OBJECTIVE: To correlate the presence of baseline variability and the duration of a prolonged deceleration/bradycardia in intrapartum fetal heart rate (FHR) tracings with the development of neonatal acidemia.
METHODS: We identified 186 patients with term gestations who had continuous electronic fetal monitoring for at least 2 hours before delivery, with an identified bradycardia during that period. Each patient had umbilical artery cord analysis done and delivery within 30 minutes of that bradycardia. One investigator blinded to the cord gas outcome reviewed the last 2 hours of the tracing using the National Institute of Child Health and Human Development guidelines for FHR monitoring. We assessed the presence or absence of variability before the bradycardia and recovery or no recovery of the bradycardia and placed the patients into four groups. Group 1 (128 patients) with normal variability and recovery, group 2 (40 patients) with normal variability and no recovery, group 3 (nine patients) with decreased variability and recovery, and group 4 (nine patients) with decreased variability and no recovery. We compared the incidence of neonatal acidosis defined as a pH of less than 7.0 at birth among the four groups. The relationship between the various groups was assessed using analysis of variance and the χ2 test. In addition, a multiple logistic regression model was developed with the parameters of amplitude and recovery used to predict pH at birth.
RESULTS: The presence of decreased variability and no recovery of the FHR of a bradycardia was associated with the lowest pH 6.83 ± 0.16 and a 78% incidence of significant acidosis. Decreased variability before FHR bradycardia was the FHR parameter significantly correlated with low pH.
CONCLUSION: The most significant factor predicting the development of pathologic neonatal acidemia and indicating the need for urgent delivery in the presence of a bradycardia is decreased variability before the bradycardia.
The most significant factor predicting the development of pathologic neonatal acidemia in the presence of a bradycardia is decreased variability before the bradycardia.
Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut.
Address reprint requests to: Keith P. Williams, Yale University School of Medicine, Department of Obstetrics and Gynecology, 333 Cedar Street/PO Box 208063, New Haven, CT 06520–8063; E‐mail: firstname.lastname@example.org.
The authors thank Vesna Popovsua for her review of the fetal heart rate tracings.
Received February 19, 2002. Received in revised form May 1, 2002. Accepted May 30, 2002.
Intrapartum electronic fetal heart rate (FHR) monitoring gained worldwide acceptance in the 1970s as an objective mechanism to assess FHR patterns and thereby predict the development of neonatal asphyxia/acidosis.1–5 The development of acidosis with a pH of less than 7 is thought to be associated with an increased incidence of the significantly poor outcome of fetal death or early neurologic injury.6–9 The predictive capability of FHR patterns are difficult to quantify because of different methods used for their interpretation and different duration of time used for assessment of different monitoring parameters.
One FHR parameter assessed is a bradycardia (a prolonged deceleration), which leads to immediate operative delivery, yet many of these infants are delivered with normal Apgar scores and no evidence of acidosis. Previous reports in the literature have, therefore, tried to identify which parameters associated with a bradycardia carry a poor prognostic outcome.10–18 Factors including the role of abnormal baseline variability before the bradycardia recovery or nonrecovery of the bradycardia in predicting the development of acidosis have not been appropriately assessed. Our study aim, therefore, was to identify preexisting baseline variability changes in FHR patterns before a significant prolonged deceleration and determine the influence of these changes and recovery/ nonrecovery of the intrapartum FHR on the development of significant fetal acidosis.
MATERIALS AND METHODS
This is a retrospective analysis performed at BC Women's Hospital (Vancouver, British Columbia, Canada) between January 1997 and January 2000. Antenatal records were reviewed for patients who fit the following inclusion criteria: 1) term pregnancies greater than or equal to 37 completed weeks' gestation; 2) an identified prolonged deceleration/bradycardia for greater than 2 minutes with a fall to less than 100 beats per minute; 3) delivery of the neonate within 30 minutes of the bradycardia; 4) continuous electronic FHR monitoring for 2 hours before delivery; and 5) umbilical artery and cord blood gases done at the delivery. Patients who fit these inclusion criteria had their medical and monitoring records abstracted from the health records department. At this institution, cord gases are done at birth mostly in the presence of abnormalities in the intrapartum FHR pattern. Although 2 hours of tracing before delivery were available to be reviewed, only the last hour was used for interpretation. The last hour of all electronic intrapartum fetal monitoring records were identified and reviewed by a research associate (VP) blinded to all aspects of the fetal outcomes. The fetal monitoring tracings were assessed according to the criteria of the National Institute of Child Health and Human Development18 workshop. We defined decreased baseline variability as amplitude of less than or equal to 5 beats per minute. One investigator, KPW, randomly reviewed 25 FHR tracings without knowledge of the neonatal outcome. The interoperator agreement in the evaluation of each of the 25 FHR tracings was done by comparison between two investigators and showed a good correlation with a κ score of 0.85. The National Institute of Child Health and Human Development18 guidelines were used to define a prolonged deceleration/bradycardia.
