Short-Term Effects of Betamethasone Administration on Fetal Heart Rate Patterns in Preterm Contraction

Abstract

Background:

Preterm labor is a leading cause of neonatal morbidity and mortality worldwide. Antenatal corticosteroid therapy, particularly betamethasone, is widely used to improve neonatal outcomes.

Aim:

To evaluate the short-term effects of maternal betamethasone administration on fetal heart rate variability using nonstress test (NST) tracings in preterm labor.

Methods:

A prospective study was conducted on 62 pregnant women with preterm contractions between 28–34 weeks of gestation admitted to St. John’s Medical College Hospital. Participants received two intramuscular doses of betamethasone (12 mg each, 12 hours apart). Serial cardiotocography recordings were performed at baseline and at 12, 24, 36, 48, 60, 72, and 84 hours after administration. NST parameters assessed included baseline FHR, beat-to-beat variability, accelerations, and decelerations. Data were analyzed using ANOVA and paired proportion tests, with significance set at P < 0.05.

Results:

Betamethasone administration was associated with a transient reduction in baseline FHR and beat-to-beat variability, most pronounced at 24–36 hours postadministration, with subsequent normalization by 72 hours (P < 0.0001). Accelerations also decreased initially but recovered over time, while decelerations remained absent across all recordings.

Conclusion:

Maternal betamethasone causes temporary, reversible alterations in fetal heart rate variability and accelerations without adverse perinatal outcomes.

INTRODUCTION

Preterm labor, defined by the WHO as the onset of labor before 37 weeks of gestation but after 20 weeks, is a major contributor to neonatal morbidity and mortality. It is further classified into early (<34 weeks) and late (34–36 weeks) preterm contractions.[1] Globally, 9.6% of all births are preterm, with India accounting for the highest number—about 3.5 million annually. Although early preterm births constitute only 1–2% of live births, they contribute to nearly 60% of perinatal deaths and most neurological morbidity.[1]

Prevention of preterm labor remains difficult, as more than 40% of women who deliver prematurely have no identifiable risk factors.[2] Preterm delivery is responsible for three-fourths of neonatal deaths unrelated to congenital anomalies[3] and is linked to conditions such as respiratory distress syndrome, intraventricular hemorrhage, necrotizing enterocolitis, and long-term neurodevelopmental impairment.[4,5]

The introduction of corticosteroid therapy in 1972 marked a breakthrough in reducing complications of prematurity.[6] Subsequent systematic reviews confirmed their significant benefit in decreasing neonatal morbidity and mortality.[7,8] A meta-analysis further supported reductions in neonatal death, RDS, IVH, and NEC with antenatal corticosteroid use.[9] However, side effects, though usually minor, must be considered.[10]

Studies on the short-term effects of betamethasone on fetal heart rate (FHR) patterns have shown conflicting results—ranging from transient cessation of fetal movements and nonreactive tracings[11,12] to altered heart rate variability.[13,14,15,16]

Aim of the study

The aim was to study the short-term effects of maternal betamethasone administration on the fetal heart rate variability using Fetal Heart Rate trace from nonstress test (NST) in preterm labor.

METHODOLOGY

This prospective study was conducted on 62 pregnant women with preterm contractions between 28–34 weeks of gestation, admitted as inpatients to the labor room of St. John’s Medical College Hospital over a period of 18 months (October 2014–March 2016).

Selection criteria

The inclusion criteria consisted of primigravida singleton pregnancies between 28–34 weeks of gestation presenting with preterm contractions who were clinically stable. Exclusion criteria included women who had already received betamethasone in the current pregnancy, those with multiple pregnancy, pregnancy complications or fetal anomalies.

Data collection

Eligible patients were recruited after informed consent and assigned a unique code. Routine laboratory investigations including blood tests and urine culture were performed. A baseline non-stress test (NST) was done using the Sonicaid^® 8000 system to assess fetal well-being.

Intervention

All patients received two intramuscular doses of betamethasone, 12 mg each, administered 12 hours apart as per hospital protocol. Cardiotocography (CTG) recordings were performed for 20 minutes at baseline and subsequently at 12, 24, 36, 48, 60, 72, and 84 hours after betamethasone administration. In cases where CTG showed nonreassuring features, it was repeated after one hour, and if abnormalities persisted, a biophysical profile (BPP) was carried out. Pregnancies with a BPP score less than 6 were terminated, while those with normal BPP were monitored further.

Statistical analysis

Data analysis was performed using ANOVA and paired proportion tests, with significance set at P < 0.05. Statistical analysis was carried out using SPSS software, while graphs and tables were prepared using Microsoft Word and Excel.

