fetal anomaly scan - chest,git,gut

FETAL ANOMALY SCAN [PART TWO]

BY-DR. SAHIL CHAUDHRYMODERATOR-DR.GURURAJ SHARMA

AJIMS MANGALORE

INTRODUCTION ChestGastrointestinal tract Urinary tract

CHEST

Axial view of the thorax: 4-chamber view. In this view,the two lung fields (L), the heart, and the descending thoracic aorta(arrow) behind the left atrium are visible. Laterally, two complete ribsare evident (arrowheads); posteriorly, one thoracic vertebra can beseen. The cutaneous outline, outside the ribcage, is also evident.

The reference to cardiac position and situs is identified by noting the left atrium lies posteriorly, closest to the spine, and the right ventricle lies anteriorly, close to the chest wall

Normal appearance of fetal thymus (arrowheads)at 37 weeks’ gestation.

Coronal T2-weighted MR image shows normal lungs and diaphragm at 37 weeks. I, Axial T2-weightedimage of thymus (arrows) anterior to heart. The thymus is relatively hypoechoic to the surrounding lungs on ultrasound and relatively low intensity on MR

The normal thymic average transverse measurement is12 mm at 19 weeks’ gestation and 33 mm at 33 weeks.The normal thymic average perimeter is 128 mm at 38Weeks.

Acute fetal thymic involution has been reportedin association with chorioamnionitis

Prenatal identification and measurement of thefetal thymus is important when DiGeorge syndrome isSuspected(E/O CLEFTING WITH TOF)

PULMONARY HYPOPLASIAPulmonary hypoplasia (PH) refers to deficient or incomplete development of parts of the lung. It can develop as a result of a number of other in-utero anomalies.There are several key factors required for the adequate development of the lung. These are:sufficient amniotic fluid volumesadequate thoracic space-sizenormal breathing movementnormal fluid within the lungA deficiency in any of these could lead to pulmonary hypoplasia.

Most cases of pulmonary hypoplasia are secondary to other congenital anomalies or pregnancy complications. Some cases however can occur as a primary event.

Intra-thoracic causes include:congenital diaphragmatic hernia: most common intrathoracic causeextralobar sequestrationagenesis of the diaphragmmediastianal massdecreased pulmonary vascular (arterial) perfusion:from a congenital cardiovascular anomaly: e.g tetralogy of Fallotunilateral absence of the pulmonary artery 

Extra-thoracic causes include:oligohydramnios: and its causesPotter sequence: fetal renal anomaliespreterm premature rupture of membranes (PPROM)skeletal dysplasias: especially those causing a narrow fetal thorax

large intra-abdominal mass compressing the thorax

neuromuscular conditions interfering with fetal breathing

Other associations include:Fryns syndromeMeckel Gruber syndromeNeu-Laxova syndromePena-Shokeir syndrome

CONGENITAL PULMONARY AIRWAYS MALFORMATION (CPAM)

A congenital pulmonary airways malformation (CPAM) is a multicystic mass of segmental lung tissue with abnormal bronchial proliferation . CPAMs are considered part of the spectrum of bronchopulmonary foregut malformations and until recently were described as a congenital cystic adenomatoid malformation (CCAM).Five subtypes are currently classified, mainly according to cyst size.type Imost common,one or more dominant cysts: 2-10 cm in size,may be surrounded by smaller cyststype II15-20% of cases,cysts are <2 cm in diameterassociated with other abnormalities

• renal agenesis or dysgenesis• pulmonary sequestration• congenital cardiac anomalies

type III~10% of cases,microcysts: <5 mm in diametertypically involves an entire lobe,has a poorer prognosis

Lesions are usually unilateral and involve a single lobe. Although there is no well-documented lobar predilection, they appear less frequently in the middle lobe

Associationshybrid lesion: e.g. CPAM and pulmonary sequestration renal agenesis

A, Axial sonogram at 28 weeks shows a homogeneously echogenic mass (calipers) in the mid–left hemithorax with no large cysts or feeding vessels. There is mild mediastinal shift tothe right. B, Axial sonogram of right-sided CCAM (arrow) at 20 weeks with small cysts, the largest of which is 8 mm (arrowhead). Thereis moderate mediastinal shift to the left C, Sagittal oblique sonogram shows CCAM everting the hemidiaphragm (arrow).

