Electronic FetalMonitoring: Past,Present, and Future

Molly J. Stout, MDa,*, Alison G. Cahill, MD, MSCIb

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 than3 million pregnancies are monitored during labor in the United States annually usingEFM.1 The use of such technology can be easily taken for granted in most labor suitesbecause physicians and other medical personnel follow continuous paper or elec-tronic tracings of fetal heart rate (FHR) and contraction patterns and virtually allpatients arrive to labor and delivery expecting the tool to be used in their care. Despiteits now ubiquitous use, continuous electronic monitoring and its associated risks andbenefits are worth considering. To meaningfully evaluate the current use of EFM andmake educated decisions regarding future research goals, it is imperative to analyzethe research and clinical practices of several past decades, which have shaped andmolded 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 werenot significantly different from modern obstetric goals: to decrease morbidity andmortality both in the mother and the newborn. The standard of care for intrapartumfetal assessment before the introduction of EFM was intermittent auscultation of fetalheart tones and fetal scalp pH sampling. FHR characteristics are, in part, a productof central nervous system’s sympathetic and parasympathetic outflow.2 If oneaccepts the theory that intrapartum hypoxia leads eventually to changes in the fetalcentral 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 BarnesJewish 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: stoutm@wudosis.wustl.edu

Clin Perinatol 38 (2011) 127–142doi:10.1016/j.clp.2010.12.002 perinatology.theclinics.com0095-5108/11/$ – see front matter � 2011 Elsevier Inc. All rights reserved.

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(CP) and other permanent neurologic damage, the goal then becomes to identifyhypoxia during labor via identifiable FHR characteristics in an effort to intervenebefore permanent damage occurs. The hope was that continuous EFM wouldbe the answer—a continuous window into the fetal central nervous system and theopportunity 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 preceding20 minutes of FHR findings. If a mixture of findings were present in the tracing, themost “ominous” finding was used (eg, it would be classified according to a prolongedlate deceleration preferentially over a mild variable deceleration). Their data showedthat moderate variable decelerations are associated with a lower mean pH comparedwith tracings with no decelerations, early decelerations, or mild variable decelerations.Severe variable decelerations and late decelerations were associated with a furthershift toward lower pH. Most (but not all) of the tracings with late decelerations hada pH less than 7.25.3 They published that their single most important result was theabsence 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 bloodoxygen tension. Rhesus monkey fetuses underwent continuous fetal monitoring andwere catheterized in utero to directly examine blood pH. Maternal monkeys had a peri-aortic loop inserted to manipulate uterine perfusion. The investigators found thatduring 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 resultantbradycardia, pH remained essentially unchanged during the event. It was also notedthat even a well-oxygenated fetus responds with late deceleration if the uterinecontractions are sufficiently prolonged. It was concluded that fetal blood oxygentension 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. Inthe 9 fetuses observed, accelerations were initially present at the time of appearanceof late decelerations. By the time the late decelerations became repetitive, the fetalblood oxygen saturation was significantly decreased, but pH and PaCO2 had notchanged significantly. The complete absence of accelerations with persistent latedecelerations characterized the phase immediately preceding fetal death and wasassociated 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 intofetal 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 reduceintrapartum fetal death and improve neonatal survival. In 1976, a prospective cohortstudy was published comparing continuous EFM to intermittent auscultation butwas stopped early because of the evidence of what the investigators described asa clear benefit in the EFM group observed as decreased neonatal intensive careunit (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 continuousEFM to 241 patients undergoing intermittent auscultation. They reported an increasedrisk of cesarean delivery in the EFM group but no difference in Apgar scores and nodifference in cord blood gas values between the groups. There were no intrapartumdeaths but 3 perinatal deaths; 2 in the EFM group, 1 in the intermittent auscultationgroup. The 2 deaths were because of congenital anomalies, and the 1 death wasthought to be due to meconium aspiration. This study was followed by another studyof a low-risk obstetric population in England of 254 women undergoing continuousEFM compared with 251 women undergoing intermittent auscultation.9 Again, theyreported increased cesarean delivery rates, with no difference in Apgar scores, inthe 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 havingpreviously 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 eitherintermittent auscultation alone, continuous EFM alone, or continuous EFM with pHsampling. Women in the continuous EFM group were more likely to undergo cesareandelivery, independent of whether pH sampling was performed or not. No differences inApgar score or acid-base parameters were found. They summarized: “Two primaryconclusions emerge from this investigation on the differential effects of fetal moni-toring: (1) electronic fetal monitoring with or without scalp sampling did not improveperinatal outcomes over that achieved by intermittent auscultation alone; (2) thecesarean 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 wasunclear whether there truly was no improvement in neonatal outcomes with EFM orwhether the outcomes of neonatal morbidity and mortality were so rare that thestudies were not powered appropriately to detect a difference. In 1985, the Dublinrandomized controlled trial of intrapartum FHR monitoring was published. The studyincluded more than 12,000 women (as compared with prior studies of 400–600women) and a power calculation that dictated that 10,000 women in each group wouldyield a sufficient sample size.11 Contrary to the prior studies, there was no increasedrate of cesarean delivery in the EFM group. The investigators present that in theneonates who survived, there was a significant decrease in the incidence of neonatalseizures in the EFM group. However, despite the difference noted in the incidence ofneonatal seizures, in the 1-year follow-up, equal number in each group was found tohave severe disabilities, suggesting that neonatal seizures by their definition were nota reasonable surrogate marker for the clinically important outcome of long-termcentral 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. Thisprospective randomized study, conducted at 2 university hospitals in Greece, includedall 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 conservativeintrauterine resuscitation (maternal oxygen and intravenous fluids, maternal position

