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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
Fetal anomaly scan pt2
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
Fetal anomaly scan pt2
◦ 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.
Fetal anomaly scan pt2
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.
Fetal anomaly scan pt2
Fetal anomaly scan pt2
Fetal anomaly scan pt2
Fetal anomaly scan pt2
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.
Fetal anomaly scan pt2
Fetal anomaly scan pt2
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
Fetal anomaly scan pt2
URINARY TRACT 
ANOMALIES
Fetal anomaly scan pt2
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
Fetal anomaly scan pt2
Fetal anomaly scan pt2
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.
Fetal anomaly scan pt2
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, 
AND 
BLADDER 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.
Fetal anomaly scan pt2
◦ 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
Fetal anomaly scan pt2
HYDRO-URETERONEPHROSIS
Fetal anomaly scan pt2
Fetal anomaly scan pt2
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.
Fetal anomaly scan pt2
Fetal anomaly scan pt2
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.
Fetal anomaly scan pt2
Fetal anomaly scan pt2

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Fetal anomaly scan pt2

  • 1. FETAL ANOMALY SCAN [PART 2] DR. ARIF KHAN S
  • 2. 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.
  • 3. Introduction ◦ Gastrointestinal tract ◦ Urinary tract ◦ Msuculo-skeletal dysplasias
  • 5. 5
  • 6. GIT
  • 7. ◦ 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
  • 8. 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
  • 9. ◦ • 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.
  • 10. ◦ 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
  • 11. 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.’
  • 12. 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.
  • 13. ◦ 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.
  • 14. ◦ 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
  • 16. ◦ 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)
  • 17. 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).
  • 18. ◦ 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
  • 19. 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
  • 20. ◦ 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%
  • 21. ◦ 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.
  • 22. 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.
  • 23. ◦ 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.
  • 24. ◦ 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
  • 25. ◦ 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.
  • 26. ◦ 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
  • 27. ◦ 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
  • 28. 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.
  • 29. ◦ 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.
  • 30. ◦ 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
  • 31. 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).
  • 32. ◦ 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
  • 33. ◦ 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.
  • 35. 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
  • 36. ◦ 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.
  • 41. 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).
  • 42. ◦ 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
  • 43. ◦ 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.
  • 46. 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
  • 47. ◦ 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
  • 51. 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).
  • 52. ◦ 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
  • 55. 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.
  • 57. 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
  • 58. ◦ 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.
  • 59. HYDRONEPHROSIS, HYDRO-URETERONEPHROSIS, AND BLADDER 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.
  • 61. ◦ 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
  • 66. 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.
  • 69. 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
  • 70. ◦ 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.

Notas del editor

  1. Axial view of the upper abdomen in a 35-week-old fetus. Note the dilatation of the colon with the haustra. This finding may be indicative of an obstruction or may be completely normal, as it happened to be in this case Finally, it should be underlined that, as far as obstructive GI lesions are concerned (duodenal atresia, esophageal atresia, ileal atresia, etc.), the dilatation of the tract proximal to the obstruction can become sonographically evident only in the 3rd trimester
  2. Axial abdominal views (stomach, bowel, liver, and spleen). (a) Axial view of the upper abdomen: the stomach is visible on the left, the right hepatic lobe on the right, and the intrahepatic tract of the umbilical vein on the midline. (b) Axial view of the lower abdomen (ventral approach): the bowel (ileus and jejunum) and a small segment of the umbilical vein (arrow) are visible
  3. • left parasagittal view: spleen (Figure 7.5c) • coronal view (VCI-C): general approach (Figure 7.6)
  4. Power or color Doppler may be used to exclude its vascular origin (a) Sagittal view of the fetal neck, showing the course of the esophagus (arrowheads), which is temporarily dilated by the swallowing of some amniotic fluid. (b) The same region (arrowheads)is shown in the coronal view, using three-dimensional volume contrast imaging (VCI-C). (c) More caudally, the parasagittal view demonstrates the esophagus behind the left atrium (arrowheads). (d) The same region, on the 4- chamber view: on this view, it is necessary to differentiate the temporary dilatation of the esophagus (arrowhead) from an abnormal venous return (systemic or pulmonary). If the anechoic area is due to esophageal dilatation, it disappears after a few minutes; in addition, the use of color/power Doppler may easily confirm or rule out a cardiovascular anomaly.
  5. Vertebral anomalies, Anal atresia, Cardiac defects, Tracheoesophageal fistula and/or Esophageal atresia, Renal & Radial anomalies and Limb defects. refers to the non-random co-occurrence of birth defects. . The reason it is called an association, rather than a syndrome is that while the complications are not pathogenically related they tend to occur together more frequently than expected by chance. In general, the etiology of "associations" are not defined.