D, Transverse view of chest with CCAM containing small cysts and mild mediastinal shift. E and F, Axial and oblique coronal images at 25 weeks in amacrocystic CCAM (arrow) with eversion of the hemidiaphragm, trace ascites (arrowhead), and severe mediastinal shift with compressionof the heart (HT)

Congenital lobar emphysema.

D/D

BRONCHOPULMONARY SEQUESTRATION Refers to aberrant formation of segmental lung tissue that has no connection with the bronchial tree or pulmonary arteries. It is a bronchopulmonary foregut malformation (BPFM).Intralobar sequestrationsvenous drainage commonly occurs via the pulmonary veins, but can occur through the azygous/hemi-azygous system, portal vein, right atrium or the IVCclosely connected to the adjacent normal lung and do not have a separate pleuraExtralobar sequestrationsvenous drainage most commonly through the systemic veins into the right atriumseparate from any surrounding lung with its own pleuraOverall, sequestration preferentially affects the lower lobes. 60% of intralobar sequestrations affect the left lower lobe, and 40% the right lower lobe. Extralobar sequestrations almost always affect the left lower lobe, however approximately 10% of extralobar sequestrations can be sub-diaphragmatic

FEEDING VESSEL SIGN

CONGENITAL HIGH AIRWAYS OBSTRUCTION SYNDROMECongenital high airways obstruction syndrome (CHAOS) refers a rare often lethal congenital laryngo-tracheal condition and is primarily characterised by obstruction to the fetal upper airway.

A CHAOS can be of 3 possible types :complete laryngeal atresia without an oesophageal fistulacomplete laryngeal atresia with a tracheo-oesophageal fistulanear-complete high upper airway obstruction 

diffusely enlarged, echogenic lungs bilaterally with eversion of the hemidiaphragms

CONGENITAL DIAPHRAGMATIC HERNIADiaphragmatic development is usually complete by ~9th week of gestation. Congenital diaphragmatic hernias result from failure of fusion of one of the pleuroperitoneal canals at about 8 weeks gestation. They may contain stomach, intestines, liver or spleen.  Congenital diaphragmatic herniation can be classified into two basic types on location:Bochdalek herniamost common foetal congenital diaphragmatic hernia,commoner on the left: 75-90%Posterolateral,presents earlierMorgagni hernialess common,anterior.presents later 

Compression of the heart, impaired swallowing, and partial obstruction of the gastrointestinal tract lead to polyhydramnios, which is present in up to 69% of cases, particularly late in gestation (by the third trimester)Sonographic findings that should prompt a search for CDH include :polyhydramnioscardiomediastinal shift inability to demonstrate the normal stomach bubbleabsent bowel loops in the abdomenintra-thoracic herniation of the liver; noted in up to 85% of cases and is associated with a worse prognosisLeft-sided CDHstomach and small bowel (echo-free) at the same transverse level as the heart on four-chamber view: this makes left sided hernias comparatively easier to detect on ultrasound (as opposed to herniaion of echogenic liver on the right side)stomach and small bowel superior to the inferior margin of the scapulaleftward displacement of the gallbladder 

A, Axial view of chest at 28 weeks’ gestation shows the stomach (arrow) in the chest with mediastinal shift to the right. B, Coronal image in a different fetus at 28 weeks shows a slightlydistended stomach (arrow) in the chest.

C, Oblique sagittal image shows a large amount of liver (Li) in the chest.

D, Axial view of abdomen shows abnormal course of umbilical vein (arrowhead) resulting from the liver herniation into thechest. E, Oblique axial view of chest shows kinked hepatic vessels.

F, Axial view in the right lower quadrant shows the associated polyhydramnioscomplicating the pregnancy in the same fetus.

RIGHT SIDED CDH

EVENTRATION

EFFUSIONS

EXIT

GIT

ABDOMINAL VIEWS

axial view of the upper abdomen: the stomach is visible onthe left, the right hepatic lobe on the right, and the intrahepatic tract ofthe umbilical vein on the midline.

(b) Axial view of the lower abdomen(ventral approach): the bowel (ileus and jejunum) and a small segmentof the umbilical vein (arrow) are visible

• 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)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.

ESOPHAGUS Ultrasound appearance of the esophagus is a pouch full of amniotic fluid, especially if the fetus has just swallowedCan 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 ATRESIAIn 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.

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.