Table 1Summary of studies comparing continuous EFM to intermittent auscultation

Author Year Study Type; Population NPowerCalculation Rate of Cesarean Delivery Apgar Score Neonatal Outcomes

Renou et al7 1976 Prospective cohort;high risk

Cases, continuous EFMControls, no EFM, no fetal

scalp sample

440 None No difference No difference Increased NICU admission andother symptoms inintermittent auscultationgroup. Study stopped early.

Haverkamp et al8 1976 Prospective randomizedEFM vs intermittentauscultation; high risk

483 None Increased in EFM group No difference No difference in NICUadmission, pH, intubations,or seizures

Kelso et al9 1978 Prospective randomizedEFM vs intermittentauscultation;normal risk

504 None Increased in EFM group No difference No difference in NICUadmission or pH

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

690 None Increased in EFM groups No difference No difference in pH or NICUadmission

Wood et al40 1981 Prospective randomizedEFM vs intermittentauscultation;normal risk

504 None Increased in EFM group No difference No difference in neurologicsymptoms

MacDonald et al11 1985 Prospective randomizedEFM vs intermittentauscultation; mixedhigh and normal risk

12,964 Yes No difference No difference Decreased neonatal seizureswith EFM. 1-year follow-upno difference in severedisabilities between groups

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

1428 Yes Increased in EFM group No difference No difference in NICUadmission or neonatalseizures. Decreased perinataldeath

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change, discontinuation of oxytocin administration) followed by operative vaginaldelivery or cesarean delivery if the nonreassuring pattern persisted for more than20 minutes. No crossover between groups occurred (eg, no patients undergoing inter-mittent auscultation were transitioned to continuous monitoring because of identifiedabnormal auscultation), and no pH sampling was undertaken to confirm or rejectFHR findings. Similar to previous studies, it was found that the incidence of cesareandelivery for nonreassuring FHR patterns was increased in the EFM group. All neonatalcomplications (such as NICU admission, assisted ventilation, hypoxic-ischemicencephalopathy [HIE], seizures) were not significantly different between EFMand inter-mittent auscultation groups. However, the researchers commented that their datasupport the use of EFM because the perinatal death rate was significantly decreasedin 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 concernsregarding 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 nodemonstrable benefit, the question remained as to whether continuous EFM wasmore appropriately applied in specific pregnancies at higher risk of intrapartum andneonatal 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 atthat time at the investigators’ institution was to “selectively” monitor pregnancieswith a high-risk condition using continuous EFM and use intermittent EFM if none ofthe high-risk criteria were met. The definition of high risk as used by the investigatorswas 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. Theyfound that universal monitoring had no significant improvement in stillbirth, Apgarscores, assisted ventilation at birth, NICU admission, or seizures compared withselective monitoring. Luthy and colleagues14 studied 246 pregnancies with pretermlabor at 26 to 32 weeks with estimated fetal weight of 700 to 1750 g randomized toeither EFM or intermittent auscultation. There was no difference in the rate of cesareandelivery between the 2 groups. Fetal acidosis, neonatal seizures, respiratory distresssyndrome, 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 monitoringdoes 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 infantsaged 18 months.15 Neurologic development at 18 months was not improved in thegroup that had been monitored with EFM compared with the intermittent auscultationgroup. An unexpected finding was an increased diagnosis of CP in the EFM group(20%) compared with the intermittent auscultation group (8%). They speculated thatperhaps 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 EFMprovides 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 andHuman Development (NICHD) proposed that 1 roadblock to a useful interpretationof research on EFM was lack of agreement in definitions and patterns on EFMtracings.16 A consensus workshop put forth standardized interpretations for FHRpatterns, 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 ofdecelerations. These components are reviewed in the following sections.

