Gastrointestinal & Abdominal Wall

A systematic Level II assessment of the fetal gastrointestinal (GI) tract includes the stomach, bowel, abdominal contour, abdominal wall insertion, and amniotic fluid volume. Bowel findings must always be interpreted in the context of gestational age and overall fetal anatomy.

Physiologic midgut herniation

During early development the rapidly growing intestine temporarily herniates into the base of the umbilical cord. This physiologic umbilical herniation is normally present in the first trimester and should resolve by about 11–12 weeks. A persistent midline abdominal wall mass after this period suggests an omphalocele or other pathologic defect.

Normal stomach and small bowel

• Stomach typically visualized in the left upper abdomen as an anechoic, round or ovoid structure.
• Size varies with swallowing and gastric emptying; occasional transient nonvisualization may be normal.
• Small bowel loops are usually low echogenicity, with a “speckled” pattern, and diameter generally < 7 mm.

Normal colon

• Colon develops increasing echogenicity and haustral markings in the third trimester.
• Filled with hypoechoic to mildly echogenic meconium close to term.

An apparently “normal” GI tract on ultrasound does not completely exclude atresias or functional disorders, especially when obstruction is partial or late in onset. Serial imaging and postnatal follow-up may still be warranted based on clinical context.

The fetal stomach is expected to be seen in the left upper abdomen on routine surveys. Deviations in visibility, size, or position may suggest structural or functional abnormalities.

Nonvisualization of the stomach

• Transient nonvisualization can be normal, particularly early in gestation or between swallowing cycles.
• Persistent nonvisualization (on repeated scans) may be associated with:
  • Esophageal atresia or tracheoesophageal fistula (TEF).
  • Severe oligohydramnios (e.g., renal agenesis, severe early PPROM).
  • CNS anomalies or neuromuscular disorders severely limiting swallowing.

Enlarged stomach / “gastric outlet” concerns

• Markedly enlarged stomach with little distal bowel filling may suggest distal obstruction (e.g., duodenal atresia).
• Look for:
  • “Double bubble” sign (stomach + proximal duodenum).
  • Polyhydramnios.
  • Associated anomalies or aneuploidy markers.

Position

• Right-sided or midline stomach may accompany situs abnormalities or diaphragmatic hernia.
• Confirm cardiac situs and overall thoracoabdominal arrangement when the stomach is not left-sided.

Any persistent abnormality of stomach visualization (absent, markedly enlarged, malpositioned) should prompt a comprehensive anatomic survey and consideration of aneuploidy and syndromic associations depending on the pattern.

Dilated fetal bowel is a descriptive term, usually reserved for small bowel loops with an internal diameter ≥ 7 mm. The finding may represent mechanical obstruction, functional ileus, or inflammatory processes.

Key sonographic points

• Measure the internal diameter of the most dilated loop in a transverse plane.
• Assess:
  • Number of dilated loops (focal vs diffuse).
  • Wall thickness and echogenicity.
  • Associated ascites or calcifications (e.g., meconium peritonitis).
  • Polyhydramnios (upper GI obstruction) vs normal or low fluid (more distal obstruction).

Key differentials for dilated bowel

• Jejunal or ileal atresia / stenosis.
• Meconium ileus (often associated with cystic fibrosis).
• Volvulus or internal hernia (may have rapid evolution and concerning sonographic changes).
• Infectious or inflammatory ileus (e.g., viral infections, meconium peritonitis).

Isolated mild bowel dilatation can be transient. Progressively increasing bowel diameter, thickened walls, ascites, or calcifications increase concern for significant obstruction or meconium peritonitis and warrant closer follow-up and neonatal surgical planning.

Intestinal atresias may occur anywhere from the duodenum to the colon. Sonographic clues depend on the level of obstruction and may be absent in partial or very distal lesions until late in gestation.

Duodenal atresia (“double bubble”)

• Classic “double bubble” sign: distended stomach and proximal duodenum, with little or no distal bowel gas/fluid seen.
• Frequently associated with:
  • Polyhydramnios (impaired intestinal absorption of swallowed fluid).
  • Aneuploidy, especially trisomy 21, and other structural anomalies.
• Can be unilateral or bilateral when associated defects are present (e.g., annular pancreas, other GI anomalies).

Jejunal / ileal atresia

• Multiple markedly dilated small bowel loops, often more irregular in distribution than duodenal obstruction.
• Polyhydramnios may occur, but is less constant than for proximal obstruction.
• Meconium peritonitis or intra-abdominal calcifications may point to in utero perforation.

Colonic obstruction

• Less conspicuous prenatally; may present with enlarged, echogenic colon in late gestation.
• Can be associated with anorectal malformations or Hirschsprung disease.

Intestinal obstruction has a broad prognosis spectrum depending on level, associated anomalies, and timing. With modern neonatal surgery, isolated atresias often have good outcomes, whereas complex or syndromic cases may be more challenging.

Echogenic bowel refers to fetal bowel that appears as bright as, or brighter than, adjacent bone when ultrasound settings are optimized. It is a sonographic marker rather than a specific diagnosis, associated with multiple conditions and, frequently, normal variants.

Technical considerations

• Compare bowel echogenicity to that of adjacent iliac bone at similar depth and gain.
• Beware of artifact from high gain or suboptimal presets, which can mimic echogenic bowel.

Key associations

• Aneuploidy (especially trisomy 21) in some series.
• Intrauterine infection (e.g., CMV, toxoplasmosis, parvovirus).
• Cystic fibrosis and meconium ileus.
• Intra-amniotic bleeding (swallowed blood products).
• Growth restriction or placental insufficiency.
• Normal variant (particularly when isolated and mild).

