o_1977r8vv9vk1ts2ms0kd8pksa.pdf

528 W. J. Ott
Fig. 35.10. Regression of the peak velocity of the middle
cerebral artery [converted to multiples of the mean (MOM)
for gestational age] against the fetal/neonatal hematocrit
(converted to MOM for gestational age) at cordocentesis or
delivery. The right side of the figure shows the peak velocity
in the middle cerebral artery in anemic vs non-anemic
fetuses or neonates
crease in the A/E ratio at both atrioventricular valves
[60]. The increased cardiac output seen in these anemic
fetuses my be due to a decrease in blood viscosity
which, in turn, leads to increased venous return
and cardiac preload; and/or to peripheral vasodilatation
caused by a fall in blood oxygen content and
therefore reduced cardiac afterload. There is no evidence
for a redistribution of cardiac output similar to
that described in hypoxic IUGR fetuses [60].
The traditional method of evaluating fetal anemia
in sensitized patients is the serial determination of
amniotic fluid changes in optical density at 450 nm
[61, 62]. The use of Doppler ultrasound to measure
peak velocity in the fetal middle cerebral artery has
been shown to be an accurate, non-invasive method
of evaluating fetal anemia [63±65]. Figure 35.10 shows
the correlation between fetal/neonatal hematocrit and
peak velocity in the fetal middle cerebral artery in 36
patients with suspected fetal anemia (primarily due
to isoimmunization) followed at the author's institution.
Doppler ultrasound appears to be as accurate as
serial amniocentesis in evaluating suspected fetal anemia,
and has the important advantage of being a
non-invasive test [66].
Non-Immune Hydrops
As has been mentioned previously non-immune fetal
hydrops may be secondary to a multitude of different
causes. The first step, therefore, in the evaluation and
management of fetuses with suspected non-immune
hydrops is to attempt to determine its etiology. Some
of the more common causes of non-immune fetal
hydrops include chromosomal abnormalities, mass
lesions that affect fetal blood flow, lymphatic abnormalities,
metabolic diseases of the fetus, and infection
Table 35.5. Evaluation of non-immune fetal hydrops.
TORCH toxoplasmosis, other, rubella, cytomegalovirus,
herpes. (From [57])
Evaluation Test Etiology?
Maternal Antibody screen Rule out isoimmunization
Complete blood
count and indices
Hematological disorders
Electrophoresis Thalassemia
Kleihauer-Betke stain Fetal±maternal
hemorrhage
VDRL and TORCH Fetal infection
titers
Glucose tolerance Maternal diabetes
test
Fetus Level II ultrasound
and color Doppler
Anatomical or physiological
abnormalities
of the fetus
Cordocentesis Karyotype (chromo-
Amniocentesis
Paracentesis
Thoracenteses
somal anomalies)
Cultures/immunology
(infection)
[67±72]. Table 35.5, modified from a review by Holzgreve
et al., lists many of the tests necessary to appropriately
evaluate cases of non-immune hydrops [57].
A study by Saltzman et al. reviewed the ultrasonic
differences seen in anemic and non-anemic fetuses
with hydrops [60]. The lack of a thickened placenta,
and the presence of pleural effusions and/or marked
edema, was more frequently associated with non-anemic
causes of fetal hydrops. Doppler echocardiography
may be useful in the additional differentiation between
cardiac and non-cardiac causes of non-immune hydrops
[45, 71]. Increased velocity in the middle cere-