  6. fistula does not prevent normal stomach filling in most instances, and only in a reduced number of cases is a constantly underfilled stomach found
  7. Esophageal atresia. (a) At 23 weeks of gestation, a suspicion of esophageal atreria (without TE fistula – see text) arises due to persistent non-visualization of the gastric bubble in the abdomen. The amount of amniotic fluid is normal. (b) At 30 weeks of gestation, polyhydramnios has developed and the stomach is still not visualized: the diagnosis of esophageal atresia is confirmed
  8. Risk of chromosomal anomalies. This is high, reaching 20–44% of cases in the fetus, with a prevalence of trisomies 21 and 18. This high risk is related to the fact that only type A esophageal atresia (atresia without concurrent TE fistula), which is the one most frequently associated with Down syndrome, is diagnosable in utero.
  9. when the midtrimester anomaly scan is carried out (at 18–21 weeks of gestation in most countries), only by demonstrating this communication can the rare occurrence of enteric duplication cysts or other upper abdominal cysts cn be ruled out
  10. Ileal atresia. (a) Before 24 weeks of gestation, there is hardly any evidence of intestinal dilatation. The only doubtful sign is represented by a moderate dilatation (> 7 mm) of a single ileal/jejunal loop, possibly associated with a hyperechoic aspect of the wall (arrowheads). (b) In the 3rd trimester, the obstruction becomes evident, with moderately severe dilatation of various loops. In the dilated bowel loops cranial to the obstruction, increased intestinal peristalsis is seen, with the intestinal content moving from one loop to the adjacent one. (c) At 36 weeks, by following the course of the dilated loops, it is possible to demonstrate the communication between the various dilated segments (the maximum transverse diameter of the loops was 23 mm).
  11. Only the timing and the rapidity of the appearance of the loop dilatation may be roughly indicative of the likely diagnosis: gradual for atresia, and sudden (in 3–4 days) for volvulus The evidence of diffuse intra-abdominal calcifications would suggest the occurrence of meconium peritonitis, which follows intestinal perforation Fgr : if the atresia is in Ileum due to protein malabsorption
  12. Anorectal atresia. (a) Normal filling of the rectal pouch (arrow), behind the bladder (BI). (b) Evident dilatation of the rectum, which also shows a hyperechoic content (arrows). (c) The fetus after termination of pregnancy. In addition to other anomalies, anorectal atresia was confirmed: the anal orifice is not visible
  13. In fact, the first step of cardiac failure in the fetus is an increase in central venous pressure, which in turn causes venous congestion in the liver, due to the fact that because of the patency of the two shunts (foramen ovale and ductus arteriosus), all increases in cardiac pressure are reflected in the right heart. Zellweger syndrome, also called cerebrohepatorenal syndrome, is a rare congenital disorder characterized by the reduction or absence of functional peroxisomes in the cells of an individual. Characterised by hypoplstic supra orbital ridges.  chondrodysplasia punctata (punctate calcification of the cartilage in specific regions of the body), Beck wiith syndrome (/ˈbɛkˌwɪθ ˈviːdə.mən/; abbreviated BWS) is an overgrowth disorder usually present at birth, characterized by an increased risk of childhood cancer and certain congenital features. Common features used to define BWS are:[1] macroglossia (large tongue), macrosomia (above average birth weight and length), midline abdominal wall defects (omphalocele/exomphalos, umbilical hernia, diastasis recti), ear creases or ear pits, and neonatal hypoglycemia (low blood sugar after birt h
  14. Hepatomegaly. This patient had had serologically confirmed hepatitis A infection in the 1st trimester. At 19 weeks, ultrasound demonstrated the following: (a) Axial view: evident hepatomegaly, with capsular macrocalcification and moderate ascites. (b) Left parasagittal view: The ascites and moderate enlargement of the left hepatic lobe (LL, arrowheads) are shown; in such a situation, the left hepatic lobe should not be mistaken for the spleen, which was normal in this case (c) (SPL and arrowheads).
  15. Severe hepatomegaly due to CMV infection. (a) on the axial view of the upper abdomen, it is possible to recognize the enlarged, hyperechoic, and rather inhomogeneous liver (arrows). (b) On the right parasagittal view, the degree of hepatomegaly is easily evaluated and the prominence of the abdomen in comparison with the normal thorax is evident (arrowheads).
