o_1977r8vv9vk1ts2ms0kd8pksa.pdf

340 A. Lysikiewicz
[11]. Hypoproteinemia that develops from impaired
protein synthesis in the liver contributes to development
of fetal hypervolemia and hydrops. Fetal hydrops
can present as a spectrum of ultrasonographic
findings, from a mild form with little fetal circulatory
overload to an end-stage disease, involving all major
systems that, with no intervention, will progress to fetal
death. Development of fetal hydrops is associated
with significantly increased fetal loss even if intervention
with fetal intravascular transfusion is attempted
[12].
The fetus appears to be resistant to decreased oxygen-carrying
capacity in fetal anemia as there is little
of fetal hypoxemia in anemic fetuses [13]. Increased
dynamic of fetal circulation compensates well initially
for the decreased fetal erythrocyte mass, maintaining
adequate oxygenation. Fetal hypoxia develops relatively
late in the process as fetal hemoglobin oxygencarrying
capacity is efficient even at low concentrations.
Fetal Cardiovascular Changes
in Alloimmunization
A substantial amount of information has been collected
about fetal circulation during the course of alloimmunization.
Fetal anemia consists of reduced red
cell mass/cc and ªthinningº of the fetal blood. Significant
fetal anemia has been reported as 5 g/dl below
the mean hemoglobin concentration for gestational
age, since at this level risk for development of fetal
hydrops increases [14]. Lower fetal hemoglobin levels
reduce oxygen-carrying capacity that could eventually
lead to fetal hypoxia. Hypoxia is, however, not observed
until late in the process, presumably due to increased
2,3-diphosphoglycerate concentration and increased
cardiac output that maintain adequate tissue
oxygen delivery [15]. At this level, anemia leads to reduction
of fetal blood viscosity that is further multiplied
by decreased fetal plasma protein production in
the fetal liver. The compensatory increase of cardiac
output and faster blood circulation, a combination
described as the fetal hyperdynamic state [16], prevents
development of hypoxia and acidosis early in
the process.
Increase of the fetal blood flow velocities is not
equally consistent in all vessels. Selective redistribution
of the blood flow, similar to those of chronic
hypoxic growth restriction, has not been confirmed
[16]. With terminal hydrops, however, hypoxia is
likely and some redistribution of the fetal blood flow
may be expected. In early fetal anemia, however, the
selection of the most representative vessels reflecting
the fetal condition is important to obtain pertinent
measurements [17].
Cardiac Blood Flow
In early fetal Rh disease, in the absence of fetal hydrops,
there are no indications that fetal anemia of
less than 5 g/dl of hemoglobin deficit from the mean
hemoglobin concentration expected for gestational
age value affects fetal cardiac functions.
At the end stage of alloimmunization generalized
fetal hydrops develops. Decreased serum oncotic
pressure owing to reduced liver albumin production,
umbilical venous and portal hypertension, hypoxic
endothelial damage, and congestive heart failure are
postulated as mechanisms of hydrops, with congestive
heart failure being infrequent. Hecher et al. [15]
examined fetal flow-velocity waveforms from the atrioventricular
valves, ductus venosus, right hepatic
vein, inferior vena cava, middle cerebral artery
(MCA), and descending thoracic aorta with concurrent
cordocentesis in 38 fetuses with red blood cell
isoimmunized pregnancies. Increased blood flow
velocities in the thoracic aorta, MCA, and the ductus
venosus were consistent with hyperdynamic state. In
this study, increased velocity in the thoracic aorta
was associated with fetal anemia as in other previous
reports [18, 19]. The authors did not notice major
changes in the venous blood flow. They concluded
that congestive heart failure is not a major factor in
development of fetal hydrops and that it happens late
in the process, if at all.
Fetal Heart Rate
Fetal hypoxia is often a concern in anemic fetuses in
alloimmunization because of presumed reduced oxygen-carrying
capacity. Hypoxic fetal response can be
expected to involve compensatory tachycardia and redistribution
of the fetal blood flow similar to chronic
hypoxia in intrauterine growth restriction; however,
several studies have shown that the correlation between
fetal anemia and fetal acid base is inconsistent
[13, 20]. Fetal hypoxia does not appear until late in
the process and fetal hemoglobin, even if diluted, can
carry a sufficient amount of oxygen. Fetal tachycardia
that may be observed is more likely to result from
the fetal hyperdynamic state [16]; therefore, only in
the very late stage of fetal disease in alloimmunization,
reduced oxygen-carrying capacity will lead to
hypoxia and fetal tachycardia. With fetal tachycardia
a higher end-diastolic flow can be recorded with
shortened diastole period. This represents a nonspecific
finding related to tachycardia itself.
Sinusoidal Fetal Heart Rate
Abnormal cardiac rhythm characteristic for fetal anemia
is a sinusoidal rhythm (Fig. 22.1). It has been
observed in severely anemic fetuses, regardless of the