Baseline Rate

The baseline rate is the mean FHR rounded to 5 beats per minute and incrementsduring a 10-minute segment. The normal baseline rate is from 110 to 160 beats perminute. Fetal bradycardia is a baseline FHR of less than 110 beats per minute, andfetal 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 andfrequency (Fig. 1). Variability amplitude is visually quantified as absent, amplituderange 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 than25 beats per minute. The sinusoidal pattern is not to be confused with variability and isinstead defined as a wavelike pattern with regular frequency and amplitude.

Acceleration

Acceleration is a visibly apparent abrupt increase (onset to peak in <30 seconds) inFHR 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 for15 seconds from start to finish (it is not required to remain at the peak throughoutthe 15 seconds). At less than 32 weeks’ gestation, an increase of 10 beats per minuteabove 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 moderatevariability.

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defined as lasting from 2 to 10 minutes. Any acceleration lasting more than 10 minutesis 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 contractionsover 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 calculatedfrom the baseline to the nadir. It is termed late relative to the contraction becausethe 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 thefetus, causing vagal stimulation, and thus there is a decrease in the FHR. A secondmechanism for late deceleration involves the relatively deoxygenated blood fromthe placenta during the contraction, causing direct hypoxic depression of themyocardium.2

Variable decelerations are termed as such because they can occur in any locationwith 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 cordcompression.2

Early decelerations are a visibly apparent gradual decrease (onset to nadir, �30seconds) and return to baseline that occurs with uterine contraction (Fig. 5). Thebeginning, nadir, and recovery are coincident with the beginning, peak, and releaseof 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 EFMshould 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 wasbeing used in more than 70% of all live births, making it the most common obstetricprocedure.18 Among members of the 1997 NICHD consensus meeting, there was

Fig. 2. FHR tracing demonstrating prolonged deceleration.

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 normallyoxygenated fetus at delivery. Similarly, members agreed that certain patterns suchas recurrent late decelerations with absent variability and prolonged or significantbradycardia are almost uniformly nonreassuring. However, the intermediate group,those tracings not belonging to either end of the spectrum of normalcy, lacked uniformconsensus on evidence-based management. The planning workshop put forth severalresearch goals regarding EFM, including studying the correlation between specificFHR 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 timepoints during labor: early labor, active labor 1 hour before complete dilation, andthroughout the entire second stage of labor in 30-minute segments. It was concludedthat variability alone cannot be a single predictor for fetal well-being because most ofthe cases with adverse fetal outcomes demonstrated normal variability.19 A case-control study reviewing FHR tracings of cases of known neonatal encephalopathycompared with controls without encephalopathy was performed in 1997. The studyreported that most cases of neonatal encephalopathy were preceded by an abnormalFHR tracing but that 52% of normal controls also had an abnormal FHR tracing beforedelivery.20

Another case-control study of 71 term infants with metabolic acidosis (basedeficit >16 mmol/L) and a control group of 71 term infants without metabolic acidosisevaluated the FHR tracings in the 4-hour period before delivery.21 Spontaneous accel-erations occurred significantly more frequently in the control group. Absent or minimalvariability in the 1-hour period before delivery occurred in 68% of the caseswith 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 beacidemic. Sameshima and Ikenoue22 retrospectively reviewed FHR tracings of morethan 5000 low-risk pregnancies and correlated FHR patterns with umbilical bloodgas and CP diagnosis. They reported that decreasing variability in tracings with lateor prolonged decelerations was associated with decreasing pH. The false-positiverate 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 fetalmonitoring 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 accordingto the 2 factors variability and recovery of bradycardia as follows: group 1, normalvariability, recovery of bradycardia; group 2, normal variability, no recovery ofbradycardia; 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 pathologicacidosis. Specifically, the presence of decreased variability before bradycardia, irre-spective of whether the bradycardia recovered, was associated with a 44% incidenceof fetal acidosis.

