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Chapter 35 ■ The Fetal Spine 1267
CAUSES OF SCOLIOSIS OR KYPHOSIS
Hemivertebrae
Butterfly vertebrae
Block vertebrae
Spina bifida
Ventral abdominal wall defects
Limb–body wall complex
Amniotic band syndrome
Arthrogryposis
Skeletal dysplasias
VACTERL* association
Caudal regression syndrome
*Vertebral abnormalities, anal atresia, cardiac
abnormalities, tracheoesophageal fistula, renal agenesis,
and limb defects.
Possible associated anomalies must then be sought
because prognosis depends on the coexistent
anomalies.
A hemivertebra represents underdevelopment or
nondevelopment of one half of a vertebral body; that is,
one of the two early chondrification centers is deficient.
The remaining ossification center is displaced laterally
with respect to the vertebrae above and below it, leading
to a short-segment mild scoliosis. The abnormalities can
be detected prenatally and may be best portrayed with
3-D ultrasound.
30-33
Fetuses with an isolated hemivertebra have an excellent prognosis, whereas those with other
fetal anomalies (e.g., Potter’s syndrome; cardiac, intestinal, intracranial, and limb anomalies) have a poor prog-
107
nosis.
survival to approximately 50%. If oligohydramnios is
also present, the mortality approaches 100%.
The presence of associated anomalies reduces
108
SACRAL AGENESIS
Sacral agenesis is an uncommon fetal abnormality that
may be present in conditions such as caudal regression
sequence, sirenomelia sequence, cloacal exstrophy
sequence, and the VACTERL association (vertebral
abnormalities, anal atresia, tracheoesophageal fistula,
renal dysplasia, and limb defects). The caudal regression
sequence (caudal regression syndrome) and the sirenomelia sequence are thought to be separate pathologic
entities.
109,110
CAUDAL REGRESSION
In caudal regression or dysplasia, abnormalities of the
lower spine and limbs occur, including sacral agenesis,
lumbar spine deficiency, and leg anomalies such as
femoral hypoplasia (Fig. 35-20). Defects of the neural
tube and the genitourinary, gastrointestinal, and cardiac
systems are common. Occurrence is sporadic; caudal
regression is more common in infants of mothers with
diabetes mellitus. The etiology is not established. Sonography can demonstrate absence of the sacrum and shortened femurs. The legs can be flexed and abducted at the
hips, and there may be clubfoot. Sonography may detect
associated urinary anomalies (renal agenesis, cystic dysplasia, caliectasis) and gastrointestinal abnormalities
(e.g., duodenal atresia).
111
The prognosis depends on the
severity and extent of the skeletal abnormalities and associated anomalies. In sacral agenesis with no internal
organ involvement, there are usually deficits in the legs
and deficient control of bladder and bowel functions. In
infants with internal organ involvement, the prognosis
is related to these defects.
SIRENOMELIA
Sirenomelia sequence is a rare disorder in which the legs
are fused and the feet are deformed or absent
35-21). The cause is probably an aberrant fetal artery
that branches from the upper abdominal aorta and passes
into the umbilical cord to the placenta.
113
flow bypasses the lower fetal body. The distal abdominal
aorta, the aorta’s distal branches, and subtended structures are small and underdeveloped. This leads to malformations of spine, legs, kidneys, gut, and genitalia.
Normally the umbilical arteries, which arise from the
fetal iliac arteries, carry blood from the fetus into the
umbilical cord and then into the placenta.
At sonography, there is advanced oligohydramnios
because of reduced or absent renal function. The legs are
fused, or there is a single leg. The feet are absent, or there
may be a single foot. There may be sacral agenesis, deficiency of the lower lumbar spine, and thoracic anomalies. These findings may be difficult to appreciate because
of the advanced oligohydramnios or anhydramnios.
The prolonged anhydramnios causes pulmonary hypoplasia, which is usually fatal. The risk of recurrence is the
same as in the general population.
112
(Fig.
