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CHAPTER 38
The Fetal Abdominal Wall
and Gastrointestinal Tract
Jodi F. Abbott
Chapter Outline
EMBRYOLOGY OF THE
DIGESTIVE TUBE
STOMACH
Small or Absent Fetal Stomach
Esophageal Atresia
Dilated Fetal Stomach
Midline or Right-Sided Stomach
LIVER
BILIARY SYSTEM
PANCREAS
SPLEEN
SMALL BOWEL AND COLON
Duodenal Stenosis and Atresia
Jejunal and Ileal Atresias
Anorectal Atresia
Megacystis and Microcolon
Echogenic Bowel
Aneuploidy
Cystic Fibrosis
Swallowed Fetal Blood
Fetal Viral Infection
Later Diagnosis of Gastrointestinal
Atresias
Intrauterine Growth Restriction and
Fetal Demise
Summary
MECONIUM PERITONITIS AND
PSEUDOCYST
Identification and confirmation of a normal fetal
abdominal wall and gastrointestinal (GI) tract is critical
to ascertain the risk of isolated and multiple fetal abnormalities. Anomalies of the fetal abdomen may be the
only sonographic evidence of multisystem organ derangement. The National Center for Biotechnical Information (NCBI) with the Online Mendelian Inheritance in
Man has recommended new diagnostic categorization
(recategorization) of abdominal wall defects. This chapter
places these updated diagnostic categories in the context
of previous information, sonographic diagnostic criteria,
hypothesized etiology, and current management of these
abnormalities. Detection of fetal intra-abdominal masses
or abnormalities is important because they may be undetected on newborn examinations.
EMBRYOLOGY OF
THE DIGESTIVE TUBE
The lumens of both the digestive and the respiratory
tubes are lined by the embryonic endoderm, which differentiates distal to the pharynx after formation of the
pharyngeal pouches. The digestive tubes are a differentiation of the lateral plate endoderm. The stomach forms
as an inferior outpouching below the pharynx. The
regional specification of the digestive tube into the
esophagus, stomach, and small and large intestines is
in response to different mesodermal mesenchymes.
1-3
ENTERIC DUPLICATION CYST
ABDOMINAL WALL
Embryology
Gastroschisis
Omphalocele
Ectopia Cordis
Amniotic Band Syndrome and
Limb–Body Wall Complex
Bladder Exstrophy
Omphalocele-Exstrophy–Imperforate
Anus–Spinal Defects
CONCLUSION
The sonic hedgehog gene (Shh) has been implicated in
this differentiation.
gresses, the expressivity of Shh increases from proximal
to distal.
5
4
As digestive differentiation pro-
STOMACH
The fetal stomach can be seen as early as 7 weeks and
should be noted routinely by 13 to 14 weeks’ gestation
(Fig. 38-1). The stomach should be in the left upper
abdomen. It is important in every fetal survey to confirm
situs of the stomach because a midline or right-sided
stomach is associated with heterotaxy syndromes. Presence of a right-sided stomach and a right-sided heart
is termed total situs inversus. A right-sided stomach
and a left-sided heart result in partial situs inversus.
During the 11 to 14-week evaluation of the fetal
abdomen, numerous abnormal findings have been
reported, including ascites, abdominal cysts, and intestinal obstruction.
Small or Absent Fetal Stomach
Fluid in the stomach should be reliably visualized on
first-trimester screening or fetal anatomic survey and
all subsequent fetal evaluations. The absence of a visualized stomach on an anatomic survey, although potentially a normal finding, has an increased risk of fetal
7
6
1327
1328 PART IV ■ Obstetric Sonography
St
L
St
Dia
A
C D
B
St
E F
FIGURE 38-1. Normal fetal abdomen. A, In first trimester the fetal stomach (St) is an echolucent structure below the diaphragm.
