Finally, we excluded all women who delivered neonates with any evidence of neonatal morbidity (composite neonatal morbidity). After excluding women who gave birth to a neonate with any of the following: arterial umbilical cord gas pH less than 7.20, 5-minute Apgar score less than 7, or neonatal intensive care unit or special care admission, the frequency and distribution of atypical decelerations were described (Table 5). Even in apparently normal term neonates, decelerations with atypical characteristics occurred commonly; 54% had one or more “shoulders” and 48% had one or more “slow returns.” Twenty-two percent women had more than five atypical decelerations in the 30 minutes before delivery but still delivered a neonate without evidence of neonatal morbidity.
We found no association between atypical deceleration characteristics in the final 30 minutes before delivery, alone or in combination, and risk of acidemia at birth. Specifically, we found that “shoulders,” “slow returns” with varied definition, and minimal or marked variability within the deceleration demonstrated no association with acidemia or metabolic acidemia at birth. Given the high frequency of these atypical deceleration characteristics in neonates born with a normal arterial umbilical cord gas pH, normal 5-minute Apgar score, and admission to the low-risk nursery, they are likely a normal variant, at least in the final 30 minutes before term birth.
The Practice Bulletin from the American College of Obstetricians and Gynecologists addressing electronic fetal heart monitoring nomenclature in 2009,4 after the 2008 workshop on electronic fetal heart monitoring guidelines sponsored in part by American College of Obstetricians and Gynecologists, the Society for Maternal-Fetal Medicine, and the NICHD5 specified atypical deceleration features including “slow returns,” “shoulders,” and “overshoots” as periodic or episodic decelerations within category II (also termed indeterminate category).4 However, no published evidence was available to guide this portion of the classification system with respect to neonatal acid base status or outcome.6 This is particularly important because the association data between category II tracings and outcomes is void,7 leaving health care practitioners with no guidance when these atypical decelerations are noted in practice.
In 1983, Krebs et al1 published their findings of a retrospective cohort study of electronic fetal heart monitoring tracings during labor after 34 weeks of gestation in 1,996 women between 1975 and 1977. Similar to the present study, they examined the presence of atypical decelerations in the 30 minutes before delivery. They found 988 women with decelerations before delivery and described their association to fetal pH from scalp sampling and 1- and 5-minute Apgar scores. The authors reported that atypical decelerations (having any one of the atypical features) were present in 19% of electronic fetal heart monitoring tracings but predicted 38% of 1- and 5-minute Apgar scores less than 7. Among other limitations, because women without fetal scalp samples were not included, it is not possible to calculate the test performance of these features and the reduced sample size further restricted the information that could be gleaned from these data. However, this was one of the largest studies to examine these atypical deceleration characteristics in human electronic fetal heart monitoring tracings and remains so through the present time.
More recently, Hamilton et al8 examined the last 4 hours on electronic fetal heart monitoring patterns before birth after 37 weeks of gestation in 3,695 women. The authors compared electronic fetal heart monitoring patterns of women with normal neonates with two groups: those with metabolic acidosis but phenotypically normal and those with acidosis and evidence of encephalopathy using computer recognition software. The authors stated that as a result of the rare occurrence of the third group, cases were collected from other sources including other hospital series and medicolegal files. They reported loss of (moderate) variability within the deceleration, but none of the other atypical features, to be discriminatory between neonates with metabolic acidosis (defined by base excess) and those who were normal. However, the area under the receiver operator curve was only slightly better than chance (0.56), which others might argue is nondiscriminatory. The definition of acidemia used by these authors and the processes to acquire their sample identified a greater number of cases of acidemia, offering greater power compared with the present study. However, despite this, they similarly found a lack of discriminatory ability of all features in common with our study excess variability within the deceleration. The significant possibility of selection bias as well as the inability to adjust for relevant confounding factors known to be associated with acidemia resulting from the lack of clinical data makes the interpretation of these findings limited. In our unselected birth cohort, we were able to adjust for relevant confounding factors to best estimate the association between atypical deceleration features and acidemia.
A unique strength of this cohort study was the interpretation of the fetal heart rate tracing deceleration characteristics by to dedicated obstetric research nurses formally trained in electronic fetal heart monitoring interpretation who were blind to all clinical factors and outcome data, including arterial umbilical cord gas pH. Although some may argue that human interpretation can be unreliable, we would offer that these nurses underwent formal inter- and intraobserver reliability testing and ongoing retraining and further that human interpretation is how electronic fetal heart monitoring is used in everyday practice and thus offers generalizability. We were also able to use a composite marker of neonatal morbidity to exclude any neonates with short-term markers of at-risk neonates to enable the description of the frequency with which atypical decelerations occur in apparently normal term neonates. Lastly, we assigned a score to objectively estimate any evidence of dose–effect in the setting of multiple atypical decelerations and acidemia.
In contrast, there are some potential limitations that are important to consider with respect to our study. Choosing the 30 minutes before delivery may limit generalizability of our findings, specifically in the interpretation of atypical deceleration characteristics at other times during labor. However, we chose this time period because it is most proximal to the measurement of acidemia in modern practice (at birth). Although we chose atypical deceleration features that are most commonly referenced in historical texts and have been previously described, our study was certainly not exhaustive and there are many other possible features of electronic fetal heart monitoring patterns, and decelerations specifically, that might be associated with acidemia but have yet to be tested. Lastly, despite our large sample size, acidemia at term occurs rarely, and thus the lack of association found in our study could be the result of type II error. Although we had 80% power to detect a 2.1-fold increased risk of acidemia in the setting of atypical decelerations, which we would offer is a reasonable threshold for clinical significance, it is possible that associations exist of lesser magnitude that could not be detected among this term-born sample.
Despite these potential limitations, we feel that our findings contribute to the existing literature associating electronic fetal heart monitoring patterns with acidemia and birth outcomes. We found no evidence that “shoulders,” “slow returns,” or nonmoderate deceleration variability, alone or in combination, are associated with acidemia. It remains to be studied whether the persistence of these deceleration features for longer than 30 minutes before delivery might have an association with acidemia. However, given the high incidence of atypical features in apparently normal term-born neonates, it appears more likely that these are normal variants within the definitions used in this study. These data support the absence of these specific atypical deceleration characteristics from the recognized definitions of decelerations stipulated by the NICHD in 20085 given their lack of association with acidemia or neonatal depression.
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© 2012 by The American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. All rights reserved.
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