Diagnostic ultrasound ( PDFDrive )

1322 PART IV Obstetric and Fetal Sonography
A
B
FIG. 38.26 Splenic Cyst. (A) Oblique transverse color Doppler image through the fetal abdomen at 34 weeks shows a simple cyst (arrow) in
the left upper quadrant. The arrowheads outline the diaphragmatic surface of the spleen. The kidney was clearly separate from the mass. (B)
Coronal image of the neonatal abdomen conirms that the cyst is in the spleen (arrowheads) and separate from the left adrenal and left kidney.
See also Video 38.11.
these cysts, when detected antenatally, should be followed by
serial ultrasound. Detailed anatomic assessment is indicated for
the presence of associated anomalies or cysts involving other
organs such as kidneys and liver.
ABDOMINAL WALL
he most common types of abdominal wall defects are gastroschisis
and omphalocele. Other, less common types include
bladder exstrophy, cloacal exstrophy, ectopia cordis, and more
severe ventral body wall defects including pentalogy of Cantrell,
body stalk anomaly, and abdominoschisis in amniotic band
syndrome. he overall incidence of abdominal wall defects is
6.3 per 10,000 pregnancies. 180 Because of the loss of integrity in
the epidermal covering, abdominal wall defects are associated
with elevated levels of maternal serum alpha-fetoprotein (MS-
AFP). In the past 3 decades, with both maternal serum screening
and fetal anatomic surveys becoming routine, the majority of
abdominal wall defects are diagnosed by the second trimester.
Centers that practice universal irst-trimester screening have
documented conirmation of diagnoses earlier than 14 weeks. 14,181
With increased access to early scanning, earlier diagnosis is
expected to become more common.
Embryology
he embryonic abdominal wall develops from the lateral plate
mesoderm and ectoderm between day 16 and day 26 of embryonic
life. Each lateral plate of mesoderm splits into parietal and visceral
layers, the space between which becomes the body cavity (coelom
or celum), which later diferentiates into the peritoneal, pericardial,
and pleural cavities. 182-184 he lateral folds (consisting of
the parietal layer of the lateral plate mesoderm and the overlying
ectoderm) then fold around the coelom caudally, cephalad, and
laterally. In the normal enfolding process, the lateral folds come
together and fuse to form the ventral body wall. Failure of this
process to be completed because of teratogenic or vascular factors
lead to a defect in the ventral body wall. Depending on the
location of the defect in the ventral abdominal wall, the result
can be gastroschisis (abdominal region), ectopia cordis (thoracic
region), or bladder exstrophy (pelvic region).
In parallel to the development of the ventral body wall, rapid
growth and elongation of the bowel takes place, and the abdominal
cavity is temporarily too small to accommodate all of its contents.
his results in transient protrusion of the intestine into the
extraembryonic coelom at the base of the umbilical cord, a process
termed physiologic midgut herniation 185 (Figs. 38.27 and 38.28).
his herniation is usually visible on ultrasound from 9 to 11
weeks and resolves (or undergoes reduction) by 12 weeks of
gestation. 181,186 herefore if prominent material is seen at the
cord insertion site, and it is unclear whether this inding represents
an abdominal wall defect or physiologic bowel herniation, a
follow-up scan in 1 to 2 weeks will resolve the issue. Failure of
the gut loops to return to the body cavity beyond that point has
been suggested as the underlying cause in cases of omphalocele. 184
hus persistence of the midgut herniation beyond 12 weeks or
the presence of content other than intestine (e.g., liver) in the
herniation should be considered as evidence of true abdominal
wall defect (i.e., omphalocele).
Gastroschisis
Gastroschisis is a relatively small (<4 cm in most cases), fullthickness
paraumbilical defect of the abdominal wall, most oten
located to the right of the umbilicus. Free-loating loops of bowel
in the amniotic luid are the key inding on ultrasound.
Epidemiology
In population-based studies in Europe, Australia, and Japan,
the incidence of gastroschisis has increased from 0.4 to 1.6