Note similar echogenicity of liver, lung, and bowel. B, In second trimester in sagittal view, the stomach (St) is seen below the diaphragm
(Dia), and the liver (L) extends anteriorly to the abdominal wall. C, In second trimester in transverse view with the spine to the left, the
stomach is superior, and bowel echogenicity is similar to liver. The liver occupies most of the right abdomen and is relatively homogeneous.
D, Normal spleen (arrows) in the transverse view of second-trimester fetal abdomen. E, Normal echogenic appearance of meconium filling
the colon in the third trimester. F, Normal cord insertion site in midtrimester fetus. (E from McNamara A, Levine D. Intraabdominal fetal
echogenic masses: a practical guide to diagnosis and management. Radiographics 2005;25:633-645.)
Chapter 38 ■ The Fetal Abdominal Wall and Gastrointestinal Tract 1329
ABSENT STOMACH
Normal stomach that recently emptied
Displaced stomach into chest in hernia
Displaced stomach into abdominal wall defect
Esophageal atresia
Aneuploidy
Anhydramnios
Microgastria
abnormality, including aneuploidy, tracheoesophageal
fistula, and oligohydramnios.
When the stomach appears small or absent, it is
important to allow sufficient time for it to fill, in case it
has recently emptied. Generally, the stomach will fill
during a 30-minute examination. Careful attention must
be paid to the thorax; the stomach can be herniated into
the chest in congenital diaphragmatic hernia.
In one retrospective study, an abnormal outcome
(structural abnormalities, intrauterine fetal or postnatal
death) occurred in 23 (85%) of 27 fetuses with an absent
stomach and 27 (52%) of 52 fetuses with a small stomach
(combined, 63%). Karyotype was abnormal in eight
(38%) of 21 fetuses with an absent stomach and two
(4%) of 46 fetuses with a small stomach.
8
Amniotic fluid
in cases of absent stomach is typically normal early in
the second trimester, but polyhydramnios is common by
the third trimester. The finding of a persistently absent
stomach on serial ultrasound scans should trigger genetic
counseling and consideration of chromosomal testing.
Esophageal Atresia
Developmentally, the trachea and esophagus differentiate inferiorly from the posterior pharynx. Incomplete
differentiation of the respiratory and GI tracts can lead
to esophageal atresia with or without tracheoesophageal
(TE) fistulas. The incidence of TE fistulas, all types, is
2.8 per 10,000 pregnancies.
atresia (90%)
11
are associated with TE fistulas, and there-
9,10
Most types of esophageal
fore the stomach (although often small) will be visualized
on ultrasound. Occasionally, fluid in the upper esophagus can be appreciated (Fig. 38-2). For this reason, the
term “tracheoesophageal fistula” is usually the working
in utero diagnosis when esophageal atresia is suspected,
even though this diagnosis cannot be definitively made
in utero. The ability of prenatal diagnosis to detect this
condition is 42%.
12
The combination of inability to see a stomach
on ultrasound and the presence of polyhydramnios
is more suggestive of esophageal atresia than absent
stomach alone. The positive predictive value of this combination is still relatively modest, 56% in the largest
12
Esophageal atresia is associated with other sys-
study.
temic anomalies, and a detailed evaluation, including
echocardiography, should be performed in a fetus with
this suspected diagnosis. It is reported that as many as
half of TE fistulas are part of the VACTERL sequence,
a nonrandom group of coexisting defects: vertebral
defects, anal atresia, cardiac anomalies, tracheoesopha-
geal fistula with esophageal atresia, renal and radial
dysplasia, and limb defects. VACTERL has sporadic
inheritance. The corrective surgery for esophageal atresia
has a success rate of 90% and is related to the presence
of associated anomalies.
11
Dilated Fetal Stomach
In the second or third trimester a prominent or transiently dilated fetal stomach may be seen on ultrasound.
However, diagnosing a dilated fetal stomach requires
that the stomach be persistently dilated throughout a
30-minute assessment. Use of a nomogram can aid in
identifying true outliers (Table 38-1).