REVISITING THE LINK BETWEEN INTRAPARTUM HYPOXIA AND CP

The original intention of EFM—to reduce intrapartum stillbirth and improveneonatal outcomes—is revisited in this section. In the 1970s, Quilligan and Paul6

suggested that brain damage is “merely an intermediate point on the pathwayto 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, nodecrease in the incidence of CP has been noted.24 HIE is a small subset of thebroader 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 andbase excess of 12 mmol/L or more, 13 cases had neurologic complications(8 neonates with seizures, 1 with bilateral grade 3 intraventricular hemorrhage, and4 died).26 There was no difference in total, late, or prolonged decelerations in theneurologically injured group when compared with the noninjured group. However,neurologically injured infants were more likely to have a positive result in blood culturein the neonatal period. The researchers concluded that although late decelerationsweremore common in the presence of metabolic acidosis, they were unable to identifythe 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 CPwas 1.1 per 1000 patients. The finding of multiple late decelerations was associatedwith a quadrupling of the risk for CP and that of decreased variability with a triplingrisk 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% (studyincidence of abnormal tracing) or 9300 children would have abnormal tracings withmultiple 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 pregnanciesintervened on without benefit or 2324 nonbeneficial interventions for each case of CPprevented.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 hadevidence of intrapartum hypoxia without any preconception or antepartum abnormal-ities that put them at risk for newborn encephalopathy. Similarly, more than two-thirdsof neonates with encephalopathy had only antepartum risk factors (and no intrapartumrisk 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 therewas any association between nonreassuring FHR patterns and subsequent CPdiagnosis.30 The incidence of nonreassuring FHR patterns was increased overall rela-tive to a population not affected with chorioamnionitis; however, there were nospecific 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 thesole cause of neonatal encephalopathy or CP. Neonatal encephalopathy is definedclinically from several abnormal neurologic findings in a term or a near-termneonate, 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 thedevelopment of spastic CP must pass through neonatal encephalopathy. Thecriteria of an acute intrapartum hypoxic event sufficient to cause CP as definedby the task force are as follows:

1. Evidence of metabolic acidosis in umbilical cord arterial blood (pH <7.0 and basedeficit �12 mmol/L)

2. Early onset of moderate or severe neonatal encephalopathy in infants born at orafter 34 weeks of gestation

3. CP of the spastic or dyskinetic type4. 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 labor2. A sudden or sustained fetal bradycardia in the absence of FHR variability in the

presence of persistent, late, or variable decelerations, usually after a sentinelhypoxic event when the pattern was previously normal

3. Apgar score of 0 to 3 beyond 5 minutes4. Onset of multiorgan involvement within 72 hours of delivery5. Early imaging showing evidence of acute nonfocal cerebral abnormality.

Understanding the link between intrapartum acute hypoxic events, neonatalencephalopathy, and CP requires understanding the idea of attributable risk. Theattributable 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 casesof 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 suggestedthat the best available evidence indicated that the incidence of neonatal encephalop-athy with intrapartum hypoxia in the absence of other antepartum abnormalities isapproximately 1.6 per 10,000 births. Approximately 70% of neonatal encephalopathyis 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 bulletinsacknowledge 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 samplesizes 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 than2500 g, the positive predictive value is 0.14% (or only approximately 1 or 1000 fetuseswith an abnormal tracing will progress to CP). ACOG suggests that either EFM orintermittent auscultation is an acceptable form of monitoring but that continuousmonitoring should be used for women in labor with high-risk conditions (eg,preeclampsia, fetal growth restriction, or type 1 diabetes). If intermittent auscultationis being used in the absence of risk factors, there are no data to suggest the optimalfrequency at which intermittent auscultation should be performed. The 2009 level Arecommendations and conclusions were as follows: (1) the false-positive rate ofEFM for predicting CP is high (>99%); (2) the use of EFM is associated with increasedoperative 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. Thelevel B conclusions of the 2009 recommendation are that there is high interobserverand intraobserver variability in FHR interpretation and re-interpretation, especially inthe context of knowing neonatal outcome, may not be reliable. Lastly, the use ofEFM 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 commentson possible disadvantages of EFM are difficult standardization of the complexity ofFHR 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 measurethe effect on perinatal death (given an incidence of 0.1%) would require 50,000 womento be randomized.34

