Objective
The objective of this study was to estimate the predictive ability of electronic fetal monitoring (EFM) patterns immediately prior to delivery for acidemia at term birth.
Study Design
This was a 4-year retrospective cohort study of 5388 consecutive singleton, nonanomalous gestations of 37 weeks or longer. The primary exposure was the EFM pattern in the 30 minutes preceding delivery. EFM patterns were prospectively interpreted using Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) nomenclature as well as non-NICHD measurements of decelerations. The primary outcome was umbilical cord arterial pH of 7.10 or less.
Results
Four NICHD-defined EFM features within the 30 minutes prior to birth demonstrated the greatest association with acidemia: repetitive prolonged decelerations (area under the curve [AUC] 0.81), baseline tachycardia (AUC 0.80), repetitive variable decelerations (AUC 0.79), and repetitive late decelerations (0.78) after adjusting for nulliparity, fever, prolonged first stage, and obesity. A non-NICHD measure, total deceleration area, demonstrated superior predictive ability for acidemia (AUC 0.83, P = .04).
Conclusion
A non-NICHD measure of deceleration frequency and severity in the second stage performed superior to 4 NICHD EFM features for predicting fetal acidemia.
Intrapartum electronic fetal monitoring (EFM) is ubiquitous in obstetrics, despite the lack of evidence for improvement in birth outcomes and its substantial contribution to the rise in the national cesarean delivery rate. In a 2008 consensus conference, sponsored by the American College of Obstetricians and Gynecologists, the Society of Maternal Fetal Medicine, and the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), the leading experts in obstetrics and fetal monitoring reconvened to prioritize areas for research and to reevaluate the definitions that were set forth by a similar group 11 years before. The group acknowledged that virtually no evidence had emerged on EFM since the 1997 consensus conference, that the use of common nomenclature was paramount and specified a 3-category system. They again called for well-designed studies to fill the significant knowledge gaps that continue to exist. One of the areas of highest importance cited was observational studies focused on indeterminate EFM patterns.
For Editors’ Commentary, see Contents
Indeterminate fetal heart rate patterns, specified as category II tracings, are characterized most often by the presence of decelerations. The NICHD system describes 4 deceleration definitions. However, visual inspection reveals that several decelerations may meet a single NICHD definition but have different characteristics such as length, depth, and shape. These additional features, if they have meaning, are lost in the currently broad system. Furthermore, none of the 4 deceleration types (variable, early, late, prolonged) has been consistently associated with acidemia or birth outcomes. Although this may be due to the paucity of study, it more likely is due to the summary nature of the current NICHD nomenclature that specifies assignment into 1 of 4 deceleration types and may result in loss of information.
We hypothesized that non-NICHD measures of fetal heart rate decelerations, which account for properties such as depth, deceleration duration, and number immediately prior to delivery, would have a greater predictive ability for acidemia compared with the NICHD category system or nomenclature for decelerations. To test this hypothesis, we studied the 30 minutes of EFM patterns prior to delivery because it is the most proximal to the measurement of acidemia.
Materials and Methods
We conducted a 4-year, retrospective cohort study of all consecutive term births from the second stage of labor at a large tertiary care medical center. Women were identified for possible inclusion in the study by diagnosis and procedure codes for the delivery of a live-born infant during the study period and then confirmed for complete ascertainment by the labor and delivery log.
Women were included in the study if they delivered at or beyond 37 0/7 weeks’ gestation. Gestational age was determined by the last menstrual period (LMP) if known and concordant with ultrasound (within 7 days of first-trimester ultrasound or 14 days of second-trimester ultrasound) or by the earliest ultrasound when the LMP was unknown or discordant. Additional inclusion criteria included cephalic presentation, reaching the second stage, and no known fetal anomalies.
Women who underwent cesarean prior to labor or cesarean in the first stage of labor prior to complete dilation were excluded because infants delivered from the first stage of labor tend to have higher umbilical cord pH than those delivered from the second stage. Women were also excluded if they did not have at least 10 minutes of EFM tracing in the 30 minutes prior to delivery (insufficient EFM) and were excluded if an arterial umbilical cord gas (UCG) was not obtained. Finally, women carrying twins or higher-order multiple gestations were excluded.