13
The differential
diagnosis of a dilated fetal stomach includes normal fetus
(Fig. 38-3) and gastrointestinal atresia (primarily duodenal atresia). For a dilated stomach when other fetal
parameters are normal, follow-up is recommended.
Midline or Right-Sided Stomach
When an apparently malpositioned stomach is noted,
the situs must again be carefully determined. Complete
situs inversus is uncommon but can be prenatally
detected. A midline stomach can represent intestinal
malrotation
14
(Fig. 38-4). However, heterotaxy syn-
drome, including right isomerism and left isomerism is
more common. It is characterized by an abnormal symmetry of the viscera and veins and may be associated with
complex cardiac anomalies, intestinal malrotation, and
splenic (asplenia or polysplenia; Fig. 38-5), and hepatic
abnormalities.
heterotaxy syndromes is 0.45 per 10,000 pregnancies.
15,16
The incidence of asplenia/polysplenia
17
Because of the combined cardiovascular and GI abnormalities, infant mortality is high, with 1-year mortality
reaching 32% in a Canadian retrospective trial.
18
LIVER
The fetal liver is clearly visualized in the upper abdomen
in the second half of gestation, although earlier in gestation it has an echogenicity similar to renal echoes. In the
fetus, the left side of the liver is larger than the right
19
The liver increases in size during pregnancy.20
side.
Hepatic enlargement has been documented in fetal
anemia caused by isoimmunization,
diseases, and fetal infection.
Hepatic calcifications may be noted in utero (Fig.
38-6). The pathophysiology of the calcifications in
otherwise normal fetuses is unknown. These are typically
isolated and of no clinical consequence.
hepatic calcifications have been reported in aneuploid or
21
22
glycogen storage
23
However,
9
1330 PART IV ■ Obstetric Sonography
AC
A
B
FIGURE 38-2. Esophageal atresia. A, Transverse
view of abdomen shows absent fetal stomach in second-trimester fetus with trisomy 13. B, Third-trimester fetus with
absent stomach and polyhydramnios. C, In a different fetus,
C
coronal view of upper thorax shows a distended esophageal
pouch (arrow).
TABLE 38-1. DIAMETER MEASUREMENTS OF FETAL STOMACH*
GESTATIONAL AGE (WK) N ANTEROPOSTERIOR (CM) TRANSVERSE (CM) LONGITUDINAL (CM)
13-15 15
16-18 29
19-21 17
22-24 11
25-27 14
28-30 17
31-33 18
34-36 15
37-39 16
From Goldstein I, Reece EA, Yakoni S, et al. Growth of the normal stomach in normal pregnancies. Obstet Gynecol 1987;70:641.
* Data are presented as mean ±2 SD.
0.4 ± 0.1 0.6 ± 0.2 0.9 ± 0.3
0.6 ± 0.2 0.8 ± 0.2 1.3 ± 0.4
0.8 ± 0.2 0.9 ± 0.2 1.6 ± 0.5
0.9 ± 0.3 1.8 ± 0.3 1.9 ± 0.6
1.0 ± 0.5 1.9 ± 0.5 2.3 ± 1.0
1.2 ± 0.3 1.6 ± 0.4 2.3 ± 0.5
1.4 ± 0.3 1.6 ± 0.4 2.8 ± 0.2
1.4 ± 0.4 1.6 ± 0.4 2.8 ± 0.9
1.6 ± 0.4 2.0 ± 0.4 3.2 ± 0.9
Chapter 38 ■ The Fetal Abdominal Wall and Gastrointestinal Tract 1331
S
FIGURE 38-3. Dilated fetal stomach in the second
trimester. In sagittal view the stomach is visible extending
inferiorly into the pelvis. Although this fetus had a persistently
dilated stomach during an anatomic survey, it resolved by the next
ultrasound, and the fetus had a normal outcome.