RESULT

The study included 62 antenatal women aged 18–37 years (mean age: 24.92 ± 4.24 years), with most in the 21–25-year age group. The mean gestational age was 31.5 weeks (range: 28–34 weeks). All participants received two intramuscular doses of betamethasone (12 mg each) 12 hours apart. Preterm contractions were the most common presentation (67%), followed by urinary complaints (19%) and vaginal discharge (12%) [Tables 1 and 2].

Table 1.

Comparison of NST recording between baseline, 12 hours, 24 hours, 36 hours, 48 hours, 60 hours, 72 hours and 84 hours following betamethasone administration (n=62)

Characteristics	Baseline FHR (bpm)	Beat to beat variability (bpm)	No. of accelerations	No. of decelerations
NST1 Pretreatment	159.16 (140–180)	5.19 (2–8)	2.63 (1–4)	0
NST2 12 hrs	160.50 (144–180)	4.55 (2–8)	2.53 (0–4)	1.72
NST3 24 hrs	160.09 (152–180)	3.25 (2–5)	2.26 (1–4)	0
NST4 36 hrs	146.28 (140–154)	3.39 (2–5)	2.96 (1–5)	0
NST5 48 hrs	157.12 (144–170)	3.37 (2–5)	2.37 (1–4)	0
NST6 60 hrs	158.56 (146–176)	5.16 (1–9)	2.77 (0–5)	0
NST7 72 hrs	153.14 (155–170)	5.96 (3–9)	2.91 (1–5)	0
NST8 84 hrs	152.20 (160–175)	6.13 (4–8)	2.73 (1–4)	0
P	0.0001	0.0001	0.0001	–

Table 2.

Comparison of NST recording over 8 NSTS following betamethasone administration – >34 weeks

Characteristics	Recording period	Baseline FHR (bpm)	Beat-to-beat variability (bpm)	No. of accelerations	No. of decelerations
NST1 Pretreatment	20 mts	159.38 (150–180)	5.1 (2–8)	2.69 (1–4)	0
NST2 12 hrs	20 mts	160.92 (154–180)	4.6 (2–8)	2.62 (1–4)	0
NST3 24 hrs	20 mts	159.83 (152–180)	3.2 (2–5)	2.31 (1–4)	0
NST4 36 hrs	20 mts	146.31 (140–154)	3.3 (2–5)	3.02 (1–5)	0
NST5 48 hrs	20 mts	157.29 (144–170)	3.3 (2–5)	2.38 (1–4)	0
NST6 60 hrs	20 mts	158.77 (146–176)	5.2 (3–9)	2.83 (1–5)	0
NST7 72 hrs	20 mts	152.52 (158–170)	5.8 (3–8)	2.96 (1–5)	0
NST8 84 hrs	20 mts	151.56 (150–175)	6.1 (4–8)	2.75 (1–4)	0
P	–	0.0001	0.0001	0.0001	–

DISCUSSION

The American College of Obstetricians and Gynecologists (ACOG) and the NIH consensus have confirmed that short-term antenatal corticosteroid therapy is highly effective in reducing neonatal morbidity, especially respiratory distress syndrome (RDS), and does not impair neonatal adrenal function.[17] Consequently, corticosteroids have become a cornerstone of preterm labor management.

In this study, 62 low-risk antenatal women were included, reducing confounding from maternal or fetal comorbidities. Betamethasone administration resulted in a transient reduction in fetal heart rate (FHR) variability and baseline FHR, particularly between 24–36 hours, with normalization by 72 hours (P < 0.0001). These changes likely reflect a pharmacological effect of corticosteroids. Similar transient suppression of FHR has been reported in studies by Magee, Mulder, and Dukes,[18] reinforcing the interpretation that such findings should not be mistaken for fetal hypoxemia.

Additional supportive evidence comes from several clinical studies. Rotmensch et al.[19] demonstrated that betamethasone causes a profound but transient suppression of FHR parameters, sometimes mimicking fetal distress. Subtil et al.[13] compared different corticosteroid formulations and found significant reductions in FHR variability with betamethasone but not with dexamethasone, a result consistent with the present findings. Mulder et al.[20] also documented a considerable but temporary reduction in fetal activity and FHR variation, which could otherwise be misinterpreted as deterioration of fetal condition. Similarly, Shamsi et al.[21] reported that while fetal movements decreased transiently after corticosteroid administration, other indices such as BPP and AFI remained unchanged.

Collectively, these studies underscore that the observed FHR changes postbetamethasone are transient, reversible, and pharmacological in origin rather than indicative of true fetal compromise.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.