1. Introduction
Maternal anemia is frequently associated with premature delivery,
reduced neonatal weight, infant iron deficiency [1–4], neonatal death,
and low Apgar scores at 1 min [5]. It is also suspected to reduce the
oxygen supply to the growing fetus, leading to the redistribution of
fetal blood flow [6]. In the presence of fetal hypoxemia, fetal blood
flow becomes centrally distributed to preserve cerebral oxygenation,
known as the brain-sparing reflex; this plays a major role in fetal
adaptations to oxygen deprivation.Maternal anemia is a hypoxic condition
that could be responsible for the redistribution of fetal blood flow;
however, no evidence of placental insufficiency has been documented
currently [6]. The combination of increased placental resistance and decreased
cerebral resistance, measured using Doppler ultrasonography,
is quantified by calculating the cerebral-to-umbilical artery resistance
ratio [7]. This Doppler parameter is not influenced by the duration of a
pregnancy and is always greater than 1.1 during normal pregnancy
[8,9]. However, this ratio is decreased in the presence of hypoxia due
to increased placental resistance and cerebral vasodilatation [8,9] and
correlates closely with fetal growth, hypoxia, and behavior, particularly