DOI: 10.1148/rg.253045124
RadioGraphics 2005;25:633-645
© RSNA, 2005
Intraabdominal Fetal Echogenic Masses: A Practical Guide to Diagnosis and Management1
Ann McNamara, MB, FFR (RCSI) and
Deborah Levine, MD
1 From the Department of Radiology, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Ave, Boston, MA 02215. Recipient of a Certificate of Merit award and an Excellence in Design award for an education exhibit at the 2002 RSNA Scientific Assembly. Received June 3, 2004; revision requested August 5 and received September 2; accepted September 8. All authors have no financial relationships to disclose.
Address correspondence to D.L. (e-mail: dlevine{at}bidmc.harvard.edu).
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Abstract
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Intraabdominal calcifications and other echogenic masses are relatively common findings during fetal sonography. Many are associated with no additional risk for the fetus or neonate. They may arise from the liver, gallbladder, spleen, kidneys, adrenal glands, gastrointestinal tract, or peritoneal cavity. Detection of such lesions should prompt a detailed survey for additional findings and a review of the maternal history. In some cases, fetal karyotyping may be indicated. In most cases, the diagnosis, management, and outcome are determined according to a combination of specific ultrasound appearances and at least one additional maternal or fetal factor. In utero diagnosis can often be achieved with careful evaluation of the lesion echotexture, associated calcifications, additional findings, and evolution over time. In most cases, expectant management is sufficient, but some patients require transfer to a facility where early postnatal intervention is available. A systematic approach to the findings aids in differential diagnosis and management.
© RSNA, 2005
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LEARNING OBJECTIVES
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After reading this article and taking the test, the reader will be able to:
- List the differential diagnoses for echogenic bowel in the fetus.
- Describe the possible causes of hepatic and peritoneal calcifications.
- Discuss the features that allow differentiation between adrenal hemorrhage and neuroblastoma.
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Introduction
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The fetal abdomen is a common site for congenital anomalies. Many of these lesions can be documented during routine examination of the fetus, particularly in the current era of high-quality scanning equipment combining variable-frequency transducers with improved spatial resolution compared to that available with earlier scanning equipment. Improved visualization of the intraabdominal structures can, however, lead to documentation of previously undetected anomalies and normal variants.
Fetal abdominal echogenic lesions are common, and many carry little or no additional risk to the fetus or neonate. Accurate presumptive in utero diagnosis can be made with careful evaluation of the lesion echotexture, associated calcifications, additional findings, and evolution over time. The purpose of this review is to illustrate a practical approach to the interpretation and management of echogenic lesions observed within the fetal abdomen. Such lesions include echogenic bowel, gastric pseudomass, abdominal calcifications, noncalcified liver lesions, enteric duplication cysts, and lesions of the adrenal region.
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Echogenic Bowel
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Echogenic bowel is the most common echogenic mass in the fetal abdomen. To ensure that the bowel is truly echogenic, it must be as bright as adjacent bone. This finding is seen in 1% of second-trimester fetuses (1). It is seen predominantly in the lower fetal abdomen and pelvis as a uniformly hyperechoic, well-defined lesion that does not shadow (Fig 1). In about 50% of cases of isolated echogenic bowel, the appearance resolves over time with no clinical sequelae. The use of high-frequency transducers can increase the finding of echogenic bowel (2). Vincoff et al (2) showed that use of an 8-MHz transducer (compared to 4 MHz) simulated echogenic bowel in 63% of fetuses examined. An additional problem in interpretation of the significance of echogenic bowel is the wide interobserver variability in the diagnosis in the same patient (3). When echogenic bowel is found in the third trimester, it is commonly a normal variant, since meconium in the colon can be echogenic (Fig 2).
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Figure 1a. Echogenic bowel. (a) Sagittal sonogram obtained at 20 weeks gestation shows a bright mass in the fetal pelvis (arrows), a finding consistent with echogenic bowel. The bowel is as bright as bone. (b) Axial sonogram of the lower abdomen of another fetus, obtained at 22 weeks gestation, shows the masslike appearance of echogenic bowel.