In 2008, a joint meeting cosponsored by the NICHD, the ACOG, and the Society forMaternal Fetal Medicine was undertaken with 3 goals: to review and update definitionsfrom the previous 1997 meeting, to assess classification systems for interpretations ofEFM tracings, and to make research goals and priorities for continued investigation ofEFM in clinical practice.35,36 The guidelines regarding FHR baseline, tachycardia,bradycardia, variability, acceleration, and characteristics of decelerations remainedthe same as the definitions from the 1997 conference (discussed earlier). In addition,uterine contraction pattern was classified as normal (�5 contractions in 10 minutesaveraged over a 30-minute period) or as a tachysystole (>5 contractions in 10 minutesaveraged over a 30-minute period). Tachysystole can occur from spontaneous orstimulated labor, and documentation of tachysystole should always be accompaniedby a notation regarding any associated FHR decelerations. The negative predictivevalue 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, neitherthe 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 FHRparameters. The decision was to enact a 3-tiered system as explained in the followingsections.

Category I (Normal)

Unambiguously normal and should be followed routinely. Category I tracings includeall of the following: normal baseline (110–160 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 throughintrauterine resuscitation (maternal position change, maternal oxygen, maintenanceof 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 recurrentdeceleration 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 theintermittent variable deceleration in the context of an otherwise reassuring tracingto persistent late or variable decelerations in the context of moderate variability. Cate-gory II includes the following:

Baseline rate

Bradycardia not accompanied by absent variabilityTachycardia

VariabilityMinimal baseline variabilityAbsent variability not accompanied by recurrent decelerationsMarked variability

AccelerationsAbsence of induced accelerations after fetal stimulation

Periodic or episodic decelerationsRecurrent variable decelerations accompanied by minimal or moderate

variabilityProlonged deceleration for 2 minutes or more but less than 10 minutesRecurrent 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 tracingsand specific components of EFM tracings that may be more useful, such as ST-segment analysis. Elliot and colleagues37 evaluated a computerized interpretationsystem that graded the FHR tracings according to a 5-tired color-coded systemranging from green (normal) to red (markedly abnormal). Their data suggest that theseverity and the duration of the abnormality are both associated with biochemicalevidence of acidemia. For example, they noted that it would take a shorter amountof 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 thedata 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 questionsregarding the incidence of false-positive results and the association with useful clinicaloutcomes 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 fetalmyocardial ischemia and could be picked up by fetal electrocardiography as a specificmarker of physiologic effects of hypoxemia. However, in a retrospective case-controlstudy of 787 fetuses, ST-segment analysis did increase the probability of detection ofa fetal acid-base abnormality. However, abnormal ST-segment changes were alsofound 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 patternsincluding frequency, changes over time, and the effect of duration (eg, the evolutionof recurrent late decelerations with minimal variability) on useful clinical outcomes.In addition, attention should be paid to the importance of maternal contractionpattern—frequency, strength, duration, relaxation—and the effect of contractionpattern on FHR and clinical outcomes. Furthermore, standardized educationalprograms 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 newtechnology without adequate testing and scientific proof of benefit.39 The prematureadoption of these technologies has consequences, which are typically consideredonly after the integration of the technology into clinical care. Dr Freeman39 suggeststhat the intervention on abnormal FHR tracings is responsible for increased (andpotentially unnecessary) surgical procedures, with the associated economic costs,as well as the legal ramification of malpractice suits with the assumption (potentiallyerroneously) that earlier and more expeditious intervention may have produced animproved outcome.Present-day obstetricians cannot undo 40 years of practice and well-engrained clin-

ical habits. But they can commit to knowing the history fromwhich these clinical habitsstemmed and continue to put forth useful research efforts to improve clinical care. It isequally important to remember the promise with which EFM was put forth and thepotential 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.

