Introduction

Intraabdominal solid masses and cystic lesions are not commonly identified during the routine 20-week anomaly ultrasound (US) scan and are uncommon findings at later gestations. However, intraabdominal masses occasionally are seen as an incidental finding during a third-trimester US scan assessing fetal growth and wellbeing. Potential differential diagnoses are numerous, but the differential diagnosis typically can be restricted through a detailed assessment of the site and appearance of the lesion. Prenatal intervention is not indicated in most circumstances, but further postnatal investigation or surgical repair may be required shortly after birth, so effective prenatal diagnosis avoids delay in treating the neonate.

Disease

Definition

An intraabdominal mass is a space-occupying lesion within the abdominal cavity that appears either cystic or solid.

Prevalence and Epidemiology

Intraabdominal masses are rare. The prevalence of congenital anomalies, such as bowel atresias, is low. Duodenal, small and large bowel, and rectoanal atresias affect 5.1 : 10,000 births, accounting for 2.2% of congenital anomalies. The prevalence of atresia of the common bile duct is even lower (0.3 : 10,000 births).

Some lesions, such as ovarian cyst or hydrometrocolpos, affect only female fetuses. A significant ovarian cyst is subjectively defined as greater than 2 cm in diameter and occurs approximately in 4 : 10,000 female live births. Choledochal cysts are more common in females (4 : 1 prevalence) and in Asian populations. Other anomalies, such as enteric duplication cysts, are more common in males than in females (2 : 1). However, because of the low birth prevalence, it is often difficult to determine accurate epidemiologic differences between populations. Abdominal cysts are discussed in more detail in Chapter 24 .

The most common echogenic intraabdominal mass is echogenic bowel ( Chapter 22 ). In contrast to other intraabdominal masses, this acquired anomaly may be seen at the 20-week scan and has a prevalence of 0.3% at this gestation. Greater than 80% of fetuses with echogenic bowel have no underlying pathology, but there are associations with chromosomal abnormality, cystic fibrosis, fetal infection, and intrauterine growth restriction.

Etiology and Pathophysiology

The etiology of intraabdominal masses varies widely depending on the organ or system involved. Numerous abnormalities, in particular, cystic masses, are truly congenital with failure in the development of hollow viscera, such as a portion of the bowel (e.g., duodenum, small or large bowel, rectum-anus; Chapter 26 ), or of drainage channels (e.g., common bile duct; Chapter 25 ). Most of these anomalies, with the exception of duodenal atresia, are not associated with chromosomal abnormality.

Small bowel atresia is thought to result from an episode of vascular impairment during embryologic development. It may occur in isolation or in association with gastroschisis (the cause of which is also considered to be a vascular accident), or a volvulus. In contrast, enteric duplication cysts appear to arise from a failure of separation between the notochord and endoderm, which explains an association with vertebral anomalies. Some congenital anomalies, such as cystic fibrosis, cause secondary changes that are visible as an intraabdominal mass. The increased echogenicity of the bowel is acquired owing to thick, abnormally viscous meconium, and the development of a pseudoobstruction.

Some intraabdominal masses are acquired rather than congenital. The inflammatory response to fetal infection can lead to the development of echogenic bowel and foci of calcification. The obstructed or hypoxic small bowel may become distended, and perforation may lead to a sterile chemical peritonitis with calcified foci being seeded through the peritoneal cavity as part of the inflammatory response. These foci represent a subacute sign of injury that may take a few weeks to evolve (see Chapters 22 and 26 ).

Focal calcification is also occasionally seen within the liver, with a prevalence of approximately 6 : 10,000 fetuses (see Chapters 23 and 28 ). These calcifications may result from localized vascular disruption within the liver causing infarction or ischemia and subsequent fibrosis and calcification. Calcifications are generally found in three sites: on the surface of the liver, where they may be associated with meconium peritonitis; as discrete lesions within the liver capsule, associated with vascular emboli; or more diffusely throughout the liver parenchyma as a result of more widespread ischemia and necrosis that may occur secondary to fetal infection.

Ovarian folliculogenesis occurs from 20 weeks' gestation, and fetal ovarian cysts are often not recognized until the third trimester. The hypothalamic-pituitary-ovarian endocrine axis is active from the end of the first trimester, and cyst formation is thought to be related to gonadotropin, placental human chorionic gonadotropin, or placental estrogen release.

Tumors are rarely seen in the fetus, but hemangioma (60%), mesenchymal hamartoma (23%), and hepatoblastoma (17%) are the most common among perinatal hepatic tumors (see Chapter 28 ). Neuroblastoma and teratoma have also been reported, but are rare, except for sacrococcygeal teratomas that often have a pelvic component ( Chapter 31 ). Hepatic tumors may manifest as a solitary or multifocal hypoechoic or hyperechoic mass within the liver and may have associated areas of calcification. Hepatoblastoma is associated with increased alpha-fetoprotein, and this may be reflected in maternal serum alpha-fetoprotein levels.

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