The cerebroplacental ratio: a new standard diagnostic tool at term gestation to assess fetal risk in labour?

SC Reale, MK Farber - The Lancet, 2024 - thelancet.com
The Lancet, 2024thelancet.com
The cerebroplacental ratio is a Doppler-derived fetal ultrasound metric that can reflect
alterations in cerebral blood flow due to fetal hypoxia and increased placental resistance. 1
The cerebroplacental ratio has emerged as a clinical risk assessment tool for placental
insufficiency at term gestation in both small for gestational age (SGA) and appropriate for
gestational age (AGA) birthweight groups. 2–5 A key clinical goal before labour onset is to
predict fetal intolerance to labour, intrapartum fetal compromise from hypoxia, emergency …
The cerebroplacental ratio is a Doppler-derived fetal ultrasound metric that can reflect alterations in cerebral blood flow due to fetal hypoxia and increased placental resistance. 1 The cerebroplacental ratio has emerged as a clinical risk assessment tool for placental insufficiency at term gestation in both small for gestational age (SGA) and appropriate for gestational age (AGA) birthweight groups. 2–5 A key clinical goal before labour onset is to predict fetal intolerance to labour, intrapartum fetal compromise from hypoxia, emergency caesarean delivery, and subsequent serious perinatal morbidity and mortality. Previous studies have associated low cerebroplacental ratios with higher rates of emergency caesarean delivery for fetal distress in labour in both AGA2 and SGA3, 4 fetuses, and higher rates of stillbirth and perinatal mortality. 5 In a trial evaluating cerebroplacental ratios among both SGA and AGA fetuses, a low cerebroplacental ratio was a better predictor of emergency operative delivery than low birthweight. 6 A randomised trial that screened for cerebroplacental ratio and placental growth factor with recommended planned delivery for abnormal screening versus standard care found no differences in intrapartum interventions or adverse neonatal outcomes. 7 However, the study was probably underpowered, and those who screened positive for a low cerebroplacental ratio had a higher likelihood of operative delivery for fetal distress, meconium, or fetal heart rate abnormalities. Given the promise of cerebroplacental ratios but inconclusive evidence for their clinical integration, a large randomised controlled trial evaluating cerebroplacental ratio screening for delivery decision making was needed. In The Lancet, Marta Rial-Crestelo and colleagues evaluated cerebroplacental ratio screening in conjunction with standard ultrasound growth assessment and its effect on perinatal mortality and severe neonatal morbidity. 8 This randomised controlled trial of 11 214 women with confirmed singleton pregnancies from nine hospitals in Spain, Israel, Poland, the Czech Republic, Chile, and Mexico randomly allocated those without known congenital malformations, infections, or other comorbidities requiring delivery before 37 weeks’ gestation in a 1: 1 ratio to a concealed (cerebroplacental ratio unavailable to clinical management) or revealed (cerebroplacental ratio available to clinical management) group. The majority of patients (78· 3%) in both groups were White, 18· 2% were Latin American, and 2· 1% were Asian. The mean gestational age at random allocation was 21 weeks and 6 days. Both groups received ultrasonography for fetal growth assessment and Doppler for cerebroplacental ratio at 36+ 0 to 37+ 6 weeks’ gestation. Clinicians managing the revealed group received cerebroplacental ratio values, with a recommendation of planned delivery after 37 weeks by induction of labour or elective caesarean delivery for cerebroplacental ratio values below the fifth centile. Clinicians managing the concealed group did not have access to cerebroplacental ratio values, and delivery planning was per standard of care. There was no difference between revealed and concealed cerebroplacental ratio groups for the primary outcome of perinatal mortality (odds ratio [OR] 1· 45 [95% CI 0· 76–2· 76]) or the secondary outcome of severe neurological morbidity (OR 0· 56 [0· 25–1· 24]). However, there was a reduction in the secondary outcome of severe non-neurological morbidity (0· 58 [0· 39–0· 87]), as well as a post-hoc analysis of overall severe morbidity (0· 58 [0· 40–0· 83]) in the revealed group. The number
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