The study was conducted with the approval of the institutional review board. Our institution utilizes a universal arterial umbilical cord gas acquisition policy and similarly uses universal continuous EFM during labor.
The primary outcome of the study was fetal acidemia, defined as an umbilical arterial cord gas of 7.10 or less. The primary exposure of the study was the EFM characteristics in the 30 minutes immediately prior to delivery, given the temporal proximity to the primary outcome measure. Each EFM tracing was prospectively extracted by 2 dedicated obstetric research nurses, formally trained and credentialed in the interpretation of EFM, blind to all clinical and outcome data. EFM tracings were extracted in 10 minute epochs as well as over the entire 30-minute period. Extraction was performed using the strict NICHD criteria for contractions and EFM patterns as well as extraction of deceleration-specific elements such as duration, depth, and number of decelerations, which allowed additional calculations to be made.
When considering the overall category assignment for the 30 minutes prior to delivery, category I and III were specified when they were the category throughout, and category II throughout or category II in combination with epochs of other categories yielded a category II assignment (to mimic what is done in practice). The depth and duration allowed the area within each deceleration to be calculated, which was approximated as half (width × depth) of the deceleration. A feature called total deceleration area was also calculated as the sum of the area within all decelerations in the final 30 minutes of EFM as a measure of both quantity and severity. All extraction was completed using a closed-ended tool. Blind reextraction by the second reader was performed at 500 patient intervals to allow assessment of interobserver reliability. A total of 270 (5.0% of tracings) were reabstracted.
Detailed maternal sociodemographics information, obstetric and medical history, antepartum course, and complications data were extracted from the electronic medical record. Additional data extracted included admission diagnoses and physical examination; tobacco, alcohol, and drug exposures; labor and delivery course including all cervical examinations; labor type; and mode of delivery; and medication exposures with doses and timing. Time from incision to delivery was extracted for women who delivered by cesarean. Fetal umbilical cord gas analysis was also extracted. Birth outcomes included maternal postpartum complications, neonatal Apgar scores, weight, and nursery disposition.
Women who delivered an infant with a pH of 7.10 or less (acidemia) were compared with those without acidemia (pH >7.10). Baseline characteristics were compared between groups using a Student t test or Mann-Whitney U for continuous variables as appropriate and a χ 2 test for categorical variables. Continuous variables were tested for normality visually and with the Kolmogorov-Smirnov test. Relative risks and 95% confidence intervals were calculated to estimate the association of individual EFM features with acidemia.
Individual features included categories and NICHD-defined baseline, variability, and deceleration characteristics as well as measures such as deceleration severity using the system described by Kubli et al, total number of decelerations overall, and total deceleration area. These non-NICHD features and calculations were compared between groups as continuous measures as well as dichotomously using the 95th percentile from the entire cohort to define abnormal. Deceleration types were considered dichotomously, both if they ever occurred and if they occurred repetitively (with ≥50% of contractions), as specified by the NICHD classification system. Stratified analyses were used to identify potentially confounding variables in the EFM feature–acidemia association.
Multivariable logistic regression was used to refine the estimate of risk for acidemia in the presence of each feature in the 30 minutes prior to delivery. Biologically plausible and historically known factors associated with acidemia were included in the initial models along with factors identified in the stratified analyses. Additionally, 6 a priori specified interaction terms of EFM characteristics were considered in the models. Backward, step-wise logistic regression was used to develop the final models. Covariates were retained in the model if they changed the effect size around the primary covariate by more than 10%. Labor type (induced vs augmented vs spontaneous), maternal race, and length of the second stage did not remain significant and thus were not included in the final models.
To estimate and compare the predictive ability for individual categories or factors for acidemia in the 30 minutes prior to delivery, sensitivity, specificity, positive predictive value (PPV), and negative predictive values were calculated. Receiver-operator curves were constructed from the final logistic regression models for the 5 EFM features with the highest magnitude of association with acidemia and were compared by area under the curve (AUC). The analyses were repeated for the association and predictive ability of categories and features in the 10 minutes prior to delivery. In addition, a planned subgroup analysis of women with infants with metabolic acidemia, which we defined as an arterial UCG of 7.10 or less and base excess less than –8.0, was performed.
