Diagnostic ultrasound ( PDFDrive )

CHAPTER 36 The Fetal Chest 1245
second and third trimesters. On a normal four-chamber transverse
view of the heart, the heart should occupy one-third to one-half
the sonographic diameter of the thorax.
Stages of Human Lung Development
1. Embryonic stage. Extends to about 7 weeks
2. Pseudoglandular stage. Extends from 6 to 16 weeks;
the lungs resemble tubuloacinar glands, with epithelial
tubes sprouting and branching into the surrounding
mesenchyme
3. Canalicular stage. Extends from 16 to 28 weeks; the
cuboid epithelium differentiates into type I and type II
cells, with production of surfactant and formation of the
irst, thin, air-blood barriers
4. Saccular stage. Extends from 28 to 36 weeks; the
pulmonary parenchyma forms, the surrounding
connective tissues thins, and the surfactant system
matures
5. Alveolar stage. Extends from the 36th week of gestation
to the irst 3 years of life
he cardiac position and axis are constant in normal fetuses.
he apex of the heart points let and touches the anterior chest
wall. he posterior aspect of the right atrium lies to the right of
midline 8 (Fig. 36.1E).
Familiarity with the normal anatomy and position of the fetal
heart is crucial, along with in utero establishment of the right
and let sides of the fetus. he reference to cardiac position and
situs is identiied by noting that the let atrium lies posteriorly,
closest to the spine, and the right ventricle lies anteriorly, closest
to the chest wall. Any deviation in the position of the heart
should prompt a search for cardiac or pulmonary abnormalities.
Anatomy of the fetal heart, including size and position, can be
easily inluenced by extracardiac thoracic anomalies.
Normal Diaphragm
Early in embryogenesis, the narrow pleuroperitoneal duct connects
the pleural and peritoneal cavities. he development of the
diaphragm, at 9 weeks’ gestation, divides the two cavities. he
normal diaphragm can be visualized as early as 10 weeks of
gestation. 9,10 he diaphragm appears as a thin, hypoechoic, arched
line separating the chest from intraabdominal contents (Fig.
36.1C-F). It is best recognized as a dome on each side on sagittal
and coronal views, with no diference in the height of the diaphragm
on either side. 11 he intact let hemidiaphragm is more
easily veriied by the presence of the luid-illed stomach in the
abdomen. On the right side, however, meticulous efort is required
to identify the hypoechoic linear muscular diaphragm between
the liver and lung.
Normal Thymus
he fetal thymus can be identiied as early as 14 weeks’ gestation
in the anterior mediastinum. By the third trimester, the thymus
is visualized as an ovoid, relatively hypoechoic structure 12,13
(Fig. 36.1G and I). he thymus contains spindle-shaped echogenicities
that diferentiate it from the surrounding echogenic
lungs. 14 hymus size varies greatly during gestation. hymic
imaging and measurements are not performed routinely on
prenatal scans. However, prenatal identiication and measurement
of the fetal thymus is important when DiGeorge syndrome (with
thymic aplasia or hypoplasia) is suspected. At times a large thymus
will be confused with a mediastinal mass. Homogeneity and
lack of mediastinal deviation can help diferentiate normal thymus
from a mediastinal teratoma or thymic cyst. he normal thymic
average transverse measurement is 12 mm at 19 weeks’ gestation
and 33 mm at 33 weeks. 14 he normal thymic average perimeter
is 128 mm at 38 weeks. 12 Acute fetal thymic involution has been
reported in association with chorioamnionitis. 15
Mediastinal teratomas 16,17 are rare anterior mediastinal
complex masses. By ultrasound, the mass is heterogeneous and
calciications may be noted. MRI is a useful adjunct in the
assessment of the mass for potential in utero and postnatal surgical
treatment. he mass can cause polyhydramnios secondary to
esophageal compression, and hydrops due to impaired venous
return with resultant fetal demise. 16 Fetal intervention with
aspiration of the tumor cyst has been described with a resultant
decrease in intrathoracic pressure, which may stop the progression
to hydrops and prevent lung hypoplasia. he ex utero intrapartum
treatment (EXIT) procedure may be recommended to establish
a proper airway at delivery. 16
PULMONARY HYPOPLASIA, APLASIA,
AND AGENESIS
Pulmonary hypoplasia is deined as a reduction in the number
of cells, airways, and alveoli that results in an absolute decrease
in the size and weight of the fetal lungs relative to gestational
age. 18 Aplasia is the presence of rudimentary bronchi with no
associated lung parenchyma. Agenesis is the complete absence
of bronchi, vessels, and lung parenchyma. he earlier the insult
to the fetal lungs occurs, the more severe is the degree of pulmonary
hypoplasia, aplasia, or agenesis. 19 Pulmonary hypoplasia
can result in postnatal respiratory distress and associated high
neonatal mortality. 20 Pulmonary hypoplasia can be primary or
secondary and can be unilateral or bilateral depending on the
cause and time of insult to the lungs. Primary pulmonary
hypoplasia is rare and is caused by a primary process in which
the lung does not form normally. Unilateral pulmonary agenesis
has an incidence of 1 in 15,000 births and is associated with
other congenital anomalies. 21 Bilateral pulmonary agenesis is
incompatible with postnatal life.
Secondary causes of pulmonary hypoplasia include masses
that compress the lungs (e.g., CDH), skeletal malformations that
do not allow the lungs to grow (e.g., thanatophoric dysplasia)
(Fig. 36.2), and severe prolonged oligohydramnios (e.g., bilateral
renal agenesis). Other factors that contribute to pulmonary
hypoplasia include hormonal inluences, pulmonary luid dynamics,
and abnormal fetal breathing movements. 22 he majority of
cases of pulmonary hypoplasia are associated with major structural
or chromosomal abnormalities (Table 36.1).