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. It originates when, at 8 weeks of gestation, the primitive foregut does not divide into the ventral tracheobronchial part and the dorsal digestive partType 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 fistulasType E: is tracheoesophageal fistula without atresia.

Ultrasound diagnosis

More than 85% of cases of esophageal atresia are not detected in utero due to the existence of a concurrent TE fistula: this fistula aids 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 trimesterFGR : 40% of cases of TE fistulaDown’s syndrome 50 percent association with Type A

23 weeks 30 weeks

Differential diagnosis. This includes all conditions possibly associated with non-visualization of the gastricBubble . severe oligohydramnios(and consequent lack of amniotic fluid ingestion)in the case of premature rupture of membranes or bilateral renal agenesis; FADS( fetal akinesia deformation sequence) and related syndromes; diaphragmatic hernia; and cleft lip/palate.Association with other malformations in decreasing order, of GI (28%), cardiovascular(24%), genitourinary (13%), and osteomuscular (11%) malformations. 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)

DUODENAL ATRESIA

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 complete atresia. In the remaining 20% of cases, the obstruction can be due to a diaphragm or membrane located within the lumen .

Diagnosis. Double bubble, with communication between the two parts; late polyhydramnios.Risk of chromosomal anomalies. High (20–50%): mainly trisomy 21.

ULTRASOUND DIAGNOSISThis 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 duodenumCare 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

CHOLEDOCHAL CYST

ENTERIC DUPLICATION CYST

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

Association with other malformations. Mostly GI malformations , vertebral and cardiac upto 33%

Risk of chromosomal anomalies.Overall, 40of cases of duodenal atresia are associated with Down syndrome.

SMALL-BOWEL ATRESIADiagnosis. Severe late-onset dilatation of the ileal loops proximal to the obstruction. Late-onset polyhydramnios.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 of the affected segment. This can show a fibrous string connecting the two blind-ending stumps (type II: 32% of cases)Or complete separation of the two stumps without any fibrous connection (type III: 48% of cases).type IV (17% of cases), in which the atresia involves multiple sites

Ultrasound diagnosis :Mainly on the detection of the 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.

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

20 wks 28 weeks 36 weeks

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

Differential diagnosis.Hirschsprung’s diseaseVolvuluisMeconeum ileus

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

MECONIUM ILEUS

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.

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 gestationThe 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.

Meconium ileus. (a) At 29 weeks of gestation, some ileal loops are dilated and show hyperechoic walls (arrow). The presence ofmacrocalcifications (arrowheads) demonstrates the perforation and theconsequent meconium peritonitis. (b) Specimen after surgery. (c) the presence of a secluded sac of ascites containing meconium sludge (arrow). (d) Another case showing diffuse intra-abdominal calcifications(arrows), consistent with a diagnosis of meconium peritonitis.

Differential diagnosis: Small bowell atresias

ANORECTAL ANOMALIES

All of these are malformations causing distal obstruction of the GI tract.Divided on the basis of their embryologic origin, intothe following:• external malformations, due to abnormalities of the development and fusion of the external perineal layers,Eg; imperforate anus with/without fistula internal malformations, 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,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.Of the above-mentioned malformations, only anorectal atresia is detectable by ultrasoundThe main ultrasound finding possibly indicative of 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.

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 wasconfirmed: the anal orifice is not visible

HEPATOMEGALY/SPLENOMEGALYWide spectrum of causes.Intrauterine foetal infections: CMV infection, when severe, is commonly associated with hepatosplenomegalyDown’s syndromerare benign and malignant hepatic tumors, such as hemangioma or hepatoblastoma,Venous congestion as in cardiac or extracardac causesBeckwith–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.

This patient had serologicallyconfirmed hepatitis A.

Evident hepatomegaly, with capsular macrocalcification and moderate ascites.

OMPHALOCELEOmphalocele 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).Diagnosis. Round, solid mass that deforms the anterior abdominal wall, may contain the right hepatic lobealong with 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, Pentology of Cantrell.

The cord insertion is located on the top of the sacTwo variants : presence or absence of the liver in the sac. Embryogentically different and have different prognosisRupture 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 wallAscites may be seen. 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.