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Figure 1b. Echogenic bowel. (a) Sagittal sonogram obtained at 20 weeks gestation shows a bright mass in the fetal pelvis (arrows), a finding consistent with echogenic bowel. The bowel is as bright as bone. (b) Axial sonogram of the lower abdomen of another fetus, obtained at 22 weeks gestation, shows the masslike appearance of echogenic bowel.
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Figure 2. Meconium in the colon. Coronal sonogram of the abdomen, obtained at 34 weeks gestation, shows that the colon has an echogenic appearance. Unlike echogenic bowel in the second trimester, this appearance is almost always a normal finding.
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Therefore, when echogenic bowel is suspected, before you decide that it is a real finding, check the transducer frequency, look at adjacent bone, and check the gestational age. Once the decision has been made that the bowel truly is echogenic in a second-trimester fetus, then differential diagnostic considerations include cystic fibrosis, chromosomal abnormalities, intraamniotic bleeding, and congenital infection (4,5).
Intraamniotic bleeding with subsequent swallowing of blood by the fetus can lead to echogenic bowel. Assessment for evidence of intraamniotic bleeding such as amniotic fluid debris and echogenic material in the stomach is potentially helpful. However, it has not been documented that the finding of intraamniotic bleeding significantly lessens the risk for other causes of echogenic bowel; therefore, we still perform a thorough evaluation of the fetus.
It is important to assess for morphologic abnormalities that would suggest aneuploidy and for signs of hydrops, which would suggest infection. Parental carrier status for cystic fibrosis and fetal karyotyping may be quite useful. When amniotic fluid is obtained, an extra 3 mL should be withdrawn for testing for infection, such as cytomegalovirus. If results of investigations are negative, follow-up ultrasound (US) in the third trimester is performed to document appropriate interval growth, since echogenic bowel may be associated with intrauterine growth restriction.
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Gastric Pseudomass
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At US examination from the second trimester onward, the fetal stomach appears as a uniformly anechoic, sharply circumscribed round structure in the left upper quadrant. However, debris is commonly visualized in the stomach, forming a pseudomass (Fig 3).
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Figure 3. Gastric pseudomass. Sagittal sonogram obtained at 18 weeks gestation shows a clump of debris in the fetal stomach (arrow). During real-time imaging, the debris was seen to move within the stomach. This finding resolved during follow-up.
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The origin of echogenic masses within the gastric lumen is incompletely understood. As they are seen in multiple planes, technical issues are unlikely. They may be due to swallowed cells that aggregate because of the relatively poor peristaltic activity in the stomach early in the second trimester (6). When intraamniotic bleeding has occurred, these pseudomasses are commonly visualized. They inevitably disappear during follow-up examinations and are not associated with an adverse neonatal outcome. Therefore, further evaluation of this finding is not required.
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Abdominal Calcifications
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The initial consideration when calcifications are visualized within the fetal abdomen is whether they are scattered in the abdomen and/or associated with a mass, or if they are in the liver. These issues are addressed below.
Meconium Peritonitis
The diagnosis of meconium peritonitis is made when scattered calcifications are seen throughout the peritoneum. The calcifications may be seen to line the liver (Fig 4). At times, only a focal calcification with shadowing is seen. Meconium peritonitis occurs when there is perforation of the bowel in utero, resulting in a sterile chemical peritonitis. In most cases, foreign-body giant cells and calcium deposits form within inflamed tissues, resulting in lesions that are echogenic at antenatal US. Eighty-six percent of fetuses with meconium peritonitis have intraabdominal calcifications at US (which occur at approximately 8 days after the perforation). These calcifications can be seen after 18 weeks gestation (7).
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Figure 4a. Presumed meconium peritonitis. (a) Sagittal sonogram obtained at 19 weeks gestation shows a single calcification with shadowing in the fetal abdomen. (b) Axial sonogram of the abdomen of another fetus, obtained at 20 weeks gestation, shows multiple scattered punctate calcifications without shadowing.
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Figure 4b. Presumed meconium peritonitis. (a) Sagittal sonogram obtained at 19 weeks gestation shows a single calcification with shadowing in the fetal abdomen. (b) Axial sonogram of the abdomen of another fetus, obtained at 20 weeks gestation, shows multiple scattered punctate calcifications without shadowing.