REFERENCES

1. Martin JA, Hamilton BE, Sutton PD, et al. Births: final data for 2002. Natl Vital StatRep 2003;52(10):1–113.

2. Creasy RK, Resnik R, Iams JD, et al. Maternal-fetal medicine principles and prac-tice. 6th edition. Philadelphia: Saunders Elsevier; 2009.

3. Kubli FW, Hon EH, Khazin AF, et al. Observations on heart rate and pH in thehuman fetus during labor. Am J Obstet Gynecol 1969;104(8):1190–206.

4. Myers RE, Mueller-Heubach E, Adamsons K. Predictability of the state of fetaloxygenation from a quantitative analysis of the components of late deceleration.Am J Obstet Gynecol 1973;115(8):1083–94.

5. Murata Y, Martin CB Jr, Ikenoue T, et al. Fetal heart rate accelerations and latedecelerations during the course of intrauterine death in chronically catheterizedrhesus monkeys. Am J Obstet Gynecol 1982;144(2):218–23.

6. Quilligan EJ, Paul RH. Fetal monitoring: is it worth it? Obstet Gynecol 1975;45(1):96–100.

7. Renou P, Chang A, Anderson I, et al. Controlled trial of fetal intensive care. Am JObstet Gynecol 1976;126(4):470–6.

8. Haverkamp AD, Thompson HE, McFee JG, et al. The evaluation of continuousfetal heart rate monitoring in high-risk pregnancy. Am J Obstet Gynecol 1976;125(3):310–20.

9. Kelso IM, Parsons RJ, Lawrence GF, et al. An assessment of continuous fetalheart rate monitoring in labor. A randomized trial. Am J Obstet Gynecol 1978;131(5):526–32.

Electronic Fetal Monitoring 141

10. HaverkampAD,OrleansM,LangendoerferS, etal.Acontrolled trial of thedifferentialeffects of intrapartum fetal monitoring. Am J Obstet Gynecol 1979;134(4):399–412.

11. MacDonald D, Grant A, Sheridan-Pereira M, et al. The Dublin randomizedcontrolled trial of intrapartum fetal heart rate monitoring. Am J Obstet Gynecol1985;152(5):524–39.

12. Vintzileos AM, Antsaklis A, Varvarigos I, et al. A randomized trial of intrapartumelectronic fetal heart rate monitoring versus intermittent auscultation. ObstetGynecol 1993;81(6):899–907.

13. Leveno KJ, Cunningham FG, Nelson S, et al. A prospective comparison of selec-tive and universal electronic fetal monitoring in 34,995 pregnancies. N Engl J Med1986;315(10):615–9.

14. Luthy DA, Shy KK, van Belle G, et al. A randomized trial of electronic fetal moni-toring in preterm labor. Obstet Gynecol 1987;69(5):687–95.

15. Shy KK, Luthy DA, Bennett FC, et al. Effects of electronic fetal-heart-rate moni-toring, as compared with periodic auscultation, on the neurologic developmentof premature infants. N Engl J Med 1990;322(9):588–93.

16. Electronic fetal heart rate monitoring: research guidelines for interpretation.National Institute of Child Health and Human Development research planningworkshop. Am J Obstet Gynecol 1997;177(6):1385–90.

17. Screening for intrapartum electronic fetal monitoring. 1996. Available at: http://www.uspreventiveservicestaskforce.org/uspstf/uspsiefm.htm.AccessedJanuary19,2011.

18. Advance report of maternal and infant health data from the birth certificate, 1990.Mon Vital Stat Rep 1993;42(Suppl 2). Available at: http://www.cdc.gov/nchs/products/mvsr/mvsr43_5s.htm. Accessed December 24, 2010.

19. Samueloff A, Langer O, Berkus M, et al. Is fetal heart rate variability a goodpredictor of fetal outcome? Acta Obstet Gynecol Scand 1994;73(1):39–44.

20. Spencer JA, Badawi N, Burton P, et al. The intrapartum CTG prior to neonatalencephalopathy at term: a case-control study. Br J Obstet Gynaecol 1997;104(1):25–8.

21. LowJA,VictoryR,DerrickEJ. Predictive valueof electronic fetalmonitoring for intra-partum fetal asphyxiawithmetabolic acidosis. ObstetGynecol 1999;93(2):285–91.