S
FIGURE 38-5. Polysplenia. Transverse MR image of fetus
with complex congenital heart disease (not shown) with multiple
splenules (arrows) in the left upper quadrant; S, stomach.
S
FIGURE 38-4. Midline fetal stomach in fetus with
heterotaxy. Transverse view of the abdomen shows a midline
stomach (arrow). This was the only abnormality seen at time of
fetal survey; fetal echocardiogram revealed anomalous pulmonary
venous return, and the diagnosis of heterotaxy was confirmed
postnatally.
CMV-infected fetuses with additional anomalies.24 In
the largest series of pregnancy outcomes of isolated, prenatally diagnosed calcifications, both trisomy 21 and
parvovirus were noted (each 3%).
24
Calcifications associated with vascular insult have also been reported. When
hepatic calcifications are visualized, it is important to
assess for any associated hepatic mass, for normal flow
in the liver, for signs of infection, and for any structural
or growth abnormalities. These calcifications in the
hepatic parenchyma need to be distinguished from calcifications that line the liver and peritoneal cavity in
fetuses with meconium peritonitis.
Hepatic or intra-abdominal masses can also be identified in utero. Solid masses include hamartoma,
adenoma, and hepatoblastoma. Hypoechoic liver
masses include hepatic cyst (Fig. 38-7, A), hemangioma
(Fig. 38-7, B), and abnormal myelopoiesis in fetuses
with trisomy 21.
25
Color flow Doppler ultrasound is
recommended to distinguish vascular lesions. Vascular
hepatic lesions have been noted to serve as vascular reservoirs, leading to high-output cardiac failure and fetal
hydrops.
26-30
These vascular lesions include hemangio-
mas, hemangioendotheliomas, and hepatoblastomas
and are associated with fetal hydrops. Therefore, following these fetuses sonographically with middle cerebral
artery and ductus venosus Doppler imaging may be
helpful because of the ability to predict fetal anemia of
other etiologies.
31-42
BILIARY SYSTEM
The normal fetal gallbladder is an oblong, echolucent
structure in the anterior liver (Fig. 38-8), generally
located 45 degrees to the right of midline and inferior
to the umbilical vein. The gallbladder increases in size
with gestational age.
of the gallbladder was most common from 20 to 32
44,45
weeks.
Nonvisualization of the gallbladder is asso-
ciated with cystic fibrosis, gallbladder atresia, and
biliary atresia.
et al.44 demonstrated the gallbladder between 12 and 40
weeks in 82.5%, but none of the fetuses with isolated
nonvisualization of the gallbladder had any adverse
neonatal outcome. Blazer et al.45 reported on 29,749
43
In multiple series, visualization
44,46
In a series of 578 fetuses, Hertzberg
A
C
B
FIGURE 38-6. Hepatic calcifications. A and B, Sagit-
tal and transverse views of hepatic calcification (arrows)
with shadowing posteriorly. In this fetus, chromosomes and
infectious workup were normal; the calcifications were
confirmed postnatally, with a normal newborn physical examination. C, Multiple hepatic calcifications in otherwise normalappearing fetus. (C from McNamara A, Levine D. Intraabdominal
fetal echogenic masses: a practical guide to diagnosis and management. Radiographics 2005;25:633-645.)
A B
FIGURE 38-7.
(B from McNamara A, Levine D. Intraabdominal fetal echogenic masses: a practical guide to diagnosis and management. Radiographics
2005;25:633-645.)
Hepatic masses. A, Hepatic cyst in sagittal view of the abdomen. B, Hepatic hemangioma (arrow) in 18-week fetus.