Arterial blood
109
SACROCOCCYGEAL TERATOMA
Fetal teratomas may arise from the sacrum or coccyx,
from other midline structures from the level of the brain
to the coccyx, or from the gonads.
teratomas arise from the pluripotent cells of Hensen’s
node located anterior to the coccyx. Sacrococcygeal
teratomas contain all three germ layers (ectoderm,
mesoderm, and endoderm) and thus may contain elements of many tissues, including neural, respiratory, and
gastrointestinal. Sacrococcygeal tumor is rare (1:35,000
115
births)
but the most common tumor of neonates.
Females are affected four times more frequently than
males. Sacrococcygeal teratomas are classified into four
114
Sacrococcygeal
1268 PART IV ■ Obstetric Sonography
BA
DC
FIGURE 35-20. Caudal regression. A, Sagittal sonogram of spine at 21 weeks shows abrupt termination of ossified vertebral
bodies. B, Transverse view of pelvis with legs in long axis shows lack of ossified pelvic bones and atrophic musculature about the lower
extremities. C, Transverse color Doppler image at level of bladder shows lack of ossified pelvic bones. D, In a different fetal specimen,
radiograph shows abrupt termination (arrows) of the lumbar spine and absence of the sacrum. The pelvic bones are small and deformed.
F
A B C
FIGURE 35-21 Sirenomelia. A, Sagittal view of fetus at 12 weeks’ gestation shows unusual angulation of lower extremity. B, Long-
axis view of a single lower extremity. C, In a different fetus, radiograph shows single femur (F) and single tibia (T). Note the segmented
defects in the vertebrae of the thoracic and lumbar spine (arrows).
T
Chapter 35 ■ The Fetal Spine 1269
B
SCT
S
A B
FIGURE 35-22. Sacrococcygeal teratoma. A, Sagittal sonogram shows type II sacrococcygeal teratoma (SCT) that is predomi-
nantly external but has a substantial intrapelvic component. The tumor extends up to level L5 and displaces the fetal urinary bladder (B)
anteriorly. Note the calcifications (arrows) within the tumor. B, T2-weighted sagittal MR image demonstrates the extent and internal
structure of the sacrococcygeal tumor (SCT); S, stomach. C, Lateral radiograph in a different neonate. (A and B courtesy Drs. Fong, Pantazi,
and Toi, Mt. Sinai Hospital, Toronto.)
TYPES OF SACROCOCCYGEAL
SCT
SCT
C
PRESACRAL MASSES
TERATOMAS
Sacrococcygeal teratoma
Type I (47%): external mass predominant
Type II (34%): external mass with significant
internal component
Type III (9%): internal mass predominant, with
smaller external component
Type IV (10%): presacral mass only
Chordoma
Anterior myelomeningocele
Neurenteric cyst
Neuroblastoma
Sarcoma
Lipoma
Bone tumor
Lymphoma
Rectal duplication
115
types:
type I, tumor predominantly external with only
minimal presacral involvement; type II, tumor presenting externally but with significant intrapelvic extension;
type III, tumor apparent externally but with predominant pelvic mass and extension into the abdomen; type
IV, tumor presacral with no external presentation (Fig.
114
35-22).
At birth, 75% of sacrococcygeal teratomas are benign,
12% are immature, and 13% are malignant. Because
malignant potential increases with the age of the infant,
surgery must be performed shortly after birth.
Sonography usually demonstrates a mass in the rump
or buttocks area adjacent to the spine
116
(Video 35-2).
Most teratomas (85%) are either solid or mixed (solid +
cystic); 15% are mostly cystic, which is a benign sign.
Calcifications are frequently present. Large masses may
displace and distort neighboring structures, such as the
rectum and urinary bladder (see Fig. 35-21). Compression of the distal ureters may cause hydronephrosis.
Larger solid tumors may develop substantial
venous shunting causing fetal cardiac failure and
hydrops.
117
The development of hydrops in the presence
arterio-
of a sacrococcygeal teratoma carries a poor prognosis,
and these findings should precipitate a cesarean section
for fetal salvage.
