting cosponsored by the NICHD, the ACOG, and the Society for
Maternal Fetal Medicine was undertaken with 3 goals: to review and update definitions
from the previous 1997 meeting, to assess classification systems for interpretations of
EFM tracings, and to make research goals and priorities for continued investigation of
EFM in clinical practice.35,36 The guidelines regarding FHR baseline, tachycardia,
bradycardia, variability, acceleration, and characteristics of decelerations remained
the same as the definitions from the 1997 conference (discussed earlier). In addition,
uterine contraction pattern was classified as normal (5 contractions in 10 minutes
averaged over a 30-minute period) or as a tachysystole (>5 contractions in 10 minutes
averaged over a 30-minute period). Tachysystole can occur from spontaneous or
stimulated labor, and documentation of tachysystole should always be accompanied
by a notation regarding any associated FHR decelerations. The negative predictive
value of EFM is noted as the presence of accelerations, either spontaneous or stimu-
lated (via fetal scalp stimulation, transabdominal halogen light or vibroacoustic stimu-
lation), that reliably predicts the lack of metabolic acidemia in the fetus. Similarly,
moderate variability reliably predicts the absence of fetal metabolic acidemia.
However, the reverse of these statements is not necessarily true. For example, neither
the lack of accelerations nor the lack of moderate variability reliably predicts the pres-
ence of metabolic acidemia. Notably, FHR fluctuations are a physiologic response,
thus EFM captures only the immediate physiologic state, can change over time, and
should be interpreted in context.
Multiple categorization strategies were entertained by the 2008 NICHD conference,
including 3- and 5-tiered systems, subcategorizations, color coding of various FHR
parameters. The decision was to enact a 3-tiered system as explained in the following
sections.

Category I (Normal)
Unambiguously normal and should be followed routinely. Category I tracings include
all of the following: normal baseline (110–160 beats per minute), moderate variability,
absent late decelerations, absent variable decelerations, accelerations may be
present but are not required, early decelerations may be present or absent.

Category III (Abnormal)

Abnormal and requires immediate efforts to improve the clinical situation through
intrauterine resuscitation (maternal position change, maternal oxygen, maintenance
of adequate maternal blood pressure, discontinuation of administration of labor
 Electronic Fetal Monitoring 139

stimulants), and if no resolution occurs, prompt delivery should be considered. Cate-

gory III tracings include any of the following: absent variability with any recurrent
deceleration or bradycardia, or sinusoidal pattern.
Category II (Indeterminate)
Category II necessarily includes all tracings not categorized as I or III and encom-
passes a wide range of clinical situations. Category II tracings may range from the
intermittent variable deceleration in the context of an otherwise reassuring tracing
to persistent late or variable decelerations in the context of moderate variability. Cate-
gory II includes the following:

Baseline rate
Bradycardia not accompanied by absent variability
Tachycardia
Variability
Minimal baseline variability
Absent variability not accompanied by recurrent decelerations
Marked variability
Accelerations
Absence of induced accelerations after fetal stimulation
Periodic or episodic decelerations
Recurrent variable decelerations accompanied by minimal or moderate
variability
Prolonged deceleration for 2 minutes or more but less than 10 minutes
Recurrent late decelerations with moderate baseline variability
Variable decelerations with other characteristics such as slow return to baseline,
“overshoots” or “shoulders.”

FOCUS ON FUTURE PROGRESS

Recent research efforts have focused on computerized interpretation of EFM tracings

and specific components of EFM tracings that may be more useful, such as ST-
segment analysis. Elliot and colleagues37 evaluated a computerized interpretation
system that graded the FHR tracings according to a 5-tired color-coded system
ranging from green (normal) to red (markedly abnormal). Their data suggest that the
severity and the duration of the abnormality are both associated with biochemical
evidence of acidemia. For example, they noted that it would take a shorter amount
of time for a strip in the markedly abnormal red category to be associated with alter-
ations in pH than it would for an intermediate yellow or blue category. Although the
data from this study add to the literature by suggesting that there may remain an asso-
ciation between abnormal FHR tracings and acidemia at birth, the same questions
regarding the incidence of false-positive results and the association with useful clinical
outcomes remain.
Focused efforts on EFM findings that may be more specific to underlying physio-
logic changes, such as ST-segment analysis, are also being studied.38 The premise
of ST-segment analysis is that ST-segment changes occur in the context of fetal
myocardial ischemia and could be picked up by fetal electrocardiography as a specific
marker of physiologic effects of hypoxemia. However, in a retrospective case-control
study of 787 fetuses, ST-segment analysis did increase the probability of detection of
a fetal acid-base abnormality. However, abnormal ST-segment changes were also
found in 50% of fetuses with normal blood gas parameters.
140 Stout & Cahill

The 2008 NICHD conference identified specific research priorities including obser-
vational studies to elucidate the interpretations of indeterminate FHR patterns
including frequency, changes over time, and the effect of duration (eg, the evolution
of recurrent late decelerations with minimal variability) on useful clinical outcomes.
In addition, attention should be paid to the importance of maternal contraction
pattern—frequency, strength, duration, relaxation—and the effect of contraction
pattern on FHR and clinical outcomes. Furthermore, standardized educational
programs for the interpretation of EFM patterns should be studied.
A professor of neurology, pediatrics, and bioethics points out that although
patients and practitioners want the latest and the best diagnostic and treatment inno-
vations, the use of EFM technology may be an example of the application of a new
technology without adequate testing and scientific proof of benefit.39 The premature
adoption of these technologies has consequences, which are typically considered
only after the integration of the technology into clinical care. Dr Freeman39 suggests
that the intervention on abnormal FHR tracings is responsible for increased (and
potentially unnecessary) surgical procedures, with the associated economic costs,
as well as the legal ramification of malpractice suits with the assumption (potentially
erroneously) that earlier and more expeditious intervention may have produced an
improved outcome.
Present-day obstetricians cannot undo 40 years of practice and well-engrained clin-
ical habits. But they can commit to knowing the history from which these clinical habits
stemmed and continue to put forth useful research efforts to improve clinical care. It is
equally important to remember the promise with which EFM was put forth and the
potential the technology might still offer if properly studied. Furthermore, as new tech-
nologies arise, the obstetricians owe their patients a truthful and critical examination of
the evidence as it emerges.

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