I. Isolated intestinal tube echo enhancement is mostly normal Fetal intestinal tube echo enhancement is a non-specific ultrasound sign. In more than 80%-90% of fetuses with ultrasound suggestive of simple intestinal echogenicity, the cause is not detected prenatally and the newborn is normal at birth with normal intestinal tract. When intestinal echo enhancement is not an isolated ultrasound sign, the fetus is most likely to have an underlying pathological condition. Second, the pathological condition of fetal intestinal canal echogenicity enhancement 1, blood in the intestinal cavity: after placental and meconium bleeding, there may be blood or blood components (hematocrit, cellular debris) in the amniotic fluid. Since blood produces very strong echogenicity, when the fetus swallows this amniotic fluid, the intestinal canal may show strong echogenicity. An ultrasound showing subchorionic fluid or strong echogenic material in the fetal stomach is indicative of enhanced intestinal echogenicity originating from intra-amniotic hemorrhage. Intra-amniotic hemorrhage is not necessarily associated with vaginal bleeding. 2. Aneuploidy: The detection rate of aneuploidy in fetuses with enhanced intestinal echogenicity has been reported to be 3%-25%. Intestinal tube echogenicity enhancement in aneuploid fetuses may be due to decreased intestinal motility and increased water absorption, as these alterations in intestinal function have been reported in aneuploid neonates. Two categories of fetuses are at highest risk for aneuploidy: 1) those with structural abnormalities, such as heart defects and duodenal atresia, and 2) those with ultrasound findings that suggest multiple “soft” indicators of aneuploidy, such as strong echogenic foci in the cardiac cavity, dilated renal pelvis, and slightly shortened humerus or femur. The most frequently detected aneuploidy is trisomy 21, which accounted for 17 (71%) of the 24 fetuses with clinically significant chromosomal abnormalities in a large case series that included intestinal echogenicity. Other aneuploidies were detected at a lower rate in fetuses with enhanced gut echo, including 45X, 13-trisomy, 18-trisomy, triploidy, and chimerism. 3. Cystic fibrosis: In cystic fibrosis (CF), abnormal secretion of pancreatic enzymes can lead to thick and sticky fetal feces and decreased intestinal peristalsis in the small intestine, so cystic fibrosis may be the cause of fetal intestinal tube echogenicity enhancement. Several case series have shown that CF is present in approximately 3% of fetuses with enhanced intestinal echogenicity, although a prevalence as high as 7.6% has also been reported. This is significantly higher than the expected prevalence in whites (1 in 2000-3000 live births). 4. Fetal growth restriction: Echo enhancement of the fetal gut can indicate fetal growth restriction (FGR). in FGR, fetal blood flow is redistributed toward vital organs (brain, heart, adrenal glands, placenta). Reduced perfusion of the fetal intestine may cause enhanced fetal intestinal tube echogenicity. Growth restriction is present in 4%-21% of fetuses with enhanced gut echo. A case-control study evaluating early signs of FGR found that the detection rate of enhanced fetal gut echo was 10 times higher in fetuses with estimated weight in the lowest quartile than in those with estimated weight greater than or equal to the 25th percentile. The prognosis for fetal gut echo enhancement with FGR is poor, especially in midterm pregnancies where low amniotic fluid and elevated maternal serum methemoglobin are detected. The prognosis is very poor, especially in midterm pregnancies with low amniotic fluid and elevated maternal serum alpha-fetoprotein. 4%-8% of fetuses with a combination of enhanced gut echo and early FGR die in utero. 5. Infection: Congenital infection can cause enhanced intestinal echogenicity by direct injury to the fetal intestine or by other potential sequelae (e.g. ascites, FGR). Ascites can enhance the echogenicity of abdominal structures (e.g., intestinal canal). Congenital infections are likely the least common cause of echogenic enhancement of the intestinal canal. The most commonly detected infectious agent in fetuses with echogenic enhancement of the intestinal canal is cytomegalovirus (CMV), toxoplasmosis is rare, and microviruses, varicella and herpes simplex infections have been reported, but are rare. 6. GI obstruction: anatomic structural or functional GI obstruction may result in enhanced absorption of fluid from the fetal feces in the obstructed intestine, resulting in enhanced intestinal echogenicity; however, the more typical ultrasound signs of small bowel obstruction are dilated intestinal collaterals filled with fluid and excess amniotic fluid. According to case reports and small case series studies, GI malformations associated with enhanced intestinal echogenicity include biliary atresia, intestinal or anal atresia, intestinal torsion, cloacal defects, and abdominal fissures. Fetal intestinal echogenicity is also associated with Hashburn’s disease. 7. Rare etiology: Fetuses with alpha-thalassemia have been reported to have enhanced intestinal echogenicity. The possible cause is severe anemia and hypoxemia causing intestinal edema, which subsequently leads to enhanced intestinal echogenicity. Intestinal tube echogenicity enhancement is occasionally seen in fetuses with visceral malformations with normal digestive tract and in pregnancies complicated by various placental or maternal disorders.