117-121
PRESACRAL FETAL MASS
The differential diagnosis of a presacral fetal mass also
includes chordoma, anterior myelomeningocele, neurenteric cyst, neuroblastoma, sarcoma, lipoma, bone tumor,
lymphoma, and rectal duplication. Amniotic fluid AFP is
often elevated in sacrococcygeal tumor, and AChE is often
present in the amniotic fluid. These results exclude most
other etiologies, except a myelomeningocele.
If a fetal sacrococcygeal teratoma is suspected from
prenatal sonograms, serial sonograms should be arranged
to monitor the pregnancy to assess for complications,
especially signs of fetal cardiac failure. Complete fetal
assessment should also include the internal characteristics of the tumor, the size of the tumor, and associated
fetal anomalies.
For masses less than 4.5 cm diameter, without associated abnormalities, elective vaginal delivery is recommended. For masses greater than 4.5 cm diameter,
1270 PART IV ■ Obstetric Sonography
elective cesarean section may be advisable because of the
risk of dystocia and hemorrhage during vaginal delivery.
In utero surgery for arteriovenous shunting has been
described for treatment of fetal hydrops from congestive
heart failure in early pregnancy (<30 weeks), but this
should be considered only in experienced hands.
117,118
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1272 PART IV ■ Obstetric Sonography
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Ultrasound Obstet Gynecol 2007;30:845-849.
104. Harrison LA, Pretorius DH, Budorick NE. Abnormal spinal curvature in the fetus. J Ultrasound Med 1992;11:473-479.
Scoliosis and Kyphosis
105. Patten RM, van Allen M, Mack LA, et al. Limb–body wall complex:
in utero sonographic diagnosis of a complicated fetal malformation.
AJR Am J Roentgenol 1986;146:1019-1024.
106. Van Allen MI, Curry C, Walden CE, et al. Limb–body wall complex: II. Limb and spine defects. Am J Med Genet 1987;28:549-
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107. Benacerraf BR, Greene MF, Barss VA. Prenatal sonographic diagnosis of congenital hemivertebra. J Ultrasound Med 1986;5:257-
259.
108. Zelop CM, Pretorius DH, Benacerraf BR. Fetal hemivertebrae: associated anomalies, significance, and outcome. Obstet Gynecol 1993;
81:412-416.
109. Twickler D, Budorick N, Pretorius D, et al. Caudal regression versus
sirenomelia: sonographic clues. J Ultrasound Med 1993;12:323-
330.
Sacral Agenesis
110. Sepulveda W, Corral E, Sanchez J, et al. Sirenomelia sequence versus
renal agenesis: prenatal differentiation with power Doppler ultrasound. Ultrasound Obstet Gynecol 1998;11:445-449.
111. Baxi L, Warren W, Collins MH, Timor-Tritsch IE. Early detection
of caudal regression syndrome with transvaginal scanning. Obstet
Gynecol 1990;75:486-489.
Caudal Regression
112. Stocker JT, Heifetz SA. Sirenomelia. A morphological study of 33
cases and review of the literature. Perspect Pediatr Pathol 1987;10:
7-50.
Sirenomelia
113. Stevenson RE, Jones KL, Phelan MC, et al. Vascular steal: the
pathogenetic mechanism producing sirenomelia and associated
defects of the viscera and soft tissues. Pediatrics 1986;78:451-457.
114. Bloechle M, Bollmann R, Zienert A, et al. [Fetal teratoma: diagnosis
and management]. Zentralbl Gynakol 1992;114:175-180.
Sacrococcygeal Teratoma; Presacral Fetal Mass
115. Altman RP, Randolph JG, Lilly JR. Sacrococcygeal teratoma: American Academy of Pediatrics Surgical Section Survey—1973. J Pediatr
Surg 1974;9:389-398.
116. Sheth S, Nussbaum AR, Sanders RC, et al. Prenatal diagnosis of
sacrococcygeal teratoma: sonographic-pathologic correlation. Radiology 1988;169:131-136.
117. Bond SJ, Harrison MR, Schmidt KG, et al. Death due to highoutput cardiac failure in fetal sacrococcygeal teratoma. J Pediatr Surg
1990;25:1287-1291.
118. Langer JC, Harrison MR, Schmidt KG, et al. Fetal hydrops and
death from sacrococcygeal teratoma: rationale for fetal surgery. Am
J Obstet Gynecol 1989;160:1145-1150.
