FETAL ANOMALY SCAN

[PART 2]DR. ARIF KHAN S

TYPES OF ANOMALIES ◦Physical structural defects:

◦Single structure is affected.◦Multiple structures are affected.

◦Non-structural defects◦ Inherited metabolic defects◦Functional and behavioral deficits e.g. congenital mental retardation.

Introduction ◦Gastrointestinal tract

◦Urinary tract

◦Msuculo-skeletal dysplasias

5

GIT

◦ ultrasound appearance varies significantly during pregnancy and also, for some sites, in the course of the same ultrasound examination, due to the physiology of swallowing,stomach emptying, and intestinal peristalsis.

◦ the origin of a cystic or solid mass detected in the abdominal cavity can also be difficult to identify with certainty

Abdominal views◦ (ileum , jejunum, colon, liver, spleen, and

abdominal wall).

◦ axial view of the upper abdomen: stomach and right hepatic lobe

◦ axial view of the lower abdomen: small bowel

◦ • mid-sagittal view of the abdomen: cord insertion and rectal pouch in the pelvis

◦ (a) Midsagittal view of the abdomen: the cord insertion, highlighted by power Doppler, and part of the small bowel (arrowhead)are visible.

◦ (b) With small movements of the transducer, it ispossible to visualize, in the pelvis, the bladder and, behind it, the rectalpouch (arrow).

◦ Right parasagittal view of the abdomen: the righthepatic lobe (Li), just below the hypoechoic layer of the diaphragm(arrowheads) and some ileal loops are visible. RL, right lung.

◦ esophageal atresia: non-visualization of the gastric bubble

◦ • duodenal atresia/stenosis: double bubble

◦ • hepatomegaly: increased liver volume

◦ • splenomegaly: increased splenic volume

◦ Choledochal cyst: round cystic structure under the liver

◦ • Enteric duplication cyst: round cystic structure

◦ adjacent to the stomach

◦ • Splenomegaly: increased volume of the spleen

◦ • Small-bowel atresia: severe dilatation of ileal loops proximal to the atretic tract

◦ • Meconium ileus: diffuse hyperechogenicities and

◦ calcifications within the intestinal lumen, sometimes

◦ associated with small-bowel obstruction

Esophagus ◦ ultrasound appearance of the esophagus

◦ as a pouch full of amniotic

◦ Fluid, especially if the fetus has just swallowed

◦ Can be recognized as a thin prevertebral anechoic structure, when filled with some amniotic fluid.(may resemble a vessel)

◦ Also on the 4-chamber view, the cross-sectional appearance of the esophagus distended by some amniotic fluid may be mistaken for that of an abnormal vessel, as in abnormal pulmonary or systemic (azygos continuation) venous return.

◦when empty appears as ‘two or more parallel echogenic lines.’

ESOPHAGEAL ATRESIA

◦ Incidence. Frequent: 1 /2500–1 /4000 live births.

◦Diagnosis. Non-visualization of the gastric bubble, relatively late-onset polyhydramnios. In some of the cases

◦ associated with a TE fistula, a constantly small stomach. Inconstantly, an upper esophageal pouch (pouch sign).

◦ Risk of chromosomal anomalies. High (20–44%): trisomies 21 and, to a lesser extent, 18.

◦ Risk of non-chromosomal syndromes. Relatively high: VA(C)TER(L).

◦Outcome. Generally good, but depends mainly on the extent of the atretic tract.

◦Definition. In esophageal atresia, the communication between the proximal and the distal tract of the esophagus is absent, due to a lack of development of the intermediate esophageal portion, mainly because of an interruption of the blood supply during organogenesis.

◦ Esophageal atresia can occur as an isolated anomaly (10% of cases) or, much more frequently, be associated with a tracheoesophageal (TE) fistula (90% of cases)

◦ Etiology and pathogenesis. The etiology of the defect is unknown. It originates when, at 8 weeks of gestation, the primitive foregut does not divide into the ventraltracheobronchial part and the dorsal digestive part

◦ Type A: Corresponds to pure esophageal atresia without fistula.

◦ Type B: is esophageal atresia with fistula between the proximal pouch and the trachea.

◦ Type C: is esophageal atresia and fistula from the trachea or the main bronchus to the distal esophageal segment. (most common)

◦ Type D: is esophageal atresia with both proximal and distal fistulas

◦ Type E: is tracheoesophageal fistula without atresia.

