Marked variability associated with twofold increased risk of neonatal acidosis: BJOG
Intrapartum electronic fetal monitoring has become a standard of care in the assessment of fetal well-being during labour. Despite extensive research on fetal heart rate (FHR) analysis, its interpretation is subject to low specificity and high interobserver variability and its effectiveness in reducing perinatal mortality and cerebral palsy remainscontroversial. Therefore, it seems necessary to reach a more evidence-based approach to FHR interpretation to optimise its performance.
Fetal heart rate (FHR) variability is a pattern of major importance in FHR analysis. Normal FHR variability generally ensures a normal fetal acid–base status. Reduced variability can reflect decreased autonomic activity, in situations such as fetal acidosis or the administration of some maternal medications. Fetal heart rate (FHR) variability is mainly determined by the autonomous nervous system and marked variability could reflect fetal autonomic instability resulting from impaired fetal oxygenation. A recent review stated that marked variability can indicate fetal compromise and highlighted the need for further research on this pattern.Aim of study by Loussert L et al was to assess the association between marked variability in FHR patterns during labour and neonatal acidosis.
This bicentric prospective cohort study was conducted from 1 January 2019 to 31 December 2019 in two French tertiary care maternity units (Toulouse and Poissy). Study included women in labour at ≥37weeks of gestation, with continuous FHR monitoring until delivery. Women with intrauterine fetal death or medical termination, multiple pregnancies or non-cephalic presentation were excluded.
The exposure was marked variability in FHR in the 60minutes before delivery, defined as a variability greater than 25 beats per minute, with a minimum duration of 1 minute. To assess the association between marked variability and neonatal acidosis, authors used multivariable modified Poisson regression modelling. They then conducted subgroup analyses according to the US National Institute of Child Health and Human Development (NICHD) category of the associated fetal heart rate.
The primary outcome was neonatal acidosis, defined as an umbilical artery pH of ≤7.10, obtained after delivery from a clamped segment of the umbilical cord. Secondary outcomes were severe acidosis, Apgar score of <7 at 5minutes, respiratory distress, neonatal intensive care unit admission, neonatal infection and neonatal death.
Among the 4394 women included, 177 (4%) had marked variability in fetal heart rate in the 60minutes before delivery. Acidosis occurred in 6.0% (265/4394) of the neonates. In the multivariable analysis, marked variability was significantly associated with neonatal acidosis (aRR 2.30). In subgroup analyses, the association between marked variability and neonatal acidosis remained significant in NICHD category-I and category-II groups.
In this prospective cohort study, marked variability in FHR patterns occurred in 4% of the neonates in the hour before birth. Neonates with a prenatal marked variability had a twofold increased risk of acidosis. In category-I FHR tracings, marked variability was associated with a fivefold increased risk of neonatal acidosis. However, the absolute risk remained low in this subgroup, with only 6.5% of neonates with marked variability developing neonatal acidosis. In category-II FHR tracings, neonates with marked variability had a twofold increased risk of neonatal acidosis and the absolute risk was high: 18.5% of neonates with marked variability developed neonatal acidosis. The risk of neonatal acidaemia was high for neonates with category-III FHR tracings, at nearly 20%, and marked variability did not significantly increase this risk.
Authors found that marked variability was associated with an increased risk of neonatal acidosis. Therefore, this pattern should be considered in FHR interpretation to optimise intrapartum fetal surveillance.