119. Gross SJ, Benzie RJ, Sermer M, et al. Sacrococcygeal teratoma:
prenatal diagnosis and management. Am J Obstet Gynecol 1987;
156:393-396.
120. Teal LN, Angtuaco TL, Jimenez JF, Quirk Jr JG. Fetal teratomas:
antenatal diagnosis and clinical management. J Clin Ultrasound
1988;16:329-336.
121. Robertson FM, Crombleholme TM, Frantz 3rd ID, et al. Devascularization and staged resection of giant sacrococcygeal teratoma in
the premature infant. J Pediatr Surg 1995;30:309-311.
CHAPTER 36
The Fetal Chest
Rola Shaheen and Deborah Levine
Chapter Outline
DEVELOPMENT OF STRUCTURES
IN THE CHEST
Pulmonary Development
Normal Sonographic Features of the
Fetal Chest
Normal Diaphragm
Normal Thymus
PULMONARY HYPOPLASIA AND
APLASIA
CONGENITAL PULMONARY
AIRWAY MALFORMATION
SPECTRUM
Congenital Cystic Adenomatoid
Malformation
Bronchopulmonary Sequestration
Congenital Lobar Emphysema
CONGENITAL HIGH AIRWAY
OBSTRUCTION
BRONCHOGENIC CYST
NEURENTERIC CYST
PLEURAL EFFUSION
PERICARDIAL EFFUSION
Familiarity with the normal development of the fetal
chest is important both for recognizing chest anomalies
and for understanding the consequences of these anomalies. Accurate prenatal diagnosis of noncardiac thoracic
lesions is essential in providing appropriate recommendations for fetal karyotyping and in planning for in utero
intervention and mode of delivery. Sonography is important for recognition of thoracic lesions and assessment of
their impact on mediastinal structures, because chest
lesions can lead to compromised cardiac function and
hydrops. Chest abnormalities may be associated with
lethal pulmonary hypoplasia, fatal chromosomal abnormalities, and lethal structural anomalies. However, some
chest lesions resolve in utero with minimal sequelae. In
cases with unclear sonographic diagnosis or planned in
utero interventions, fetal magnetic resonance imaging
(MRI) is helpful.
DEVELOPMENT OF STRUCTURES
IN THE CHEST
Pulmonary Development
In the human lung, there are five distinct stages of development, during which the lung matures and the number
of alveoli increases.
but structurally immature; the greatest increase in
number of alveoli occurs postnatally. During the first 3
years of life, the alveoli are formed through a septation
1,2
At birth, the lungs are functional
CONGENITAL DIAPHRAGMATIC
HERNIA
Left-Sided Hernia
Right-Sided Hernia
Other Hernias and Eventration
Associated Anomalies
Morbidity and Mortality
In Utero Therapy
CONCLUSION
process that increases the gas exchange surface area. It is
important to understand that this lung development
process is ongoing, and that space-occupying lesions,
or extrinsic abnormalities that do not allow for normal
lung growth, can lead to improper lung development.
Normal Sonographic Features
of the Fetal Chest
The fetal lungs are identified by ultrasound as homogeneously echogenic tissue surrounding the heart, separated by the hypoechoic, dome-shaped diaphragm from
the abdominal organs (Fig. 36-1, A and B). The fetal ribs
are highly echogenic, curved bony structures arising near
the spine and extending anteriorly to encompass more
than half the thoracic circumference. Lung echogenicity
varies during gestation, in general increasing in echogenicity as lung development progresses.
Assessment of pulmonary size is important for evaluation of fetuses at risk for pulmonary hypoplasia, particularly in cases of congenital diaphragmatic hernia
(CDH), pleural effusions, prolonged oligohydram-
nios, and skeletal deformities. Methods to assess pulmonary size include measurement of the thoracic
circumference
nal thoracic area minus cardiac area in diastole on a
transverse four-chamber view
(3-D) lung volumetry with ultrasound or MRI.
