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202 L. Detti et al.
Cerebral±Placental Ratio
It has been reported that the internal carotid/umbilical
artery PI ratio has a sensitivity of 70% in identifying
growth-restricted fetuses, as opposed to a 60% sensitivity
for the internal carotid artery and 48% for the
umbilical artery alone [26]. Others have selected the
middle cerebral artery/umbilical artery ratio and have
reported that in AGA fetuses this ratio remains constant
following 30 weeks' gestation. In AGA fetuses
the ratio is equal to 1 [27]. A ratio above 1 is considered
pathological. The Cerebral±Placental ratio has also
been reported to be a good predictor of neonatal outcome,
and could be used to identify fetuses at risk of
morbidity and mortality [28, 29]. Another study has
reported that in fetuses with suspected IUGR, abnormal
Cerebral±Placental ratio is strongly associated with
low gestational age at delivery, low birth weight, and
low umbilical artery pH. Abnormal Cerebral±Placental
ratio is also significantly associated with a shorter interval
to delivery and the need for emergent delivery
[30]. A question that arises is: Does the Cerebral±Placental
ratio make any difference when compared with
the umbilical artery? The answer is that the ratio is useful
on those conditions characterized by a borderline
umbilical artery. If there is absent/reversed flow of
the umbilical artery, the ratio is not helpful.
What to Do in Presence
of an Abnormal Cerebral±Placental Ratio?
The management of a pregnancy in the presence of
an abnormal cerebral±placental ratio depends on the
gestational age. Prior to 34 weeks, steroids and close
monitoring with non-stress test (NST) and biophysical
profile (BPP) twice a week, and assessment of fetal
growth every 2 weeks, is a good management option.
Following 34 weeks' gestation the cerebral±placental
ratio does not appear very helpful and, therefore, a
clinical decision based on the results of the cerebral±
placental ratio is not recommended [28]; however,
others have reported that cerebral±placental ratio
continues to be useful [31, 32]; therefore, this requires
further investigations.
Finally, maternal hyperoxygenation could improve
fetal hemodynamics in IUGR fetuses [33].
Prediction of Fetal Hematocrit
Fetal hemoglobin increases with advancing gestation
(Table 14.1) [34]. Fetal anemia is categorized as mild,
moderate, or severe, based on the degree of deviation
from the median for gestational age. Severe anemia
may cause hydrops and fetal demise.
There are many causes of fetal anemia (Table 14.2),
the most common being red cell alloimmunization in
Table 14.1. Increase of fetal hemoglobin with advancing
gestation
Weeks Mean 95 5 0.55 MoM 0.65 MoM
18 10.6 11.8 9.4 5.8 6.9
19 10.9 12.2 9.6 6.0 7.1
20 11.1 12.5 9.8 6.1 7.2
21 11.4 12.8 9.9 6.2 7.4
22 11.6 13.0 10.1 6.4 7.5
23 11.8 13.3 10.2 6.5 7.6
24 12.0 13.6 10.3 6.6 7.8
25 12.1 13.8 10.4 6.7 7.9
26 12.3 14.0 10.5 6.8 8.0
27 12.4 14.3 10.6 6.8 8.1
28 12.6 14.5 10.7 6.9 8.2
29 12.7 14.7 10.7 7.0 8.3
30 12.8 14.9 10.8 7.1 8.3
31 13.0 15.1 10.8 7.1 8.4
32 13.1 15.3 10.9 7.2 8.5
33 13.2 15.5 10.9 7.2 8.6
34 13.3 15.7 10.9 7.3 8.6
35 13.4 15.8 10.9 7.4 8.7
36 13.5 16.0 10.9 7.4 8.7
37 13.5 16.2 10.9 7.5 8.8
38 13.6 16.4 10.9 7.5 8.9
39 13.7 16.5 10.9 7.5 8.9
40 13.8 16.7 10.9 7.6 9.0
Table 14.2. Causes of fetal anemia
Red cell alloimmunization
Alpha-thalassemia
Enzyme disorder
Pyruvate kinase deficiency
Glucose phosphate isomerase deficiency
G6PD deficiency
Kasabach-Merritt sequence
Fetomaternal hemorrhage
Intracranial hemorrhage
Parvovirus B19 infection
Twin-to-twin transfusion
Blackfan-Diamond syndrome
Transient myeloproliferative disorder
Congenital leukemia
the United States. The primary cause of red cell alloimmunization
is maternal sensitization to D antigen of
the rhesus blood group system; however, many other
antigens, the so-called irregular antigens, may be responsible
for maternal sensitization. Prophylaxis with
rhesus immunoglobulins has decreased the incidence
of Rh-hemolytic disease; however, this phenomenon
is still present.
Several other conditions can lead to fetal anemia.
Hematological disorders can lead to fetal anemia and
they are implicated in approximately 10±27% of cases
of nonimmune hydrops [35±37]. Fetal anemia may
also result from excessive erythrocyte loss by hemoly-