Chapter 38 ■ The Fetal Abdominal Wall and Gastrointestinal Tract 1333
consecutive pregnant women whose fetuses were imaged
by both transabdominal and transvaginal sonography at
14 to 16 weeks for gallbladder detection. Maternal scans
were repeated in 1 week if the fetal gallbladder was not
seen on the initial examination. Of these, only 34 fetuses
were identified with nonvisualization of the gallbladder
GB
FIGURE 38-8. Normal gallbladder. Transverse view of
a third-trimester fetal abdomen shows the gallbladder (arrow) as
an elongated cystic structure to the right of the umbilical vein
(arrowhead).
(0.1%); all these women were offered amniocentesis for
karyotype and cystic fibrosis screening. In 14 of these
fetuses, other anomalies were identified. In the other
20 fetuses, the gallbladder nonvisualization was isolated,
and all 20 had a normal karyotype and appeared
normal after birth. Therefore, confirmation of a normal
gallbladder is not considered a requisite of a detailed fetal
anatomic survey.
Echodensities in the fetal gallbladder can be either
sludge or gallstones. They are primarily seen in the third
trimester.
47-49
Gallstones are generally reported to have
acoustic shadowing (Fig. 38-9). If there is no shadowing,
it is assumed that the echogenic debris represents sludge,
a precursor of gallstones. In most cases, postnatal resolution occurs, and children are asymptomatic.
Enlarged gallbladder is associated with fetal aneuploidy, but all reported fetuses also had other prenatally
visualized anomalies.
50
Cystic lesions of the biliary tree have been identified
in utero. These cysts may be anechoic, may have echogenic debris, or may represent a bilobed gallbladder.
Choledochal cysts most often represent dilation of the
common bile duct
case reports of infrahepatic cystic masses representing
both choledochal cysts and biliary atresias.
51
(Fig. 38-10). There are numerous
52-54
Although
prenatal sonographic appearance is not diagnostic; two
case series suggest that infrahepatic cysts with some echogenicity that enlarge in the third trimester are more likely
to be choledochal cysts.
52,55
A
FIGURE 38-9. Gallbladder sludge and stones. A, Transverse third-trimester abdomen shows the lumen of the gallbladder
surrounding echogenic material consistent with sludge. This fetus had a normal newborn course. B, A fetus with gallstones.
B
1334 PART IV ■ Obstetric Sonography
in the colon. All GI atresias are thought to represent a
failure of recanalization of the bowel lumen, which is a
solid tube early in fetal life.
L
S
FIGURE 38-10. Choledochal cyst. Transverse view of
abdomen shows a cyst (arrow) with stomach (s) on the left and
liver (L) on the right.
PANCREAS
Pancreatic abnormalities reported prenatally include
polycystic pancreas
diagnoses of annular pancreas were triggered by sonographic assessment for a dilated duodenum. Annular
pancreas is associated with as many as 33% of fetuses
with prenatally diagnosed duodenal atresias.
56
and annular pancreas.57 The
58
SPLEEN
The fetal spleen can be visualized as an echogenic organ
in the left upper abdomen, lateral to the spine and the
upper renal pole. The relationship to the fetal stomach
can vary (Fig. 38-1, D). Nomograms are available for
splenic size from 18 weeks until term.
59,60
Abnormalities
of the fetal spleen (asplenia or polysplenia) are associated
with heterotaxy syndromes and warrant a detailed fetal
cardiac examination. Splenomegaly in isoimmunized
fetuses correlates to the severity of fetal anemia.
addition, splenomegaly in utero has been reported due
to viral infection.
62
61
In
SMALL BOWEL AND COLON
In the first trimester and early in the second trimester,
the small and large bowel appear somewhat heterogeneous, with echogenicity similar to but increased, compared to liver (see Fig. 38-1). Later in pregnancy, fluid
can be seen in small bowel loops. Meconium can be seen
Duodenal Stenosis and Atresia
Dilation of the duodenum resulting from stenosis
(obstruction) or atresia is the most common bowel
obstruction in the fetus; occurring in 1 or 2 per 10,000
live births.
between 34% and 57% were diagnosed prenatally.