3
(Table 36-1), lung area (defined as inter-
4
), and three-dimensional
5-7
The fetal lungs, thorax, and heart grow at similar
rates, such that the normal cardiothoracic ratio remains
1273
1274 PART IV ■ Obstetric Sonography
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 first, 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 first 3 years of life.
constant in the second and third trimesters. On a normal
four-chamber transverse view of the heart, the heart
should occupy approximately one-third to one-half the
sonographic diameter of the thorax.
The cardiac position and axis are constant in normal
fetuses. The apex of the heart points left and touches the
anterior chest wall. The posterior aspect of the right
atrium lies to the right of midline.
8
Familiarity with the normal anatomy and position of
the fetal heart is crucial, along with in utero establishment of the right and left sides of the fetus. The reference
to cardiac position and situs is identified by noting the
left atrium lies posteriorly, closest to the spine, and the
right ventricle lies anteriorly, close to the chest wall. Any
deviation in the position of the heart should prompt a
search for cardiac or pulmonary abnormality. Anatomy
of the fetal heart, including size and position, can be
easily influenced by extracardiac thoracic anomalies.
Normal Diaphragm
Early in embryogenesis, the narrow pleuroperitoneal
duct connects the pleural and peritoneal cavities.
The development of the diaphragm, at about 9 weeks,
divides the two cavities. The normal diaphragm and
diaphragm motion can be visualized as early as 10 weeks
of gestation.
9-11
The diaphragm appears as a thin,
hypoechoic, arched line separating the chest from intraabdominal contents (Fig. 36-1, C, D, and F). It is best
recognized as a dome on each side on sagittal and coronal
views, with no difference in the height of the diaphragm
on either side.
12
The intact left hemidiaphragm is emphasized by the presence of the fluid-filled stomach in the
abdomen. On the right side, however, meticulous effort
may be required to identify the hypoechoic linear muscular diaphragm between the liver and lung.
Normal Thymus
The fetal thymus can be identified as early as 14 weeks’
gestation in the anterior mediastinum. By the third trimester, the thymus is visualized as an ovoid, relatively
hypoechoic structure
thymus contains spindle-shaped echogenicities that differentiate it from the surrounding lungs.
13,14
(Fig. 36-1, G and I ). The
15
Thymus size
varies greatly during gestation. Thymic imaging and measurements are not performed routinely on prenatal scans.
However, prenatal identification and measurement of the
fetal thymus is important when DiGeorge syndrome is
suspected. In addition, a large thymus will sometimes be
confused with a mediastinal mass. It is therefore important to recognize the normal appearance of the thymus.
The normal thymic average transverse measurement is
12 mm at 19 weeks’ gestation and 33 mm at 33 weeks.15
The normal thymic average perimeter is 128 mm at 38
weeks.13 Acute fetal thymic involution has been reported
in association with chorioamnionitis.
16
PULMONARY HYPOPLASIA
AND APLASIA
Pulmonary hypoplasia is defined 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.
the fetal lungs, the more severe is the degree of pulmonary hypoplasia.
20
Pulmonary hypoplasia is a relatively
common process that results in severe postnatal respiratory distress and associated high neonatal mortality,
with a high incidence of stillbirths (6.7%).
turity of the lungs contributes to the nonviability of
fetuses less than 24 weeks.
Pulmonary hypoplasia can be primary or secondary
and can be unilateral or bilateral depending on the etiology and time of insult to the lungs. Primary pulmonary
hypoplasia is very rare and is caused by a primary process
in which the lung does not form normally. Unilateral
pulmonary agenesis, in which no normal lung forms,
has an incidence of 1 in 15,000 births and is associated
with other congenital anomalies.
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), and severe prolonged oligohydramnios (e.g., bilateral renal agenesis). Other factors
that contribute to pulmonary hypoplasia include hormonal influences, pulmonary fluid dynamics, and abnormal fetal breathing movements.
of pulmonary hypoplasia are associated with major structural or chromosomal abnormalities (Table 36-2).