◦Ultrasound diagnosis

◦ The overall detection rate, considering all possible signs of esophageal atresia, should be in the range of 24–42%

◦More than 85% of cases of esophageal atresia are not detected in utero due to the existence of a concurrent TE fistula: this fistula does not prevent normal stomach filling in most instances, and only in a reduced number of cases is a constantly underfilled stomach found.

◦ Pouch sign: dilatation of proximal esophageal tract.

◦ This sign is observed transiently also in the normal fetus after swallowing; in fetuses with a small stomach and polyhydramnios, the detection of a persistent pouch sign would indicate the likely presence of a TE fistula.

◦non-visualization of the gastric bubble is the only sign if present is highly indicative of esophageal atresia (but only in the 8–10% of cases that are not associated with a TE fistula.

◦ The other sign possibly indicative of esopheagal atresia is polyhydramnios, which becomes clearly evident only in the late 2nd trimester

◦ FGR : 40% of cases of TE fistula

◦Down’s syndrome 50 percent assosciation with Type A

◦Differential diagnosis.Oligohydramnios : PROM and B/L Renal agenesis Diaphragmatic hernia

Cleft palate and cleft lip

Association with other malformations. Major anomalies are associated in 40–70% of the cases, with prevalence, in decreasing order, of GI (28%), cardiovascular(24%), genitourinary (13%), and osteomuscular (11%) malformations.

TE fistula accounts for a significant number of these anomalies.

Risk of chromosomal anomalies. This is high, reaching 20–44% of cases in the fetus, with a prevalence of trisomies 21 and 18.

◦Chromosomal syndromes •

◦ VA(C)TER(L) association: look for → esophageal atresia (+ TE fistula) + vertebral anomalies (scoliosis, hemivertebrae) + anorectal atresia + cardiac (ventricular septal defect) + renal anomalies (dysplasia, ectopia, etc.) + limb anomalies (aplasia radii)

Dudenal atresia◦ Incidence. Frequent 1 /2500–1 /10 000 live births.

◦Diagnosis. Double bubble, with communication between the two parts; late polyhydramnios.

◦ Risk of chromosomal anomalies. High (20–50%): mainly trisomy 21.

◦ Risk of non-chromosomal syndromes. Low.

◦Outcome. Mainly good.

◦Definition. In duodenal atresia, the tract between the proximal and distal portions of the duodenum is atretic.In most cases (80%), the obstruction is due to completeatresia and is caudal to the ampulla of Vater. In the remaining 20% of cases, the obstruction can be due to a diaphragm or membrane located within the lumen of the duodenum, and can be complete or partial (stenosis).

◦ Etiology and pathogenesis. The etiology of the defect

◦ is unknown. The pathogenetic mechanism involves

◦ an interruption of blood supply during organogenetic

◦ period, as for most GI tract atresias. According to

◦ another theory, the defect may be due to a lack of duodenal

◦ recanalization – always during early embryogenesis

Ultrasound diagnosis◦ . This is based upon recognition of

◦ the classic double bubble, associated with polyhydramnios,

◦which often develops in the late 2nd, early 3rd trimester. Usually, polyhydramnios is absent and the double bubble

◦ The only finding consists of an evidently dilated stomach, with initial dilatation only of the duodenum

◦ In most cases on follow up the double bubble sign becomes clearly visisble.

◦ Care should be taken in demonstrating a communication between the two anechoic bubbles, to obtain confirmation that the second bubble is actually the dilated proximal duodenum

◦ In few cases where the diuble bubble sign will be seeb only in late gestation or may even not occur and diagnosed post natally.

◦ Extremeky rare cases When Duaodenal atresia is asosciaterd with esophagela atresisa the over distention of stomach and proximal duodenum is massive.

◦Differential diagnosis. This should include all other conditions featuring a cystic structure in the middle or right upper abdomen : choledochal cysts, enteric duplication cysts, and hepatic cysts.

◦Prognostic indicators. The association with other anomalies, which is relatively frequent, represents the main poor prognostic sign.

◦Association with other malformations. Major anomalies are associated with duodenal atresia in 40–50% of cases

Mostly GI malformations , vertebral and cardiac. upto 33%

◦Risk of chromosomal anomalies. This is high. Overall, 40% (range 20–50%) of cases of duodenal atresia are associated with Down syndrome. Conversely, 5–15% of neonates with trisomy 21 have duodenal atresia.

◦Risk of non-chromosomal syndromes. This is low.