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Causes of meconium peritonitis include ileal or jejunal atresia, volvulus, and microcolon. Cystic fibrosis is associated with meconium peritonitis, although the extent of association varies depending on the series examined (7,8).
Associated abnormalities are often detected in fetuses with meconium peritonitis, particularly dilated bowel (27%–29%), fetal ascites (54%–57%), polyhydramnios (64%–71%), and meconium pseudocyst (Fig 5) (9). Meconium pseudo-cyst is seen as a well-defined hypoechoic mass surrounded by an echogenic calcified wall, indicating a contained perforation.
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Figure 5a. Meconium peritonitis with a meconium pseudocyst in a fetus at 18 weeks gestation. (a) Axial sonogram of the abdomen shows multiple punctate calcifications on the peritoneal surface of the liver. (b) Coronal sonogram obtained lower in the abdomen shows a hypoechoic structure with an irregularly calcified wall (arrow) in the anterior abdomen, an appearance consistent with a meconium pseudocyst.
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Figure 5b. Meconium peritonitis with a meconium pseudocyst in a fetus at 18 weeks gestation. (a) Axial sonogram of the abdomen shows multiple punctate calcifications on the peritoneal surface of the liver. (b) Coronal sonogram obtained lower in the abdomen shows a hypoechoic structure with an irregularly calcified wall (arrow) in the anterior abdomen, an appearance consistent with a meconium pseudocyst.
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In the evaluation of the fetal abdomen for meconium peritonitis, the following should be documented: the site, size, and location of calcifications (including the scrotum and thorax) and the presence of dilated or echogenic bowel loops, meconium pseudocyst, ascites, and signs of hydrops fetalis.
When the calcifications are isolated, there generally is a favorable neonatal outcome and intervention is not necessary (Fig 4). In the series of Dirkes et al (7), all five fetuses with isolated calcifications had a normal outcome at postnatal follow-up. These cases are thought to represent perforation of bowel that spontaneously heals in utero. Therefore, in the absence of other findings, isolated calcifications can be followed sonographically during pregnancy. Parental cystic fibrosis gene carrier status can be assessed. In this assessment, parental blood is tested for the 25 most common alleles associated with cystic fibrosis, allowing detection of 90%–97% of cystic fibrosis cases. However, it has been shown that peritoneal calcifications have a lower association with cystic fibrosis than had been previously thought (8). After birth, plain radiography of the abdomen is performed, frequently followed by upper and lower gastrointestinal tract barium studies to assess for occult perforation. If results of these studies are normal and the neonate has passed meconium, no further follow-up is needed.
When peritoneal calcifications are seen in conjunction with other findings, the outcome is more guarded (7). Closer follow-up is warranted. Post-natal imaging commonly demonstrates obstruction with or without perforation, and surgery is often indicated.
Liver Calcifications and Calcified Liver Lesions
Calcifications in the fetal liver are a relatively common finding, identified at 1 in every 1,750 second-trimester US examinations (10). The site, size, and distribution of the lesions are major factors in determining further management. The presence of an associated liver, abdominal, or retroperitoneal mass as well as the association with ascites are important considerations.
If the liver calcifications are single, no other fetal morphologic abnormalities are detected, and infectious screening tests are negative, then the prognosis is promising. Follow-up sonography typically shows stability or regression of the finding, and no further work-up is required.
Punctate echogenic lesions on the surface of the liver usually represent peritoneal calcifications, the commonest source of which is meconium peritonitis (Fig 5). Isolated subcapsular calcifications also can be due to emboli from the portal or hepatic veins (11).
Calcifications in the liver can be single or multiple (Fig 6). In the majority of cases in which isolated hepatic calcific deposits are detected, no underlying abnormality is found. Most studies document that screening tests for the infections associated with calcifications in the liver—such as cytomegalovirus infection, toxoplasmosis, rubella, syphilis, and herpes simplex—are negative, and the outcome is almost always favorable if no other abnormality is detected (10–12). A vascular etiology for these lesions has been postulated but not proved (12). The development of ascites is associated with congenital viral infection (13).