Other anomalies are usually involved; most notably,
30% to 44% have trisomy 21.
duodenal atresia have also been reported.
63-65
Of cases reported up through the 1990s,
63,67
Familial cases of
70
Duodenal
66-69
atresia is also associated with anomalies of the VACTERL
spectrum (vertebral abnormalities, anal atresia, cardiac
abnormalities, TE fistula, renal agenesis, limb defects).
71,72
Diagnosis of duodenal stenosis is most common in
the third trimester. In the early second trimester, falsenegative diagnoses as well as false-positives have been
reported.
73,74
The infrequent diagnosis in the second trimester may be caused by the relatively small amount of
swallowed amniotic fluid by the fetus at this time. In
the early second trimester, the fetus normally swallows
2 to 7 mL of fluid, compared to 450 mL at term.75
Duodenal obstruction may result from preampullary
obstruction, a diaphragm or web causing partial or
complete obstruction, or complete absence of a duodenal segment.
76-79
The classic “double bubble” sign of a second echo-
lucent mass medial to the stomach (in a transverse view
of fetal abdomen) is considered diagnostic of duodenal
obstruction. This image represents the dilated duodenum proximal to the atretic area. Because an abdominal
fluid collection can have other etiologies, it is important
to demonstrate a continuum between the stomach
and the cystic mass. A prominent incisura angularis of
the stomach may be mistaken for a “double bubble” if
these are in different planes, but a careful real-time longitudinal examination of the stomach can eliminate this
possibility. Apparent double-bubble sign is also associated with postnatal diagnoses of choledochal cyst and
duodenal duplication cyst.
have resolved in pregnancy, with normal outcomes.
67,80
Second-trimester cases
73,74
Double-bubble sign has been found the late second or
the third trimester in fetuses with echogenic bowel, in
both those with trisomy 21 and fetuses with normal
karyotypes
81
(Fig. 38-11).
When duodenal atresia is suspected based on a
“double bubble,” the presence of polyhydramnios significantly increases the likelihood of a correct diagnosis.
Polyhydramnios is frequently present in cases of duodenal atresia by the late second trimester,
66,82,83
but typically is absent in the early second trimester, at the time
of routine fetal survey. In a European study of 138 cases
of postnatally confirmed duodenal atresia, polyhydramnios was present in only 33%.
58
In this series, the
Chapter 38 ■ The Fetal Abdominal Wall and Gastrointestinal Tract 1335
S
E
D
I
A
D
S
C
B
FIGURE 38-11. Duodenal atresia in a fetus
with trisomy 21. A, Transverse fetal pelvis at 18
weeks with echogenic bowel (arrow E). The image of
the bowel is taken in a plane to include iliac crest (arrow
I) for comparison. B, Same fetus at 21 weeks. Transverse
view of abdomen with stomach (arrow S) on left and
fluid-filled duodenum (arrow D). C, Same fetus at 25
weeks. There is a “double bubble.” The stomach is
visible inferiorly (S), with the dilated proximal duodenum (D) visible crossing the midline.
pregnancies with polyhydramnios were also more likely
to be born preterm. Finding the double-bubble sign
should trigger genetic counseling and consideration of
amniocentesis because of the association with trisomy
21. Careful renal and cardiac testing should be performed, including fetal echocardiography.
Jejunal and Ileal Atresias
The prevalence of jejunoileal atresias (usually reported
together) range from .54 to 1.11 cases per 10,000 live
84
births.
Jejunal atresias are slightly more common (51%)
than ileal.85 The most common etiology hypothesized for
jejunoileal atresias is isolated vascular compromise.
animals, induced vascular compromise leads to isolated
bowel atresias.
87
Jejunal atresias have been associated
86
In
with nonbowel anomalies in up to 42% of cases, with
ileal obstructions associated with nonbowel anomalies
only in up to 2%.