22. Sameshima H, Ikenoue T. Predictive value of late decelerations for fetal acidemiain unselective low-risk pregnancies. Am J Perinatol 2005;22(1):19–23.

23. Williams KP, Galerneau F. Fetal heart rate parameters predictive of neonataloutcome in the presence of a prolonged deceleration. Obstet Gynecol 2002;100(5 Pt 1):951–4.

24. Clark SL, Hankins GD. Temporal and demographic trends in cerebral palsy–factand fiction. Am J Obstet Gynecol 2003;188(3):628–33.

25. HankinsGD, SpeerM. Defining the pathogenesis and pathophysiology of neonatalencephalopathy and cerebral palsy. Obstet Gynecol 2003;102(3):628–36.

26. Larma JD, Silva AM, Holcroft CJ, et al. Intrapartum electronic fetal heart ratemonitoring and the identification of metabolic acidosis and hypoxic-ischemicencephalopathy. Am J Obstet Gynecol 2007;197(3):301,e1–8.

27. Nelson KB, Dambrosia JM, Ting TY, et al. Uncertain value of electronic fetal moni-toring in predicting cerebral palsy. N Engl J Med 1996;334(10):613–8.

28. Badawi N, Kurinczuk JJ, Keogh JM, et al. Antepartum risk factors for newbornencephalopathy: the Western Australian case-control study. BMJ 1998;317(7172):1549–53.

29. Badawi N, Kurinczuk JJ, Keogh JM, et al. Intrapartum risk factors for newbornencephalopathy: the Western Australian case-control study. BMJ 1998;317(7172):1554–8.

Stout & Cahill142

30. Sameshima H, Ikenoue T, Ikeda T, et al. Association of nonreassuring fetal heartrate patterns and subsequent cerebral palsy in pregnancies with intrauterinebacterial infection. Am J Perinatol 2005;22(4):181–7.

31. American College of Obstetricians and Gynecologists’ Task Force on NeonatalEncephalopathy, Cerebral Palsy and the American College of Obstetriciansand Gynecologists, American Academy of Pediatrics. Neonatal encephalopathyand cerebral palsy: defining pathogenesis and pathophysiology. Washington,DC: American College of Obstetricians and Gynecologists; 2003.

32. American College of Obstetricians and Gynecologists. ACOG practice bulletin.Clinical management guidelines for obstetrician-gynecologists, number 70,December 2005 (replaces practice bulletin number 62, May 2005). Intrapartumfetal heart rate monitoring. Obstet Gynecol 2005;106(6):1453–60.

33. American College of Obstetricians and Gynecologists. ACOG practice bulletinNo. 106: intrapartum fetal heart rate monitoring: nomenclature, interpretation,and general management principles. Obstet Gynecol 2009;114(1):192–202.

34. Zarko A, Declan D, Gillian ML. Continuous cardiotocography (CTG) as a form ofelectronic fetal monitoring (EFM) for fetal assessment during labour. CochraneDatabase Syst Rev 2008;2.

35. Macones GA, Hankins GD, Spong CY, et al. The 2008 National Institute of ChildHealth and Human Development workshop report on electronic fetal monitoring:update on definitions, interpretation, and research guidelines. Obstet Gynecol2008;112(3):661–6.

36. Parer JT, Ikeda T, King TL. The 2008 National Institute of Child Health and HumanDevelopment report on fetal heart rate monitoring. Obstet Gynecol 2009;114(1):136–8.

37. Elliott C, Warrick PA, Graham E, et al. Graded classification of fetal heart rate trac-ings: association with neonatal metabolic acidosis and neurologic morbidity. AmJ Obstet Gynecol 2010;202(3):258,e1–8.

38. Melin M, Bonnevier A, Cardell M, et al. Changes in the ST-interval segment of thefetal electrocardiogram in relation to acid-base status at birth. BJOG 2008;115(13):1669–75.

39. Freeman JM. Beware: the misuse of technology and the law of unintended conse-quences. Neurotherapeutics 2007;4(3):549–54.

40. Wood C, Renou P, Oats J, et al. A controlled trial of fetal heart rate monitoring ina low-risk obstetric population. Am J Obstet Gynecol 1981;141(5):527–34.