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Figure 6a. Intrahepatic calcifications. (a, b) Axial (a) and oblique coronal (b) sonograms obtained at 18 weeks gestation show calcification in the fetal liver. The maternal history was unremarkable, and the outcome was normal. (c, d) Axial sonograms of the liver of another fetus, obtained at 20 weeks gestation, show diffuse punctate calcifications. Results of testing for cytomegalovirus were indeterminate twice, and an infectious cause was thought to be likely. The neonatal outcome was normal.
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Figure 6b. Intrahepatic calcifications. (a, b) Axial (a) and oblique coronal (b) sonograms obtained at 18 weeks gestation show calcification in the fetal liver. The maternal history was unremarkable, and the outcome was normal. (c, d) Axial sonograms of the liver of another fetus, obtained at 20 weeks gestation, show diffuse punctate calcifications. Results of testing for cytomegalovirus were indeterminate twice, and an infectious cause was thought to be likely. The neonatal outcome was normal.
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Figure 6c. Intrahepatic calcifications. (a, b) Axial (a) and oblique coronal (b) sonograms obtained at 18 weeks gestation show calcification in the fetal liver. The maternal history was unremarkable, and the outcome was normal. (c, d) Axial sonograms of the liver of another fetus, obtained at 20 weeks gestation, show diffuse punctate calcifications. Results of testing for cytomegalovirus were indeterminate twice, and an infectious cause was thought to be likely. The neonatal outcome was normal.
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Figure 6d. Intrahepatic calcifications. (a, b) Axial (a) and oblique coronal (b) sonograms obtained at 18 weeks gestation show calcification in the fetal liver. The maternal history was unremarkable, and the outcome was normal. (c, d) Axial sonograms of the liver of another fetus, obtained at 20 weeks gestation, show diffuse punctate calcifications. Results of testing for cytomegalovirus were indeterminate twice, and an infectious cause was thought to be likely. The neonatal outcome was normal.
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Calcified liver masses are suspicious for malignancy. These tumors are very rare, the most likely being hepatoblastoma (a heterogeneous mass with coarse calcifications and an osseous matrix) and metastatic neuroblastoma (a poorly differentiated neural crest cell tumor, most commonly originating in the adrenal gland).
Fetal Gallstones
The fetal gallbladder is visualized in 82%–100% of all second- and third-trimester US examinations (14). It may not be seen late in pregnancy due to the initiation of gallbladder contractions.
Gallstones and gallbladder sludge (thickened bile containing a precipitation of calcium, pigment, and cholesterol elements) have been described after 28 weeks gestation (15,16). Echogenic foci in the fetal gallbladder that cast an acoustic shadow are more likely to represent stones than sludge and are slightly less likely to resolve in the postnatal period (17). Careful evaluation of echogenic foci in the right upper quadrant is required to confirm the diagnosis of cholelithiasis (Fig 7) and exclude other causes of calcification in the region, particularly intrahepatic mass lesions.
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Figure 7a. Fetal gallstones. (a) Coronal sonogram obtained at 16 weeks gestation shows shadowing stones in the fetal gallbladder. (b) Axial sonogram of the gallbladder of another fetus, obtained at 20 weeks gestation, shows small stones. Neonatal follow-up demonstrated the expected complete resolution of the gallstones in both cases.
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Figure 7b. Fetal gallstones. (a) Coronal sonogram obtained at 16 weeks gestation shows shadowing stones in the fetal gallbladder. (b) Axial sonogram of the gallbladder of another fetus, obtained at 20 weeks gestation, shows small stones. Neonatal follow-up demonstrated the expected complete resolution of the gallstones in both cases.
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Postulated causes of fetal gallstones include hemolytic disease, cholestasis, and maternal drug use. Most studies report no associated fetal abnormalities (16,17). The detection of gallstones or sludge in the fetus is typically not associated with postnatal clinical sequelae (unlike cholelithiasis in children). In many cases, the stones resolve before or soon after delivery, possibly due to alterations in bile metabolism. In one case series, gallstones were associated with tetralogy of Fallot, trisomy 21, and gastroschisis (18). However, there may have been an element of selection bias in that study, thus rendering the interpretation as to underlying causes difficult. In general, fetal gallstones are usually an incidental finding at third-trimester US carried out for another indication. A single postnatal US study may be indicated to confirm the expected resolution. No further investigation is warranted.