58,88
Jejunal atresias, however, are more
likely to be multiple and less often associated with in
utero perforation than ileal atresias, likely because of
the lower compliance of the ileum. “Apple peel”
jejunal atresia is a subtype that involves agenesis of the
mesentery, is more often familial,
58,89,90
and is likely of a
1336 PART IV ■ Obstetric Sonography
1
FIGURE 38-12. Ileal atresia. Transverse fetal abdomen
with multiple dilated loops of bowel. The bowel lumen is measured in the largest transverse diameter (calipers).
FIGURE 38-13. Hirschsprung disease. Note multiple
dilated loops of bowel throughout the abdomen.
different etiology. Cystic fibrosis (CF) is a common
underlying etiology for ileal obstruction, with or without
meconium-increased echogenicity noted prenatally.
In ileal obstructions without meconium echogenicity,
the frequency of CF in newborns is 6% to 8%.
81,91
92-94
Diagnosis of jejunoileal obstruction is based on
dilated loops of bowel, most frequently without a dilated
stomach and sometimes with hyperperistalsis (Fig.
38-12). If peristalsis is not observed, dilated small bowel
can be difficult to distinguish from dilated colon. The
top normal lumen diameter used to diagnose bowel dilation is 7 mm.81 The diagnosis of jejunoileal atresia is
typically not made until late in the second trimester,
when the bowel dilates. Polyhydramnios is less common
in lower bowel obstructions than in duodenal atresia, not
occurring in any reported ileal atresias,
in one third of jejunal atresias.
95
95
but occurring
Anorectal Atresias
Of the large colon atresias, anorectal atresia is the most
common. The incidence is 0.8 to 4 per 10,000 live
96
births.
obstruction have also been noted.
mations have the highest incidence of associated anomalies of any of the GI atresias, 48% to 98%.
Isolated cases of prenatal diagnosis of midcolon
97
Anorectal malfor-
96,98,99
The
associated abnormalities are chromosomal and genitourinary. Additionally, anal atresia is a part of the VACTERL
sequence.
as for upper bowel obstructions, with anal atresia detected
in only 7% to 24% of affected fetuses.
98-100
However, prenatal detection is not as high
68,93,101
In prenatally detected cases, there are dilated loops of
small bowel or colon in the absence of polyhydram-
102,103
nios.
In a large series of neonates diagnosed post-
natally with VACTERL association, none of the fetuses
with anorectal atresia were detected prenatally.
of the association of colonic obstruction with non-GI
anomalies, a detailed fetal survey, fetal echocardiogram,
genetic counseling, and discussion of aneuploidy risk
should be included in the management of suspected
cases in utero.
Megacystis and Microcolon
In megacystis-microcolon–intestinal hypoperistalsis
syndrome, there is a distended bladder and at times a
dilated small bowel. There is a 4:1 female predominance,
which aids in distinguishing the large bladder associated
with posterior urethral valves. Magnetic resonance
imaging (MRI) can be helpful in identifying the micro-
105,106
colon.
Hirschsprung disease (congenital megacolon) can be detected in utero. In these cases, there are
multiple dilated loops of bowel (Fig. 38-13). Hirschsprung
disease or congenital aganglionosis of a segment of the
colon can cause functional bowel obstruction.
Echogenic Bowel
Hyperechogenicity of the bowel is described when echoes
of the bowel are as echogenic as the iliac crest with the
ultrasound gain at the lowest gain, where bone looks
white in the second trimester of pregnancy (Fig. 38-14;
see also Fig. 38-11, A; Video 38-1). Use of a high-
frequency probe (8 MHz) increases the frequency of
interpreting fetal bowel as echogenic.
5 MHz) probe should be used to confirm this finding.
(≤
107
A low-frequency
When strict diagnostic criteria are used, the incidence
of echogenic bowel in a general obstetrics population is
0.2% to 0.7%.
93,108
As the echogenicity of normal bowel
104
Because
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