Based on pilot data, we estimated the incidence of acidemia in the cohort to be 1.0% and the incidence of late decelerations in the nonacidemic group to be 10%. With an alpha error of 0.05, we estimated we needed 56 cases of acidemia to have 80% power to detect a 2-fold or greater association with any EFM feature and acidemia. The statistical analyses were performed using STATA, version 10, Special Edition (College Station, TX).
Results
Of 8622 consecutive delivery admissions, 5762 women with nonanomalous, term, vertex pregnancies delivered in the second stage. From these, 17 were excluded for no recorded EFM, 16 were excluded for lack of UCG, 338 were excluded for insufficient EFM, and 3 patients were excluded for concurrent incarceration, leaving 5388 patients included in the study. Arterial acidemia (pH of ≤7.10) occurred in 57 infants (1.1%) and 5331 (98.9%) had a pH greater than 7.10 ( Figure 1 ). Women who delivered infants with acidemia were more likely to be nulliparous and have regional anesthesia. They were also more likely to deliver by operative vaginal delivery or cesarean compared with women delivering nonacidemic infants. Women delivering acidemic infants tended to have higher rates of maternal fever and a history of a prior low-transverse cesarean, although these did not reach statistical significance ( Table 1 ).
| Characteristic | Acidemia (n = 57) | No acidemia (n = 5331) | P value |
|---|---|---|---|
| Maternal age, y a | 23 (20–28) | 23 (20–28) | .55 |
| Advanced maternal age | 15.5% | 7.0% | .30 |
| Gestational age at delivery, wks a | 39.0 (38.0–40.0) | 39.0 (38.0–40.0) | .77 |
| Maternal black race | 70.2% | 72.8% | .65 |
| Body mass index a | 32.1 (26.8–37.1) | 30.5 (26.9–35.0) | .30 |
| Preeclampsia | 5.3% | 6.5% | .70 |
| Gestational diabetes | 4.1% | 2.8% | .76 |
| Pregestational diabetes | 3.5% | 1.2% | .11 |
| Nulliparous | 57.9% | 36.8% | < .01 |
| Prior low transverse cesarean | 12.3% | 6.4% | .07 |
| Labor type | .42 | ||
| Spontaneous | 31.5% | 37.6% | |
| Augmented | 35.1% | 31.9% | |
| Induction | 33.3% | 30.5% | |
| Regional anesthesia | 94.7% | 83.7% | .02 |
| Prostaglandin | 15.8% | 12.9% | .52 |
| Foley bulb | 5.3% | 4.5% | .78 |
| Oxytocin | 64.9% | 58.8% | .35 |
| Birthweight, g a | 3210 (2995–3515) | 3250 (2960–3555) | .96 |
| Birthweight >4000 g | 5.3% | 5.4% | .94 |
| Birthweight <1800 g | 1.8% | 0.8% | .41 |
| Vaginal delivery | 47.4% | 86.1% | < .01 |
| Operative vaginal delivery | 36.8% | 12.4% | < .01 |
| Cesarean | 15.8% | 1.5% | < .01 |
| Maternal fever | 15.8% | 8.6% | .06 |
Of the 3 categories, none demonstrated statistically significant association with acidemia when considered in the last 10 minutes or in the last 30 minutes prior to delivery ( Table 2 ). Baseline, variability, and decelerations were individually considered. Compared with moderate variability, minimal variability was not associated with acidemia (adjusted odds ratio [aOR], 0.68; 95% confidence interval [CI], 0.27–1.70). Absent and marked variability occurred too infrequently to estimate association. Repetitive late decelerations (aOR, 2.07; 95% CI, 1.00–4.29), repetitive prolonged decelerations (aOR, 2.57; 95% CI, 1.19–5.53), and repetitive variable decelerations (aOR, 1.83; 95% CI, 1.09–3.10) were all significantly associated with acidemia after adjusting for fever, obesity, prolonged first stage, and nulliparity. Compared with a normal baseline, tachycardia was significantly associated with acidemia (aOR, 2.16; 95% CI, 1.22–3.83), but bradycardia occurred rarely in the nonacidemic group and not at all in those with acidemia, precluding risk estimation.