SMALL-BOWEL ATRESIA◦ Incidence. Frequent: 1 /2500–1 /5000 live births.

◦Diagnosis. Severe late-onset dilatation of the ileal loops proximal to the obstruction. Late-onset polyhydramnios.

◦Risk of chromosomal anomalies. Low.

◦Risk of non-chromosomal syndromes. Low.

◦Outcome. Generally good, but guarded in apple-peel variant and multiple-site atresia.

◦ Types . Small-bowel atresia can be single or multiple. It can be due to an intraluminal diaphragm or membrane (type I: 20% of cases) or

◦ present as complete atresia ofthe affected segment. this can show a fibrous string connecting the two blind-ending stumps (type II: 32% of cases)

◦ complete separation of the two stumps without any fibrous connection (type III: 48% of cases).

◦ Type III includes the two variants that bear the worst prognosis, due to the severely reducedactive intestinal surface: type IIIB (11% of cases),

◦ In which the bowel shows the so-called apple-peel aspect.

◦ type IV (17% of cases), in which the atresia involves multiple sites

As far as the anatomic site of the atresia is concerned,

◦ the jejunum only is involved in 50%

◦ the ileus only in 43% of cases,

◦ both intestinal tracts in the remaining 7% of cases.

Ileal atresias are more often single and show higher tendency to perforation in utero

◦ jejunal atresias are more often multiple, tend to dilate rather than to perforate, and show a significantly lower neonatal mean weight and less advanced gestational age at delivery in comparison with ileal atresias.

◦ Jejunal atresia (37 weeks of gestation). Note the extremely severe dilatation without evidence of perforation (absence of meconium peritonitis). The arrowheads indicate the site of the peristaltic wave, opening and closing the communication between adjacent loops

◦ Etiology and pathogenesis.

◦ . Investigations in animal models and in humans have demonstrated that intestinal atresia is due to a vascular insult, consisting of an atresia or torsion of the feeding artery during the rotation of the midgut.

◦ The apple-peel variant has been hypothesized to be the effect of vascular occlusion of a superior mesenteric artery branch.

◦Ultrasound diagnosis :

◦mainly on the detection of the severe dilatation of the \intestinal loops proximal to the obstruction, which is absent in most cases prior to 25 weeks of gestation.

◦ polyhydramnios is also of late onset.

◦ Hence, the first sonographic evidence of a possible small-bowel atresia Is the isolated dilatation of an ileal loop, showing a transverse diameter of greater than 7 mm.

◦ Additional signs that contribute to confirming the diagnosis are a Centro abdominal location of the affected loop, its hyper echoic walls.

◦ increased peristalsis, and the presence of endoabdominal calcifications possibly indicative of a meconium ileus.

◦ Better demonstrated in 3rd trimester with massively dilated bowel loops and increased peristalitic movements

◦ it is not possible to identify the real site of the obstruction (ileal or jejunal).

◦ The only features that may point towards one of the two sites are the evidence of intestinal perforation (ascites with particulate matter and/or calcifications) for the ileus or extreme dilatation without perforation for the jejunum .

Differential diagnosis.

Hirschsprung’s disease

Volvuluis

Meconeum ileus

◦ The detection of intra-abdominal calcifications, possibly suggesting the presence ofa meconium ileus complicated by perforation and meconium peritonitis, represents one of the most important poor prognostic signs.

◦Association with other malformations. Major anomalies are very rarely associated with intestinal atresias

MECONIUM ILEUS◦ Incidence. No data available.

◦Diagnosis. Mechanical ileal obstruction due to the increased consistency of meconium; significant risk of

◦perforation and consequent meconium peritonitis.

◦Risk of chromosomal anomalies. Relatively low.

◦Risk of non-chromosomal syndromes. If cystic fibrosis is considered here, the risk is extremely high (>90%).

◦Outcome. Depends on the underlying cystic fibrosis and its phenotypic expression

◦Definition. Meconium ileus is characterized by an ileal mechanical obstruction caused by inspissated meconium. The meconium is thicker than normal due to a high protein content, the primary cause of which is cystic fibrosis, associated with most cases of meconium ileus.

◦This obstruction leads relatively often to ileal perforation and consequently meconium peritonitis.

◦ In somecases, the obstruction occurs more distally, in the colon, where the meconium causes a mucus plug that obstruct the rectum.