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Noncalcified Liver Lesions
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The differential diagnosis of intrahepatic echogenic liver masses includes benign entities such as hemangioma, mesenchymal hamartoma, adenoma, and focal nodular hyperplasia. Other considerations include hepatoblastoma and metastatic neuroblastoma.
Hemangioma
Hemangioma is a benign tumor characterized by increased turnover of endothelium, mast cells, macrophages, and fibroblasts. It is the commonest tumor of infancy, occurring most often in the liver, lung, and gastrointestinal tract (Fig 8). Although it is the commonest vascular tumor, antenatal detection is uncommon. Hemangioma is classically a well-defined echogenic liver lesion. It tends to appear avascular at color Doppler sonography and is more likely to exhibit calcification than hamartoma. Hemangiomas up to 12 cm have been described antenatally (19). With lesions of this size, significant morbidity has been reported. Complications are related to congestive cardiac failure, thrombocytopenia, anemia, and intraabdominal hemorrhage as a result of rupture of the tumor. Maternal steroids and interferon alpha-2a have been used to treat these lesions medically with varying success (9). When these methods fail, surgery may be required postnatally. Spontaneous regression of hemangioma has been documented.
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Figure 8a. Liver hemangioma. (a) Axial sonogram of the liver obtained at 16 weeks gestation shows a single 1-cm-diameter, uniformly echogenic, well-circumscribed mass in the anterior aspect of the liver. (b) Axial sonogram of the liver obtained at 18 weeks gestation shows no change in the size or characteristics of the mass (cursors). Results of further examinations up to term were unchanged.
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Figure 8b. Liver hemangioma. (a) Axial sonogram of the liver obtained at 16 weeks gestation shows a single 1-cm-diameter, uniformly echogenic, well-circumscribed mass in the anterior aspect of the liver. (b) Axial sonogram of the liver obtained at 18 weeks gestation shows no change in the size or characteristics of the mass (cursors). Results of further examinations up to term were unchanged.
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Mesenchymal Hamartoma
This tumor is composed of connective tissue, hepatocytes, and biliary elements in a disorderly fashion. Although it is typically cystic, solid tumors have been described. It is echogenic if solid or composed of multiple microcysts with innumerable tissue-fluid interfaces.
Once the antenatal diagnosis of an intrahepatic solid lesion has been made, the following need to be documented: the number, size, and location of lesions, lesion vascularity, portal vein patency, the presence of calcifications, amniotic fluid volume, and heart size. In cases of discrete, small, uniform, noncalcified lesions with no associated abnormalities, close follow-up to document change if any in the above factors is recommended. Any significant increase in size, change in vascularity, or findings of hydrops should prompt consideration of delivery at a tertiary-care center.
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Enteric Duplication Cysts
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Enteric duplication cysts are structures in immediate contact with the alimentary tract, made up of a two-layer smooth muscle wall and an internal epithelium of a respiratory or intestinal type. They are associated with additional abnormalities in one-third of cases, particularly those of the spine and gastrointestinal tract (20). These cysts are typically anechoic but can manifest as an echogenic abdominal mass (Fig 9). The thick wall that duplication cysts possess can make differentiation from mesenteric cysts difficult (20). These cysts may or may not communicate with the lumen of the gastrointestinal tract. They are classified as cystic or tubular. The tubular type communicate with the bowel more commonly and are less likely to be identified at sonography.
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Figure 9a. Echogenic gastric duplication cyst. Axial (a) and oblique coronal (b) sonograms show a well-defined, echogenic, round mass that indents the stomach. The appearance remained constant throughout gestation and into the neonatal period.
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Figure 9b. Echogenic gastric duplication cyst. Axial (a) and oblique coronal (b) sonograms show a well-defined, echogenic, round mass that indents the stomach. The appearance remained constant throughout gestation and into the neonatal period.