Approach to isolated echogenic bowel

• Confirm echogenicity with optimized settings and appropriate comparison to bone.
• Review:
  • Aneuploidy screening results.
  • Maternal infection history and serologies where indicated.
  • Family or ethnic risk factors for cystic fibrosis, and carrier screening as appropriate.
  • Fetal growth trajectory and Doppler results.
• Serial growth surveillance is commonly recommended.

Isolated mild echogenic bowel with reassuring aneuploidy and infection evaluation, normal growth, and no additional anomalies often has a favorable outcome. Persistent or marked echogenicity, especially with growth restriction or other findings, deserves closer attention.

Meconium peritonitis results from intrauterine bowel perforation with leakage of meconium into the peritoneal cavity, leading to inflammation and sometimes calcification. Meconium ileus, often associated with cystic fibrosis, is a frequent underlying cause.

Sonographic features

• Intraperitoneal calcifications (often echogenic foci in the abdomen).
• Free fluid or large loculated ascites; sometimes meconium pseudocyst formation.
• Associated dilated bowel loops.

Clinical considerations

• Screening for cystic fibrosis where indicated.
• Evaluation for associated obstruction or atresia.
• Planning for delivery in a center with neonatal surgery and NICU support.

Many fetuses with meconium peritonitis and appropriate postnatal care can have good outcomes, although the spectrum of severity is broad and depends on underlying pathology and associated conditions.

Fetal ascites (free fluid in the peritoneal cavity) may occur in isolation or as part of hydrops fetalis. The GI tract is one of several potential sources when ascites is identified.

GI-related causes of ascites

• Meconium peritonitis / bowel perforation.
• Severe bowel obstruction with serosal leakage.
• Hepatic or portal anomalies (less common in a purely GI module but part of the abdominal differential).

A full evaluation for hydrops (cardiac function, anemia, infection, chromosomal differences, lymphatic and genitourinary causes) should accompany any case of significant ascites.

Isolated fetal ascites is uncommon and has a broad differential. Identification of a GI etiology relies on careful interrogation of bowel loops, stomach, abdominal wall, and associated findings (e.g., calcifications).

An omphalocele is a midline abdominal wall defect at the base of the umbilical cord, with herniation of abdominal viscera into a sac composed of peritoneum and amnion. The umbilical cord inserts into the apex of the sac.

Sonographic features

• Midline mass at the umbilical ring containing liver and/or bowel.
• Thin, echogenic membrane surrounding the herniated viscera.
• Umbilical cord inserting into the membrane rather than the abdominal wall.
• Polyhydramnios is not uncommon in larger lesions.

Associated anomalies & considerations

• High rate of associated structural anomalies and aneuploidy (including trisomies 13 and 18).
• Association with multiple syndromes (e.g., pentalogy of Cantrell, Beckwith–Wiedemann).
• Prognosis depends on size of defect, liver involvement, associated anomalies, and karyotype.

Distinguishing omphalocele from physiologic midgut herniation in the first trimester and from gastroschisis in the second trimester is critical for counseling and management planning.

Gastroschisis is an abdominal wall defect typically located to the right of a normally inserted umbilical cord, allowing herniated bowel to float freely in the amniotic cavity without a covering membrane.

Sonographic features

• Defect in the abdominal wall, usually right of the cord insertion.
• Free-floating bowel loops in the amniotic fluid, often thickened or dilated with time.
• Umbilical cord inserts normally into the abdominal wall (separate from the defect).

Clinical course & associations

• Typically not associated with chromosomal anomalies.
• Associated risks:
  • Intrauterine growth restriction.
  • Preterm delivery.
  • Bowel atresia, stenosis, or perforation due to vascular compromise.
• Survival is generally high in modern surgical series, but morbidity related to bowel function can be significant.

Serial assessment of fetal growth, amniotic fluid volume, and bowel appearance is common. Delivery planning in a center with neonatal surgery and NICU support is recommended.

Less common abdominal wall defects include body stalk anomalies and very large defects with limb or spine abnormalities. These often carry a poor prognosis and are frequently associated with additional malformations.

• Body stalk or limb–body wall complex:
  • Large ventral wall defect with evisceration of organs, very short or absent umbilical cord, and associated spinal or limb anomalies.
  • Prognosis is typically poor.
• Complex ventral wall defects:
  • Occasionally overlap features of omphalocele, gastroschisis, and other anomalies.
  • Detailed imaging and multidisciplinary counseling are important.

Cystic masses in the fetal abdomen can arise from the biliary tree, mesentery, gastrointestinal tract, ovary, or other structures. Location, relationship to adjacent organs, and internal features help narrow the differential.

Selected entities

• Choledochal cyst:
  • Cystic structure in the right upper quadrant near the porta hepatis.
  • May communicate with the biliary tree on detailed imaging.
• Enteric duplication cyst:
  • Cystic lesion in the abdomen sharing a wall with the GI tract.
  • “Double wall” or “muscular rim” sign may be seen.
• Mesenteric or omental cyst:
  • Cystic mass that may displace bowel loops but does not clearly arise from a solid organ.
• Ovarian cyst (in female fetuses, usually late gestation):
  • Anechoic or complex cyst in the pelvis, often unilateral.
  • May be associated with maternal hormonal stimulation; usually benign but at risk of torsion when large.

Most isolated fetal abdominal cysts have a good prognosis, particularly when small and without associated anomalies. Serial imaging and postnatal ultrasound help clarify the underlying diagnosis and guide management.