◦ Etiology and pathogenesis. Cystic fibrosis is associated in more than 90% of cases. In the

◦ few cases not associated with this genetic condition, the etiology of the intestinal obstruction remains unclear.

◦ The pathogenetic mechanism leading to the obstruction is represented by the significant changes in the components of meconium

increase in porotien content increased viscocity inspissation obstruction- dilation of proximal loops and perforation.

◦with the thick meconium spilling into the abdominal cavity, with a consequent severe adhesive peritonitis.

Ultrasound diagnosis.:

◦ This is based upon recognition of an ileal obstruction, with one or multiple dilated loops that characteristically show hyperechoic content and similarly hyperechoic walls.

◦ In meconium ileus, the obstruction is usually of late onset, becoming evident in the late 2nd trimester, after 24–25 weeks of gestation

◦ The ultrasound appearance is pleomorphic. The dilated ileal loops may show hyperechoic content or, in other cases, meconium/fluid levels; the walls may appear normal or thickened and hyperechoic.

◦Or show features of meconium peritonitis.

◦ If the obstruction involves the ileus, the colon is typically empty, since meconium transit is blocked.

◦ Firstr sign is hyperechoic Ileus. early–mid 2nd trimester

◦Differential diagnosis:

Small bowell atresias

ANORECTAL ANOMALIES ◦ Incidence. Extremely rare.

◦Diagnosis. Late-onset dilatation of sigmoid colon and rectum, often with hyperechoic meconium. Normal amniotic fluid.

◦Risk of chromosomal anomalies. High: trisomies 18 and 21.

◦Risk of non-chromosomal syndromes. High: predominantly associated with various expressions of the caudal regression sequence.

◦Outcome. Good, if isolated. If syndromic, depends on the associated malformations (as in caudal regression).

◦Definition. All of these are malformations causing distal obstruction of the GI tract.

Anorectal malformations canbe divided, on the basis of their embryologic origin, into

the following:

◦• external malformations, due to abnormalities of the development and fusion of the external perineal layers,

Eg; imperforate anus with/without fistula

◦ internal malformations, in which the developmental anomaly involves the primary partition of the cloaca by the urogenital septum –

Eg;pure rectal atresia and rectal atresia with fistula

◦• mixed malformations, including all possible sites of ectopic anus

◦Of the above-mentioned malformations, only anorectal atresia is detectable by ultrasound

◦ in a minority of cases, in the 3rd trimesterr of pregnancy. The main ultrasound finding possibly indicativeof such a malformation is overdistension of the rectum and, to a lesser extent, of the sigmoid colon,

◦ Relatively often, the mecoium in the dilated rectal pouch becomes hyperechoic.

◦ The amount of amniotic fluid is unchanged.

◦ If the anorectal atresia is associated with a rectovesical fistula, the amniotic fluid is reduced..

◦ If polyhydramnios is noted in association with anorectal atresia, this is due to the associated anomalies.

HEPATOMEGALY/SPLENOMEGALY

◦ Incidence. Rare. Often due to severe fetal infections.

◦Diagnosis. Enlarged liver/spleen.

◦Risk of chromosomal anomalies. Low, except for the myeloproliferative disease typical of trisomy 21.

◦Risk of non-chromosomal syndromes. Relatively low. Hepatomegaly can be associated with the Beckwith–

◦Wiedemann and Zellweger syndromes.

◦Outcome. Depends on the underlying cause

◦ . Definition. Hepatomegaly is defined as an increased volume of the liver. Similarly, splenomegaly refers to an increased volume of the spleen. They may be associatedor occur independently

◦ Etiology and pathogenesis

Wide spectrum of causes.

◦ Intrauterine foetal infections: CMV infection, when severe, is commonly associated with hepatosplenomegaly

◦Down’s syndrome

◦ rare benign and malignant hepatic tumors, such as hemangioma or hepatoblastoma,

◦ Venous congestion as in cardiac or extracardac causes

◦ Beckwith–Wiedemann and Zellweger syndromes, that can be associated with hepatomegaly.

◦Gaucher and Niemann–Pick syndromes, which, in the late 3rd trimester, may lead to splenomegaly.

OMPHALOCELE◦ Incidence. Relatively frequent. 1/4000 live births, but higher in utero.

◦Diagnosis. Round, solid mass that deforms the anterior abdominal wall, usually containing the right hepatic lobe

◦and some bowel loops. The cord insertion is on the mass.

◦Risk of chromosomal anomalies. High: trisomies 18 and 13 and triploidy.