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Most gastric duplications are cystic and of the noncommunicating type. They are found on the greater curve of the stomach near the pylorus. The differential diagnosis of gastric duplication includes retroperitoneal tumor (neuroblastoma) and teratoma of the stomach.
Forty percent of duplication cysts involve the ileum (20). The colon and rectum can also be affected. The most common complication is bowel obstruction. Hemorrhage and perforation have also been described. Surgery is therefore recommended in most cases. If an enteric duplication is suspected, examination should be directed toward the identification of communication with the remainder of the gastrointestinal tract, dilated bowel loops, and/or evidence of perforation. Spinal malformations are associated with foregut duplications; thus, careful evaluation of the spine should be performed. Follow-up examinations should be directed to documenting change in size, development of calcifications, and the presence of bowel obstruction.
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Lesions of the Adrenal Region
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The size of the fetal adrenal gland in the late third trimester is about 20 times its relative size in the adult, weighing approximately 2–4 g at birth (21). The adrenal can be seen routinely at US after 30–32 weeks gestation. The cortex is normally hypoechoic to the adjacent liver or spleen. The differential diagnosis for an echogenic suprarenal mass includes adrenal hemorrhage, an exophytic renal tumor, and neuroblastoma. At times, an extralobar sequestration can mimic an adrenal lesion.
Adrenal Hemorrhage
The causes of adrenal hemorrhage in utero are poorly understood. Hypoxia and increased intra-vascular pressure have been postulated (21). The right adrenal gland is involved in 75% of cases, possibly due to the relatively shorter adrenal vein (21). The key to the diagnosis is change in appearance over time. In the first few hours after adrenal hemorrhage occurs, it appears as a solid echogenic lesion. It later develops a hypoechoic center, followed by shrinkage of the lesion with involution of the cystic component with or without the appearance of dystrophic calcifications. In the latter stages, differentiation from neuroblastoma may be difficult (21).
Neuroblastoma
Neuroblastoma is the most common neoplasm of the adrenal gland (Fig 10). It is usually identified for the first time in the third trimester at a mean gestational age of 36 weeks. Associated malformations are unusual. Neuroblastoma is characteristically a heterogeneous solid mass with cystic components that displaces the adjacent kidney inferiorly and laterally. It can metastasize to the liver. Spontaneous regression occurs in up to 40% of cases. Peripheral calcification may persist.
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Figure 10a. Neuroblastoma. (a, b) Axial (a) and coronal (b) sonograms obtained at 18 weeks gestation show a homogeneously echogenic retroperitoneal mass. (c) Coronal magnetic resonance image shows the intermediate-signal-intensity lesion (arrows). s = stomach. A neuroblastoma was confirmed at surgery.
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Figure 10b. Neuroblastoma. (a, b) Axial (a) and coronal (b) sonograms obtained at 18 weeks gestation show a homogeneously echogenic retroperitoneal mass. (c) Coronal magnetic resonance image shows the intermediate-signal-intensity lesion (arrows). s = stomach. A neuroblastoma was confirmed at surgery.
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Figure 10c. Neuroblastoma. (a, b) Axial (a) and coronal (b) sonograms obtained at 18 weeks gestation show a homogeneously echogenic retroperitoneal mass. (c) Coronal magnetic resonance image shows the intermediate-signal-intensity lesion (arrows). s = stomach. A neuroblastoma was confirmed at surgery.
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Subdiaphragmatic Extra-lobar Pulmonary Sequestration
Approximately 10%–15% of extralobar pulmonary sequestrations occur below the diaphragm, where there is a 4:1 left-sided predominance (9). In contrast to this, neuroblastomas are more commonly right sided. In addition, sequestrations are generally appreciated earlier in the pregnancy, in the second trimester, and are more echogenic than neuroblastomas (Fig 11). If a feeding vessel can be seen arising from the thoracic aorta and extending below the diaphragm to the mass, this strongly favors the diagnosis (9).