The OEIS complex refers to the combined occurence of:An omphalocoeleBladder exstrophy / cloacal exstrophyAn imperforate anusAnd spinal anomalies: e.gkyphoscoliosishemivertebrae

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

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

(a) Normal fetalkidneys at 13 weeks of gestation.At this stage, the kidneys appearas bilateral hyperechoic structures in the paravertebral regions(arrows).

(b) Normal fetal kidneysat 18 weeks. The kidneyappears slightly hyperechoic(arrows) compared with surroundingtissues; the renal

Ultrasound appearance of the fetal kidney at 28 weeks ofgestation: the renal pyramids may be seen as hypoechoic structureswithin the renal parenchyma; the renal pelvis may be seen as an echofreearea medially

Axial scanthrough the fetal pelvis showingthe bladder wall (arrows).

Color flow Doppler image showingboth perivesical arteries separatingaround the bladder(arrow).

RENAL AGENESISDefinition. Renal agenesis is defined as complete absence of one or both kidneys (unilateral or bilateral renal agenesis).Incidence. Unilateral form: 1/1000. Bilateral form: 1–2/5000.Diagnosis. Bilateral form(POTTER): 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

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

PKD ABSENT RENAL ART

RENAL ECTOPIA

Pelvic kidney. (a) Oblique scan through the fetal pelvis. The kidney (arrows) is seen within the pelvis, lying superior to the bladder(BL). (b) Color flow Doppler shows the pelvic kidney artery (arrow), which originates from the aorta at a more caudal level than the contralateralrenal artery (RA). (c) Crossed fused renal ectopia. Note the two fused kidneys (arrows); the lower pole of the upper one is fused with the upper pole of the lower one.

HORSESHOE KIDNEY

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

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 , which have a more anterior location and are often slightly dilated.

AUTOSOMAL RECESSIVE POLYCYSTIC KIDNEY DISEASE (ARPKD) – POTTER TYPE I

Both kidneys are increased in volume and are hyperechogenic. The bladder cannot be visualized, and severe oligohydramnios is present.

MULTICYSTIC DYSPLASTIC KIDNEY (MCDK) – POTTER TYPE II

Unilateral: the kidney is increased in volume, with multiple non-communicating cysts of variable size; the parenchyma is hyperechoic; normal amount of amniotic fluid and bladder visualized.

Bilateral: same as above + severe oligohydramnios and inability to visualize bladder.

AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE (ADPKD) – POTTER TYPE III

Diagnosis. Kidneys moderately increased in volume, hyperechogenic (often the cortex only), with a bladder that can be visualized and normal or slightly reduced amniotic fluid

OBSTRUCTIVE CYSTIC DYSPLASIA – POTTER TYPE IVDiagnosis. Kidney(s) of normal or reduced dimensions with increased echogenicity of the parenchyma and presence of cysts in variable positions (frequently pericortical). If bilateral, oligohydramnios and a dilated bladder with thick walls are present.

MCDK VS OCD

Parenchymal rimUrethral involvementBilaterality

Algorithm for evaluation of hyperechogenic kidneys.

HYDRONEPHROSIS, HYDRO-URETERONEPHROSIS, AND BLADDER DILATATION

Diagnosis. Dilatation of the collecting system of the kidney.

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 5 mm up to 32 weeks of gestation and 7 mm from the 33rd week onwards

HYDRO-URETERONEPHROSISVUJ OBSTRUCTION HUN WITH URETEROCOELE

DUPLEX KIDNEY WITH TWO COLLLECTING SYSTEMS AND URETEROCOELE

BLADDER/CLOACAL EXSTROPHYDefinition. 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. 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.

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).

ALGORITHM FOR NON VISUALISATION OF BLADDER

RENAL TUMORS

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.Etiology and pathogenesis. Mesoblastic nephroma, which is a benign lesion, is the most common tumor, followed by the malignant Wilms’ tumorDiagnosis is generally made in the 3rd trimester. The tumor mass may occupy part of the kidney oreplace it completely . If it is very large, a mass effect on adjacent abdominal viscera may bedetected.

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

POSTERIOR URETHRAL VALVE

Rupture of an obstructed bladder (arrow) may occur,producing urinous ascites,

AMBIGUOUS GENITALIADiagnosis. It is difficult to differentiate micropenis with cryptorchidism from clitoromegaly with normal labia;

In males, the main findings are micropenis, ventral curvature of the penis, retained testicles, scrotum bifidum, and hypospadias; in females, the main finding is clitoromegaly.

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