| Variable | pH ≤7.10 (n = 57) | pH >7.10 (n = 5331) | Unadjusted relative risk (95% CI) | Adjusted OR (95% CI) a | P value |
|---|---|---|---|---|---|
| Category I | 0.0% | 2.3% | Referent | — | — |
| Category II | 100.0% | 97.6% | — | — | — |
| Category III | 0.00% | 0.09% | — | — | — |
| Moderate variability | 91.2% | 87.2% | Referent | Referent | — |
| Minimal variability | 8.8% | 12.5% | 0.68 (0.27–1.69) | 0.68 (0.27–1.71) | .41 |
| Marked variability | 0.0% | 0.3% | — | — | — |
| Absent variability | 0.00% | 0.02% | — | — | — |
| Repetitive late decelerations b | 15.8% | 7.3% | 2.35 (1.16–4.76) | 2.06 (0.99–4.27) | .05 |
| Repetitive prolonged decelerations b | 14.0% | 5.2% | 2.90 (1.39–6.07) | 2.56 (1.19–5.52) | .02 |
| Repetitive variable decelerations b | 49.1% | 32.5% | 1.99 (1.19–3.33) | 1.91 (1.07–3.08) | .03 |
| Baseline tachycardia | 12.3% | 4.5% | 2.95 (1.35–6.44) | 2.15 (1.21–3.82) | < .01 |
| Baseline bradycardia | 0.0% | 0.2% | — | — | — |
a Adjusted for nulliparity, fever, prolonged first stage, and obesity;
b Repetitive: occurring with 50% or greater of contractions.
Infants with acidemia at birth had a greater number of decelerations in the final 30 minutes compared with those without acidemia (9 vs 6, P < .01) as well as a greater number of severe decelerations (nadir of ≤60 beats/min), and a greater total deceleration area ( Table 3 ). After adjusting for fever, obesity, prolonged first stage, and nulliparity, only abnormal total deceleration area (greater than the 95th percentile) was significantly associated with an increased risk for acidemia (aOR, 3.79; 95% CI, 2.04–7.04). When the association of NICHD and non-NICHD characteristics with metabolic acidemia was tested, a similar pattern was seen ( Table 4 ).
| Variable | pH ≤7.10 (n = 57) (1.1%) | pH >7.10 (n = 5331) (98.9%) | Unadjusted relative risk (95% CI) | Adjusted OR (95% CI) a | P value |
|---|---|---|---|---|---|
| Number of decelerations, median (range) [IQR] | 9 (1–17) [6–12] | 6 (0–22) [3–9] | — | — | < .01 |
| Greater than 95th percentile b | 9 (15.8) | 427 (8.0) | 2.12 (1.05–4.31) | 1.74 (0.84–3.61) | .13 |
| Number of severe decelerations, median (range) [IQR] | 1 (0–8) [0–2] | 0 (0–12) [0–1] | — | — | < .01 |
| Greater than 95th percentile b | 5 (8.8) | 308 (5.8) | 1.56 (0.63–3.88) | 1.61 (0.64–4.06) | .32 |
| Total deceleration area, median (range) [IQR] | 21116.0 (650.0–54502.0) [6780.5–36972.5] | 8940.0 (147.0–71881.5) [3855.0–16709.5] | — | — | < .01 |
| Greater than 95th percentile b | 18 (41.9) | 558 (13.4) | 4.52 (2.48–8.24) | 3.79 (2.04–7.04) | < .01 |
a Adjusted for nulliparity, fever, prolonged first stage, and obesity;
b Greater than 95th percentile of number of decelerations, number of severe decelerations, or total deceleration area in cohort.
| Variable | Metabolic acidemia (n = 50) a | Adjusted OR (95% CI) |
|---|---|---|
| Moderate variability | 21 | 0.72 (0.42–1.22) |
| Category III | 0 | — |
| Minimal variability | 3 | 0.68 (0.27–1.71) |
| Prolonged decelerations | 7 | 3.02 (1.64–5.55) |
| Tachycardia | 10 | 2.99 (1.55–5.77) |
| Recurrent late decelerations | 8 | 2.46 (1.10–4.29) |
| Total deceleration area greater than 95th percentile | 15 | 3.79 (2.04–7.04) |
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