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Figure 11a. Subdiaphragmatic extralobar pulmonary sequestration. Axial sonogram obtained at 18 weeks gestation (a), sagittal sonogram obtained at 20 weeks gestation (b), and axial sonogram obtained at 28 weeks gestation (c) show an echogenic mass in the left retroperitoneum. No feeding vessel was identified. At surgery, the mass was an extralobar pulmonary sequestration.
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Figure 11b. Subdiaphragmatic extralobar pulmonary sequestration. Axial sonogram obtained at 18 weeks gestation (a), sagittal sonogram obtained at 20 weeks gestation (b), and axial sonogram obtained at 28 weeks gestation (c) show an echogenic mass in the left retroperitoneum. No feeding vessel was identified. At surgery, the mass was an extralobar pulmonary sequestration.
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Figure 11c. Subdiaphragmatic extralobar pulmonary sequestration. Axial sonogram obtained at 18 weeks gestation (a), sagittal sonogram obtained at 20 weeks gestation (b), and axial sonogram obtained at 28 weeks gestation (c) show an echogenic mass in the left retroperitoneum. No feeding vessel was identified. At surgery, the mass was an extralobar pulmonary sequestration.
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Congenital Mesoblastic Nephroma
Congenital mesoblastic nephroma, which is derived from the secondary mesenchyme, is the commonest primary renal neoplasm seen in the first month of life. In utero, it is seen as a large solid vascular mass (Fig 12). Owing to arteriovenous shunting, heart failure and polyhydramnios are common. Mesoblastic nephroma is benign, and postnatal nephrectomy is curative (22).
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Figure 12a. Congenital mesoblastic nephroma. (a) Axial sonogram obtained at 36 weeks gestation shows a heterogeneous mass (arrows) in the right retroperitoneum. (b) Coronal sonogram shows that the mass (cursors) originates from the right kidney. (c) Color Doppler image shows blood supply from the ipsilateral renal artery. At surgery, a mesoblastic nephroma was confirmed.
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Figure 12b. Congenital mesoblastic nephroma. (a) Axial sonogram obtained at 36 weeks gestation shows a heterogeneous mass (arrows) in the right retroperitoneum. (b) Coronal sonogram shows that the mass (cursors) originates from the right kidney. (c) Color Doppler image shows blood supply from the ipsilateral renal artery. At surgery, a mesoblastic nephroma was confirmed.
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Figure 12c. Congenital mesoblastic nephroma. (a) Axial sonogram obtained at 36 weeks gestation shows a heterogeneous mass (arrows) in the right retroperitoneum. (b) Coronal sonogram shows that the mass (cursors) originates from the right kidney. (c) Color Doppler image shows blood supply from the ipsilateral renal artery. At surgery, a mesoblastic nephroma was confirmed.
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Work-up of Adrenal Region Lesions
The following approach to assessment of lesions in the adrenal region is suggested: First, determine if the mass is of renal or adrenal origin. At times, this is not possible to determine. When a mass identified during a routine fetal survey (18–22 weeks gestation) is uniform and left sided, consider subdiaphragmatic extrapulmonary sequestration the most likely cause. If the mass is uniform with a central cystic portion, right sided, or bilateral, then adrenal hemorrhage is at the top of the differential diagnosis list, particularly if follow-up shows rapid resolution. In both cases, management is expectant.
If a highly vascular mass is identified later in pregnancy and is not clearly separate from the kidney, consider mesoblastic nephroma. Most pregnancies with mesoblastic nephroma will deliver prior to 38 weeks gestation. Postnatal nephrectomy (or partial nephrectomy) is curative. If a mass identified at this stage of gestation is right sided with cystic spaces, consider neuroblastoma and assess carefully for liver metastases. Close expectant management should be advised with resection in the neonatal period.
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Conclusions
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Fetal abdominal echogenic lesions are common, and many carry no additional risk to the fetus or neonate. The identification of such lesions in the fetal abdomen should prompt a detailed survey for additional findings and review of the maternal history. In some cases, fetal karyotyping may be indicated. In utero diagnosis can often be achieved with careful evaluation of the lesion echotexture, associated calcifications, additional findings, and evolution over time. In most cases, expectant management is sufficient, with some cases requiring transfer to a facility appropriate for early postnatal intervention.
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References
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Abstract
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