  16. Hepatomegaly. The simultaneous presence of ascites acts as a natural contrast medium, allowing 3D ultrasound (surface rendering) to visualize the enlarged liver (L), the spleen (on the left), and the bowel (arrow). However, in this case, the diagnostic role of 3D imaging is limited
  17. Splenomegaly in two cases of severe fetal CMV infection. (a) On the coronal view, at 37 weeks of gestation, it is possible to recognize the severely enlarged spleen (Spl), the lower pole of which reaches the bladder (Bl) and a concurrent similarly severe hepatomegaly (Li). (b) A similar case, at 36 weeks of gestation, showing severe hepatosplenomegaly, ascites, and intra-abdominal calcifications. Both neonates died of widespread CMV infection
  18. Omphalocele in a fetus with multiple anomalies (anencephaly, omphalocele, and bilateral aplasia radii). (a) At 23 weeks of gestation, the axial view of the abdomen demonstrates a large omphalocele containing the liver (the arrows indicate the large wall defect). (b) 3D lowmagnification maximum-mode rendering showing the anencephaly and the omphalocele (arrowheads). (c) The stillborn fetus: the omphalocele (arrowhead), with the cord insertion, and the aplasia radii with ectrodactyly are shown.
  19. polyhydramnios, possibly secondary to bowel obstruction at the level of the wall defect or within the omphalocele, may complicate one-third of Cases
  20. Omphalocele: 3D ultrasound. (a) Multiplanar imaging, showing the omphalocele on the three orthogonal planes, which enables assessment of its content and extension (arrowheads indicate the abdominal wall defect; the arrow indicates cord insertion). (b) Surface rendering demonstrates the cord insertion on the top of the omphalocele (arrows), in between the two knees (g).
  21. Gastroschisis at 31 weeks of gestation. The appearance of bowel dilatation in the 3rd trimester represents a complication, indicating a likely obstruction. This situation may evolve with perforation and/or necrosis of one or more bowel loops. (a) Sagittal view of the fetal trunk showing some normally sized loops close to the fetal arm and one severely dilated tract (arrow). (b) Axial view demonstrating also some meconium blocked in the dilated loop (arrowhead). (c) Surface rendering demonstrating the dilated loop (the same as in (b)). (d) Below the dilated loop, most of the herniated bowel is of normal size.
  22. Bilateral renal agenesis. (a) The absence of both kidneys is evident despite the associated oligohydramnios; the arrows indicate both adrenal glands in the paraspinal regions. (b) The ultrasound image shows the absence of both kidneys; the right adrenal gland appears enlarged (arrowheads); the typical ‘ice cream sandwich’ appearance of the adrenal gland is characterized by the hypoechoic cortex and hyperechoic medulla; this is quite different from the normal kidney
  23. (a) Color flow Doppler shows both renal arteries in a case of autosomal recessive polycystic renal disease (ARPKD) (b) Absence of the renal arteries is noted in a case of bilateral renal agenesis, while the aorta is clearly shown; the arrows indicate the adrenal glands.
  24. Horseshoe kidney. Ultrasound images showing (a) both renal pelvises (arrows), which have a more anterior location than normal, and (b) the slightly lower than normal location of the horseshoe kidney. The arrows indicates the renal pelvises; BL, bladder.
  25. Factors influencing the diameter of the fetal pelvis include the state of hydration of the mother, the grade of distension of the fetal bladder, and recent emptying of the bladder itself. On the contrary, what is highly indicative of an obstructive lesion is dilatation of the renal calices. Ultrasound images showing several different degrees of hydronephrosis. (a) The kidneys show moderate pyelectasia. (b) Sagittal scan of a hydronephrotic fetal kidney showing dilatation of the pelvis and calices; the calices are confluent and dilated. (c) Coronal scan of the kidney in a case of ureteropelvic junction (UPJ) obstruction; the renal pelvis (RP) and caliceal distension (arrows) end abruptly at the ureteral junction. (d) Severe UPJ obstruction presenting as an abdominal cyst; the renal parenchyma is thinned to a few millimeters
  26. Vesico-ureteric junction obstruction. (a) Hydronephrosis and dilatation of the ureter (arrow) are present. K, kidney; BL, bladder. (b) Hydroureteronephrosis and ureterocele: ultrasound image showing a tubular anechoic formation, with a tortuous path, corresponding to a dilated ureter, which extends from the renal pelvis to the retrovesical region. Hydronephrosis is associated. Note the ureterocele
  27. Duplex kidney with two collecting systems and ectopic ureterocele. (a) The arrowhead indicates the ureterocele within the bladder. (b) Color Doppler flow demonstrating two renal artery branches. (c) Ultrasound image showing hydronephrosis of the upper pole only (arrow). (d) Surface rendering of the same case, demonstrating the duplex kidney with a dilated ureter.
  28. Bladder exstrophy (a, b) Ultrasound images showing an exteriorized bladder (arrows). (c
  29. Nephroblastoma. Axial (a) and coronal (b) scans of the fetal abdomen showing a solid echogenic mass above the kidney (arrows).