◦Risk of non-chromosomal syndromes. Relatively high: Beckwith–Wiedemann, Cantrell.

◦Outcome. Good if the lesion is isolated and the liver is not completely herniated. Very poor in the case of associated malformations and/or chromosomal aberrations.

◦Definition. Omphalocele is a defect in the closure of the abdominal wall that also involves the cord insertion. The herniated organs are wrapped in a two-layered sac, (peritoneum and the amnion).

◦ The cord insertion is located on the top of the sac

◦ Two variants : presence or absence of the liver in the sac. Embryogentically different and have different prognosis

◦ Rupture of sac in 10 percent cases

◦Ultrasound diagnosis. An omphalocele is sonographically represented by a bulging structure that

◦ (i) arises from the anterior abdominal wall; (ii) contains some abdominal viscera (liver and/or bowel); and (iii) presents the cord insertion on its convexity

◦ The presence of the umbilical vein within the omphalocele is an indirect sign of the fact that this anomaly represents a primary closure defect of the abdominal wall

◦ Ascites may be seen .

If present then care should then be taken not to mistake the ascites for amniotic, as this would lead to an erroneous diagnosis of gastroschisis.

◦ Polyhydramnios may be seen .

◦ If the liver is detected within the omphalocele , the diagnosis is certain also early in gestation;

◦ if, on the contrary, only some bowel loops are seen in it, care should be taken to differentiate a real omphalocele from the physiologic herniation of the intestine within the cord that is frequently seen until the 11th week of gestation. Makes rescanning in a week’s time necessary.

GASTROSCHISIS◦ Incidence. Rare.

◦Diagnosis. Bowel loops freely floating in the amniotic fluid. Para-umbilical wall defect. Normal cord insertion.

◦ Risk of chromosomal anomalies. Very low.

◦ Risk of non-chromosomal syndromes. Low. Concurrent joint contractures of the legs with hypoplastic lower limb

◦muscles indicate the presence of congenital amyoplasia.

◦Outcome. Very good, unless rare complications including perforation, infarction or infection of the herniated loops occur.

◦Definition. Gastroschisis is characterized by a paraumbilical defect of the abdominal wall through which bowel loops herniate to float freely in the amniotic fluid

◦ The defect involves all the layers of the abdominal wall, and the herniated viscera consist, in the overwhelming majority of cases, of bowel loops only; in very rare circumstances, the stomach

◦ urogenital structures may herniate as well.

◦Ultrasound diagnosis.

the recognition of freely floating bowel outside the fetal abdomen is the main feature

URINARY TRACT ANOMALIES

RENAL AGENESIS

◦ Incidence. Unilateral form: 1/1000. Bilateral form: 1–2/5000.

◦Diagnosis. Bilateral form: lack of visualization of the kidneys and bladder associated with severe oligohydramnios

◦ (after the 16th week). Unilateral form: lack of visualization of one kidney, with normal bladder and amniotic fluid.

◦Risk of chromosomal anomalies. Low risk in isolated unilateral forms (< 1%); slightly higher in isolated bilateral

◦ renal agenesis.

◦Risk of non-chromosomal syndromes. High: 20–25%.

◦Outcome. Bilateral form: uniformly fatal. Unilateral form: good, if isolated

◦Definition. Renal agenesis is defined as complete absence of one or both kidneys (unilateral or bilateral renal agenesis).

◦ Etiology and pathogenesis. This anomaly is due to failure \of the development of the ureteric bud with absence of any interaction with the metanephric blastema.

◦ The incidence is 1/1000 newborns for the unilateral form and 1–2/5000 for the bilateral form

◦ . Ultrasound diagnosis. Sonographic diagnosis of bilateral renal agenesis is based on the impossibility of visualizing the kidneys and the bladder, associated with severe oligohydramnios after the 16th week of gestation

RENAL ECTOPIA◦ Incidence. 1/700 newborns.

◦Diagnosis. Visualization of the kidney in the pelvis, beside the bladder.

◦Risk of chromosomal anomalies. Low.

◦Risk of non-chromosomal syndromes. Low.

◦Outcome. Good in isolated forms.

◦Definition. The kidney is positioned in the fetal pelvis, either in the iliac fossa or on the midline in the pre-sacral area.

HORSESHOE KIDNEY◦Diagnosis. In axial scans, the isthmus linking the two inferior poles of the kidneys can be seen in

front

◦ of the descending aorta.