Prenatal prediction of pulmonary hypoplasia and the
degree of severity are crucial for parental counseling as
17-19
The earlier the insult to
18
The imma-
22
Bilateral pulmonary
23
The majority of cases
21
Lu
Chapter 36 ■ The Fetal Chest 1275
Li
Li
Lu
A
Left
D
Right
E F
B
Right Left
C
G H
FIGURE 36-1. Normal fetal chest. A, Sagittal view of torso at 13 weeks. Note liver (Li), lungs (Lu), and diaphragm. B, Four-
chamber view of the heart surrounded by the homogeneous echogenic lungs at 18 weeks. C, Coronal, and D, sagittal, views of chest at
18 weeks show the dome-shaped hemidiaphragms (arrow) separating the lungs (Lu) from intraabdominal organs and the relative hypoechoic
appearance of the liver (Li). E and F, Axial and sagittal views of fetal chest at 37 weeks. G, Normal appearance of fetal thymus (arrowheads)
at 37 weeks’ gestation. H, Coronal T2-weighted MR image shows normal lungs and diaphragm at 37 weeks. I, Axial T2-weighted MR
image of thymus (arrows) anterior to heart. The thymus is relatively hypoechoic to the surrounding lungs on ultrasound and relatively
low intensity on MRI.
well as for postnatal management planning, especially for
neonates requiring intensive respiratory care immediately after birth.
prenatal pulmonary hypoplasia
lung volumes by 3-D ultrasound
thoracic circumference
9,32
ratio,
lung-to-body weight ratio,24 and Doppler
studies of pulmonary arteries.
24
Proposed methods for prediction of
30,31
25
include estimation of
26,27
or by MRI,
(Table 36-1), lung-to-head
33
28,29
Prognosis and management are variable and depend
on the severity and nature of the associated conditions.
For example, absence of fetal breathing movements in
the setting of oligohydramnios in pregnancies resulting
from premature rupture of membranes (PROM) is an
accurate predictor for pulmonary hypoplasia.
the spectrum of outcomes ranges from mild respiratory
insufficiency to neonatal death.
In cases of unilateral pulmonary hypoplasia or aplasia,
there is mediastinal shift to the side of the hypoplastic
lung, with no associated mass in the contralateral lung
to explain the degree of mediastinal shift
The contralateral lung will often be enlarged and echo-
22
genic.
Unilateral pulmonary hypoplasia can also be
I
4
Clinically,
34
(Fig. 36-2).
1276 PART IV ■ Obstetric Sonography
TABLE 36-1. NORMAL THORACIC CIRCUMFERENCE AND LENGTH CORRELATED WITH
MENSTRUAL (GESTATIONAL) AGE*
Predictive Percentiles
AGE (WK)
2.5 5 10 25 50 75 90 95 97.5
16 5.9 6.4 7.0 8.0 9.1 10.3 11.3 11.9 12.4
17 6.8 7.3 7.9 8.9 10.1 11.2 12.2 12.8 13.3
18 7.7 8.2 8.8 9.8 11.0 12.1 13.1 13.7 14.2
19 8.6 9.1 9.7 10.7 11.9 13.0 14.0 14.6 15.1
20 9.5 10.0 10.6 11.7 12.9 13.9 15.0 15.5 16.0