Important to our study were the following definitions from the National Institute of Child Health and Human Development guidelines. Baseline FHR variability is deemed as fluctuations in the baseline FHR of two cycles per minute or greater and is visually quantitated as the amplitude of the peak to trough in beats per minute as follows: Amplitude range undetectable, absent FHR variability, amplitude range greater than undetectable but less than or equal to 5 beats per minute is minimal FHR variability, amplitude range 6–25 beats per minute is moderate FHR variability, and amplitude range greater than 25 beats per minute is marked FHR variability.
A prolonged deceleration of the FHR is a visually apparent decrease in FHR below the baseline. The decrease is calculated from the most recently determined portion of the baseline. The decrease from the baseline is greater than or equal to 15 beats per minute lasting 2 minutes or more but less than 10 minutes from onset to return to baseline.
In all, 186 patients with a bradycardia were identified and placed into one of four groups depending on the presence or absence of normal variability for the entire duration of the last hour before the bradycardia and recovery or nonrecovery of the bradycardia after a duration of 10 minutes. Patients were placed into four groups: group 1 with normal baseline variability and recovery of the bradycardia before 10 minutes; group 2 with normal baseline variability with no recovery of the bradycardia within 10 minutes; group 3 with decreased baseline variability and recovery of the bradycardia before 10 minutes; and group 4 with decreased baseline variability and no recovery of the bradycardia within 10 minutes. The relationship between the umbilical artery cord gas parameters of pH and base deficit was analyzed. We used two cutoffs derived from the literature to define an abnormal pH, a pH of less than 7.0, and a pH of less than or equal to 7.1. Two cutoffs were used to define an abnormal base deficit, a base deficit greater than −16, and a base deficit greater than −12.
Differences between the groups for the continuous variables were analyzed using analysis of variance with the Bonferroni correction with pairwise comparison used to identify significant differences. A significance level of P ≤ .05 was set. For categoric data, analysis was done by χ2 analysis. A multiple logistic regression model was developed with the parameters of amplitude and recovery used to predict pH at birth.
A total of 186 patients were included into the study. The majority of the patients in the study (71%) showed normal baseline variability and recovery of the bradycardia (Table 1). The two factors of decreased variability and nonrecovery of the FHR tracing resulted in a significant increase in the incidence of pathologic acidosis (2% versus 78%, P < .001). The presence of decreased variability before a bradycardia, irrespective of whether the bradycardia recovered or not, was associated with a minimum 44% incidence of pathologic fetal acidosis. The period of baseline variability available for analysis in the hour before the prolonged deceleration varied from 30 to 50 minutes. Using the multiple logistic regression model, a low pH was predicted only by decreased amplitude (odds ratio 1.28, 95% confidence interval 1.15, 1.40).
FHR parameters are used to predict the development of neonatal acidosis, which is a marker for the occurrence of hypoxic ischemia encephalopathy and long‐term neurologic dysfunction. Several authors have identified the FHR parameter of fetal bradycardia occurring before delivery to predict a poor outcome.10,11,14 However, a fetal bradycardia before delivery does not uniformly predict a poor outcome, and so several other factors related to the bradycardia have been investigated to improve the predictive capability.
Gilstrap et al10 identified a group of infants and assessed baseline variability for 10 minutes before delivery. He identified that the lack of FHR baseline variability before delivery was associated with a 1.5‐ to three‐fold increase in the incidence of acidosis in patients with a concomitant FHR bradycardia. Our study differs from theirs as we used up to 1 hour of FHR monitoring before delivery to assess variability, and they used a pH of less than or equal to 7.20 to define acidosis. Their duration of absent variability, however, was only 10 minutes or less. Piquard et al11 measured blood gases before and after the final stage of labor in an attempt to identify a predictive FHR pattern. They identified a FHR pattern, which they called type 2b, representing decreased baseline under 90 beats per minute with frequent decreased variability with one of the largest shifts in pH, but they did not assess the prebradycardia FHR pattern. Low et al12 identified the FHR variables of absent or minimal baseline variability and late or prolonged decelerations to identify significant acidosis with estimated positive predictive values from 18% to 26%. We used a longer period of assessment of FHR before the bradycardia.
Gull et al14 reviewed 27 cases of end‐stage bradycardia and identified the variables of loss of FHR variability during the bradycardia for 4 minutes or more or loss of variability after 3 minutes from the beginning of the bradycardia as predisposing to increasing degrees of acidosis. The length and depth of the bradycardia and their product had a weaker correlation. Their study did not provide any information on the FHR parameters before the end‐stage bradycardia. Krebs et al13 stressed the importance of the duration of the bradycardia (less than 15 minutes) as a good prognostic sign, but all the acidotic fetuses in the study were born when the bradycardia lasted less than 15 minutes.
