DeVore raises the prospect of an important role for cerebroplacental ratio in fetal surveillance. This Doppler parameter was introduced more than 20 years ago and has once again come to prominence. It has been thought to reflect fetal adaptation to progressive placental chronic hypoxia more sensitively than the umbilical artery and middle cerebral artery pulsatility indices on their own by showing earlier changes and unveiling hitherto unrecognized fetal compromise. Further, as summarized by DeVore, a role for the cerebroplacental ratio in the management of fetuses with late-onset small for gestational age (SGA) has been suggested where both umbilical Doppler and cardiotocography are not reliable in predicting an adverse perinatal event and may predict an increased chance of perinatal events also in apparently normal-sized fetuses. This may suggest an adaptive response to subclinical placental insufficiency and a reduced tolerance of such a fetus to labor hypoxia or to prolongation of gestation.

Active adjustment of fetal circulation leading to increased fetoplacental and reduced cerebral impedanced and not impedanced by a decrease in the cerebroplacental ratio may be considered a brain-protective mechanism. Some data have, however, suggested a worse neurological outcome in small fetuses delivered after a cerebral vasodilatation, particularly in the frontal cortex. On this basis, a rationale for introducing the cerebroplacental ratio in the routine surveillance of fetuses with late-onset SGA and of considering an elective delivery has been proposed by some.

But we still do not know if and for how long in a small fetus a reduced cerebroplacental ratio indicates a phase of adaptation of the brain circulation that would allow a full clinical recovery once delivered. Nor is it clear whether an abnormal cerebroplacental ratio is the first sign of fetal decompensation that would invariably lead to cerebral injury independent of the time of delivery. So we cannot presently, on the available evidence, conclude as to whether a reduced cerebroplacental ratio is an alert bell or alternatively a crash sound. Surely it is only when the answer to these questions is known that we can implement its use in the clinical management of late SGA or normal-sized fetuses near term. Moreover, earlier delivery of small fetuses <39 weeks must be robustly justified as such a policy would invariably lead to an increased burden of cesarean delivery and neonatal respiratory morbidity.

In a similar way, abnormal ductus venosus Doppler in early fetal growth restriction had been suggested to confer an especially poor perinatal outcome from retrospective studies but a recent prospective randomized study has shown the converse. We should treat retrospective and observational data with caution: it is hypothesis forming and does not constitute evidence on which to change clinical practice. It is with this rationale in mind that the TRUFFLE Group is planning a multicenter randomized controlled trial with the aim of assessing the clinical benefit of incorporating the cerebroplacental ratio in the clinical management of those fetuses recognized as small >32 weeks of gestation.