◦Risk of chromosomal anomalies. 5–8%: Turner syndrome and trisomy 18.

◦Risk of non-chromosomal syndromes. moderately high: 12–16%.

◦Outcome. In isolated forms, horseshoe kidney is asymptomatic in about half of cases. Increased incidence of infections and vesico-ureteral reflux..

◦Definition. The kidneys are fused, with an equal amount of renal tissue on each side of the midline. The inferior poles of the kidneys are linked by an isthmus of fibrous tissue or parenchyma. The ureters do not cross the midline before entering the renal sinuses.

◦ Etiology and pathogenesis. Fusion anomaly The anomaly originates after the interaction of the ureteral buds with the metanephric blastema, but before the migration and rotation processes.3

◦ The horseshoe kidney is usually positioned lower than normal because its ascent in the normal position is impeded by the emergence of the inferior mesenteric artery

◦Ultrasound diagnosis. On transverse or oblique views of the fetal abdomen, the isthmus connecting the inferior poles of the two kidneys can be seen in front of the descending aorta; the kidneys appear medially and anteriorly rotated.

◦ In this scanning plane, it is also possible to see the two renal pelvises , whichhave a more anterior location and are often slightly dilated.

HYDRONEPHROSIS, HYDRO-URETERONEPHROSIS, ANDBLADDER DILATATION◦ Incidence. 1–5/500 newborns.

◦Diagnosis. Dilatation of the collecting system of the kidney.

◦ Risk of chromosomal anomalies. Low in isolated cases: 1–3%.

◦ Risk of non-chromosomal syndromes. Relatively low: 6–8%.

◦Outcome. In the first 2 years of life: spontaneous regression in approximately 30–40% of cases and need for

◦ surgery in 20–50% of cases, according to the grade of hydronephrosis present during the prenatal period. In bilateral forms associated with oligohydramnios, unfavorable prognosis with the possibility, in selected cases, of in utero therapy.

◦Ultrasound diagnosis: one of the most widely accepted is the following: the anteroposterior

◦ diameter of the pelvis on a transverse view of the abdomen should not, under normal conditions, exceed 4 mm up to 32 weeks of gestation and 7 mm from the 33rd week onwards

HYDRO-URETERONEPHROSIS

BLADDER/CLOACAL EXSTROPHY◦ Incidence. Bladder exstrophy: 1/30 000 newborns. Cloacal exstrophy: 1/200 000–1/400

000newborns.

◦Diagnosis. Failure to visualize the bladder in the pelvis. Presence of a small mass on the lower abdominal wall (bladder exstrophy). Ample abdominal wall defect with presence of omphalocele or cystic anterior abdominal wall structure in contact with the amniotic fluid (cloacal exstrophy).

◦Risk of chromosomal anomalies. Low.

◦Risk of non-chromosomal syndromes. Relatively low.

◦Outcome. The survival rate is about 90% in the case of bladder exstrophy, but decreases to 75% for cloacal exstrophy. The quality of life depends on the success of surgical correction.

◦Definition. Bladder exstrophy is a very rare congenital malformation in which the anterior wall of the bladder is absent and the posterior wall is exposed to the amniotic fluid.3,14 It is caused by incomplete closure of the lower abdominal wall. The defect is associated with separation of the pubic bones, a low-set umbilicus, and abnormal genitalia.

RENAL TUMORS◦ Incidence. Extremely rare in the fetus. 1/125 000 during childhood.

◦Diagnosis. The lesion is usually unilateral. The kidney is partly or totally replaced by a mass with ill-defined

◦margins and high vascularization. It may have or have not a capsule.

◦Risk of chromosomal anomalies. Low.

◦Risk of non-chromosomal syndromes. Low.

◦Outcome. Depends on histology, but is generally good.

◦Definition. Renal tumors are benign or malignant neoplasms arising in the fetal kidney. Prenatal recognition is extremely rare.

◦ Etiology and pathogenesis. Mesoblastic nephroma, which is a benign lesion, is the most common tumor, followed by the malignant Wilms’ tumor

◦ diagnosis is generally made in the 3rd trimester.

◦ The tumor mass may occupy part of the kidney oreplace it completely (Figure 8.31). If it is very large, a mass effect on adjacent abdominal viscera may bedetected.

◦Usually, mesoblastic nephromas show illdefined margins due to the absence of a capsule, whereas neprhoblastomas are usually capsulated. Increased vascularization may be detected on color/power Doppler.