Sheiner et al19 identified that a fetal bradycardia less than 70 beats per minute had an odds ratio of 3 (95% confidence interval 1.02, 8.6) to be associated with an abnormal pH. No information on the recovery of the FHR pattern before the bradycardia was given. Our study identifies that before a prolonged deceleration, evaluation of the baseline FHR pattern is the most important component to determine the degree of acidosis at birth.
Immediate intervention in every patient with a fetal bradycardia would lead to increased operative delivery rate with the delivery of a large number of uncompromised infants and a resulting increase in maternal trauma. Our study indicates that nonrecovery is weakly correlated with a low pH, and the most significant factor indicating the need for urgent operative delivery with a fetal bradycardia is decreased variability for up to 1 hour before the bradycardia. Urgent delivery should be considered in any clinical scenario in which the FHR shows evidence of a bradycardia with prior decreased variability.
1. Edington PT, Sibanda J, Beard RW. Influence on clinical practice of routine intrapartum fetal monitoring. Br Med J 1975;3:341–3.
2. Johnstone FD, Campbell DM, Hughes GJ. Antenatal care: Has continuous intrapartum monitoring made any impact on fetal outcome? Lancet 1978;1(8077)1298–300.
3. Koh KS, Creves D, Yung S, et al. Experience with fetal monitoring in a university teaching hospital. Can Med Assoc J 1975;112:455–6.
4. Shenker L, Post RC, Seiler JS. Routine electronic monitoring of fetal heart and uterine activity during labor. Obstet Gynecol 1975;46:185–9.
5. Weinraub Z, Casp E, Brook I, Rahmani P, Bukovsky I, Schreyer P. Perinatal outcome in monitored and unmonitored high-risk deliveries. Isr Med Sci 1978;14:249–55.
6. Goldaber KGD, Gilstrap LG, Leveno KJ, Dax JS, McIntire DD. Pathologic fetal acidemia. Obstet Gynecol 1991;78:1103–7.
7. Nagel HTC, Vandenbussche FPHA, Oepkes D, Jennekens-Schinkel A, Kaan LAEM, Bennebroek Gravenhorst J. Follow-up of children with an umbilical arterial blood pH of < 7.0. Am J Obstet Gynecol 1995;173:1758–64.
8. Goodwin TM, Belai I, Hernandez P, Durand M, Paul RH. Asphyxial complications in the term newborn with severe umbilical acidemia. Am J Obstet Gynecol 1992;162:1506–12.
9. Gilstrap LG, Leveno KJ, Burris J, Williams ML, Little BL. Diagnosis of birth asphyxia on the basis of fetal pH, Apgar score, and newborn cerebral dysfunction. Am J Obstet Gynecol 1989;161:825–30.
10. Gilstrap LC, Hauth JC, Toussaint S. Second stage fetal heart rate abnormalities and neonatal acidosis. Obstet Gynecol 1984;63:209–13.
11. Piquard F, Hsiung R, Mettauer M, Schaefer A, Haberey P, Dellenbach P. The validity of fetal heart rate monitoring during the second stage of labor. Obstet Gynecol 1988;72:741–50.
12. Low JA, Victory R, Derrick E. Predictive value of electronic fetal monitoring for intrapartum fetal asphyxia with metabolic acidosis. Obstet Gynecol 1999;93:285–91.
13. Krebs HB, Petres RE, Dunn LJ. Intrapartum fetal heart rate monitoring V. Fetal heart rate patterns in the second stage of labor. Am J Obstet Gynecol 1981;140:435–9.
14. Gull I, Jaffa A, Oren M, Grisarn D, Ruben Peyser M, Lessing JB. Acid accumulation during end-stage bradycardia in term fetuses: How long is too long? Br J Obstet Gynaecol 1996;103:1096–101.
15. Boehm F. Prolonged end stage fetal heart rate deceleration. Obstet Gynecol 1975;45:579–82.
16. Katz M, Shani N, Meizner I, Insler V. Is end-stage deceleration of the fetal heart ominous? Br J Obstet Gynaecol 1982;89:186–9.
17. Gilstrap CG, Hauth JC, Hankins GDV, Beck AW. Second-stage fetal heart rate abnormalities and type of neonatal acidemia. Obstet Gynecol 1987;70:191–5.
18. National Institute of Child Health and Human Development Research Planning Workshop. Electronic fetal heart rate monitoring: Research guidelines for interpretation. Am J Obstet Gynecol 1997;177:1385–90.
19. Sheiner E, Hadar A, Hallak M, Katz M, Mazor M, Shoham-Yardi I. Clinical significance of fetal heart rate tracings during the second stage of labor. Obstet Gynecol 2001;97:747–52.