21 10.4 11.0 11.6 12.6 13.7 14.8 15.8 16.4 16.9
22 11.3 11.9 12.5 13.5 14.6 15.7 16.7 17.3 17.8
23 12.2 12.8 13.4 14.4 15.5 16.6 17.6 18.2 18.8
24 13.2 13.7 14.3 15.3 16.4 17.5 18.5 19.1 19.7
25 14.1 14.6 15.2 16.2 17.3 18.4 19.4 20.0 20.6
26 15.0 15.5 16.1 17.1 18.2 19.3 20.3 21.0 21.5
27 15.9 16.4 17.0 18.0 19.1 20.2 21.3 21.9 22.4
28 16.8 17.3 17.9 18.9 20.0 21.2 22.2 22.8 23.3
29 17.7
30 18.6 19.1 19.7 20.7 21.9 23.0 24.0 24.6 25.1
31 19.5 20.0 20.6 21.6 22.8 23.9 24.9 25.5 26.0
32 20.4 20.9 21.5 22.6 23.7 24.8 25.8 26.4 26.9
33 21.3 21.8 22.5 23.5 24.6 25.7 26.7 27.3 27.8
34 22.2 22.8 23.4 24.4 25.5 26.6 27.6 28.2 28.7
35 23.1 23.7 24.3 25.3 26.4 27.5 28.5 29.1 29.6
36 24.0 24.6 25.2 26.2 27.3 28.4 29.4 30.0 30.6
37 24.9 25.5 26.1 27.1 28.2 29.3 30.3 30.9 31.5
38 25.9 26.4 27.0 28.0 29.1 30.2 31.2 31.9 32.4
39 26.8 27.3 27.9 28.9 30.0 31.1 32.2 32.8 33.3
40 27.7 28.2 28.8 29.8 30.9 32.1 33.1 33.7 34.2
16 0.9 1.1 1.3 1.6 2.0 2.4 2.8 3.0 3.2
17 1.1 1.3 1.5 1.8
18 1.3 1.4 1.7 2.0 2.4 2.8 3.2 3.4 3.6
19 1.4 1.6 1.8 2.2 2.7 3.0 3.4 3.6 3.8
20 1.6 1.8 2.30 2.4 2.8 3.2 3.6 3.8 4.0
21 1.8 2.0 2.2 2.6 3.0 3.4 3.7 4.0 4.1
22 2.0 2.2 2.4 2.8 3.2 3.6 3.9 4.1 4.3
23 2.2 2.4 2.6 3.0 3.4 3.8 4.1 4.3 4.5
24 2.4 2.6 2.8 3.1 3.5 3.9 4.3 4.5 4.7
25 2.6 2.8 3.0 3.3 3.7 4.1 4.5 4.7 4.9
26 2.8 2.9 3.2 3.5 3.9 4.3 4.7 4.9 5.1
27 2.9 3.1 3.3 3.7 4.1 4.5 4.9 5.1 5.3
28 3.1 3.3 3.5 3.9 4.3 4.7 5.0 5.4 5.4
29 3.3 3.5 3.7 4.1 4.5 4.9 5.2 5.5 5.6
30 3.5 3.7 3.9 4.3 4.7 5.1 5.4 5.6
31 3.7 3.9 4.1 4.5 4.9 5.3 5.6 5.8 6.0
32 3.9 4.1 4.3 4.6 5.0 5.4 5.8 6.0 6.2
33 4.1 4.3 4.5 4.8 5.2 5.6 6.0 6.2 6.4
34 4.2 4.4 4.7 5.0 5.4 5.8 6.2 6.4 6.6
35 4.4 4.6 4.8 5.2 5.6 6.0 6.4 6.6 6.8
36 4.6 4.8 5.0 5.4 5.8 6.2 6.5 6.8 7.0
37 4.8 5.0 5.2 5.6 6.0 6.4 6.7 7.0 7.1
38 5.0 5.2 5.4 5.8 6.2 6.6 6.9 7.1 7.3
39 5.2 5.4 5.6 6.0 6.4 6.8 7.1 7.3 7.5
40 5.4 5.6 5.8 6.1 6.5 6.9 7.3 7.5 7.7
18.2 18.8 19.8 21.0 22.1 23.1 23.7 24.2
Thoracic Circumference (CM)
Thoracic Length (cm)
2.2 2.6 3.0 3.2 3.4
5.8
*From Chitkara U, Rosenberg J, Chevanak FA, et al. Prenatal sonographic assessment of thorax: normal values. Am J Obstet Gynecol 1987;156:1069-1074.
produced by space-occupying lesions, such as congenital
cystic adenomatoid malformation (CCAM), CDH, or
pleural effusion. The extent of pulmonary hypoplasia for
CONGENITAL PULMONARY
MALFORMATION SPECTRUM
a given amount of visualized lung is greater in fetuses
with CDH than with CCAM, suggesting that in CDH
there is a mechanism other than mass effect that limits
pulmonary development.
An echogenic lesion in the fetal thorax (Table 36-3)
or a cystic lesion in the fetal thorax (Table 36-4) can be
part of the congenital pulmonary airway malformation
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