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    E l e c t r o n i c F e t a lM o n i t o r i n g : P a s t ,

    P r e s e n t , a n d F u t u r eMolly J. Stout, MDa,*, Alison G. Cahill, MD, MSCIb

    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 andmake 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 systems 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, USAb Division of Maternal Fetal Medicine, Washington University in St Louis, 4911 Barnes JewishPlaza, Box 8064, St Louis, MO 63110, USA* Corresponding author.E-mail address: [email protected]

    KEYWORDS

    Electronic fetal monitoring Intrapartum continuous monitoring Neonatal outcomes

    Clin Perinatol 38 (2011) 127142doi:10.1016/j.clp.2010.12.002 perinatology.theclinics.com0095-5108/11/$ see front matter 2011 Elsevier Inc. All rights reserved.

    mailto:[email protected]://dx.doi.org/10.1016/j.clp.2010.12.002http://perinatology.theclinics.com/http://perinatology.theclinics.com/http://dx.doi.org/10.1016/j.clp.2010.12.002mailto:[email protected]
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    (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 answera 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 uterineblood 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 appearanceof 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 onan 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

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    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 400600women) 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 appropriatelypowered 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

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    Table 1

    Summary of studies comparing continuous EFM to intermittent auscultation

    Author Year Study Type; Population N

    Power

    Calculation Rate of Cesarean Delivery Ap

    Renou et al7 1976 Prospective cohort;high risk

    Cases, continuous EFMControls, no EFM, no fetal

    scalp sample

    440 None No difference No

    Haverkamp et al8 1976 Prospective randomizedEFM vs intermittentauscultation; high risk

    483 None Increased in EFM group No

    Kelso et al9 1978 Prospective randomizedEFM vs intermittentauscultation;

    normal risk

    504 None Increased in EFM group No

    Haverkamp et al10 1979 Prospective randomizedEFM 1 pH vs EFM alonevs intermittentauscultation; unselected

    690 None Increased in EFM groups No

    Wood et al40 1981 Prospective randomizedEFM vs intermittentauscultation;normal risk

    504 None Increased in EFM group No

    MacDonald et al11 1985 Prospective randomized

    EFM vs intermittentauscultation; mixedhigh and normal risk

    12,964 Yes No difference No

    Vintzileos et al12 1993 Prospective randomizedEFM vs intermittentauscultation; mixedhigh and normal risk

    1428 Yes Increased in EFM group No

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    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, dysfunctionallabor, 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 neonatalmortality. 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 DEVELOPMENTDEFINITIONS 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

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    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

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    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. Alldecelerations 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 uterinecontraction. 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,

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    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 partialpressure of oxygen.

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

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    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. Inthe 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 hada 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 EFMto reduce intrapartum stillbirth and improve

    neonatal outcomesis 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

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    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, approximately4 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 thyroiddisease, 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 outlinespecific 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

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    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 99%); (2) the use of EFM is associated with increased

    operative vaginal deliveries and cesarean deliveries; (3) when FHR tracing has

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    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 reviews 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 orstimulated 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, andshould 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 (110160 beats per minute), moderate variability,

    absent late decelerations, absent variable decelerations, accelerations may bepresent 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

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    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 variabilityVariable 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 theseverity 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 premiseof 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.

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    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

    patternfrequency, strength, duration, relaxationand 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 ofthe evidence as it emerges.

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