Year : 1999 | Volume
: 9 | Issue : 4 | Page : 169--182
Sonographic assessment of fetal abdominal cystic lesions : A pictorial essay
Department of Ultrasound, Meera Hospital, Shiv Marg, Bani Park, Jaipur, India
S-9, Bhawani Singh Road, C-Scheme, Jaipur
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Agarwal R. Sonographic assessment of fetal abdominal cystic lesions : A pictorial essay.Indian J Radiol Imaging 1999;9:169-182
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Agarwal R. Sonographic assessment of fetal abdominal cystic lesions : A pictorial essay. Indian J Radiol Imaging [serial online] 1999 [cited 2020 Feb 22 ];9:169-182
Available from: http://www.ijri.org/text.asp?1999/9/4/169/28349
Fetal abdominal cystic lesions are a common finding during routine antenatal ultrasonography. They may arise virtually from any abdominal organ; however, the urogenital and gastrointestinal systems are the ones most commonly involved.
Cystic masses in the fetus are reliably identified with US but it may not be possible to make a precise prenatal diagnosis. The shape, size, character and position of the lesions usually suggest the most likely diagnosis. The relationship to the adjacent organs and normality of the other organs also help in arriving at a diagnosis. Detection of associated anomalies, assessment of the liquor amnii, visualization of the genitalia, karyotyping and family history further help in the diagnosis.
Isolated lethal cystic lesions or the lesions associated with other serious structural defects and/or abnormal karyotype need no further US surveillance. In such cases, termination of pregnancy is a reasonable approach. However, isolated, non-lethal lesions should be monitored with repeated ultrasound examinations because the evolution of these lesions in utero is extremely variable. They may increase in size, decrease or even disappear or may undergo complications which carry life-threatening risks to the fetus. Serial scans not only help in the management of the pregnancy but are also valuable in therapeutic management.
This pictorial essay originates from the department of ultrasound of a 35-bedded maternity hospital and includes fetal abdominal cystic malformations recorded during routine antenatal US (about 15,000 cases) between January 1992 and December 1998. Various congenital malformations detected at this centre have been followed by serial US scans. The prenatal findings have been correlated with autopsy reports after termination of pregnancy or postnatal investigations/or surgical findings after delivery. This approach has helped in defining the natural history of congenital anomalies, determining the pathophysiologic features that affect clinical outcome and formulating management based on prognosis.
UROGENITAL CYSTIC LESIONS
In the first month of life, 40% of neonatal masses are genitourinary in origin. The common causes of cystic lesions are hydronephrosis, renal dysplasia, ovarian cyst, hydrometrocolpos and urachal cyst.
Hydronephrosis is the most common cause of fetal abdominal cystic lesions. The upper tract dilatation may range in severity from mild (only a dilated renal pelvis with or without calyceal dilatation) to severe obstruction, resulting in rupture of the renal collecting system . Minimal pyelectasis in the fetus is common and unlikely to be significant in every case . However, UPJ obstruction and reflux may manifest initially as mild fetal pyelectasis ,. In addition, karyotype abnormalities, remarkably Trisomy 21, are reported to be associated with mild pyelectasis . The exact diameter of the renal pelvis that should trigger prenatal surveillance and postnatal investigation of mild fetal pyelectasis remains controversial ,,,. Hydronephrosis is considered present if the antero-posterior fetal renal pelvis diameter is > 10 mm  [Figure 1] or if the ratio of the antero-posterior diameter of the renal pelvis to the antero-posterior diameter of the kidney is greater than 0.5 . Postnatal investigations are required if the antero-posterior pelvic diameter is > 7 mm after 33 weeks or > 4 mm before 33 weeks of gestation . Calyceal dilatation is much more significant. This indicates hydronephrosis even when the pelvis/kidney ratio is less than 0.5 and always persists into the postnatal period .
Mild fetal pyelectasis is characterised by a small amount of fluid in the fetal renal pelvis. In moderate hydronephrosis, the reniform contour is maintained and the fluid spaces are anatomically arranged and communicate with one another. Any preserved parenchyma is seen at the periphery of the fluid containing structure. In most severe cases, only a large cystic structure is seen because the normal morphology of the Kidney is lost [Figure 2]. In such cases, distinction from other abdominal cystic masses may be difficult. However documentation that the masses touch the fetal spine assists in localisation of the mass to the genitourinary system . Though, significant progress of dilatation and thinning of renal parenchyma in utero is relatively uncommon , when it occurs, the urinary tract may rupture and produce a paranephric urinoma. It then appears as a large unilocular cystic mass touching the spine . Urine ascites [Figure 3] or uriniferous perirenal pseudocysts (urinomas) from spontaneous decompression of the urinary tract may occur as early as the beginning of the second trimester .
Hydronephrosis of varying degrees is readily identified by antenatal US. However, a relative degree of hydronephrosis in utero does not always correlate with renal parenchymal function. Hydronephrosis may not be present in a fetus with chronic urinary tract obstruction. Further, US features of hydronephrosis caused by urinary tract obstruction depend on the severity of obstruction as well as the gestational age at which obstruction begins. Obstruction in the first half of gestation causes renal dysplasia [Figure 4], whereas obstruction that originates during the second half of gestation causes hydronephrosis and atrophy , [Figure 5].
US is limited in its ability to predict both renal functional loss as well as the difference between functional and anatomic obstruction . However, it has the capacity to recognise the level of obstruction accurately . Poor prognostic signs are oligohydramnios, lack of caliectasis, urine ascites, dystrophic calcification, renal dysplasia, associated multisystem abnormalities and abnormal karyotype. The assessment of amniotic fluid volume is not entirely reliable as polyuria may ccur in a failing renal function. Chemical analysis of fetal urine taken from each renal pelvis is most useful for predicting renal function.
Fetal abdominal cystic masses due to hydronephrosis may result from many obstructive and non-obstructive causes. Sites of obstruction are at the ureteropelvic junction and urethra. Non-obstructive causes of urinary tract dilatation are vesico-ureteric reflux, neurological lesions, primary mega-ureter and as part of the megacystis microcolon syndrome .
Ureteropelvic Junction Obstruction
The most common cause of neonatal hydronephrosis is obstruction at the UPJ. It can be diagnosed on a routine mid-trimester scan. US features of unilateral UPJ obstruction include varying degrees of pelvicaliectasis without any evidence of ureterectasis, ectopic ureterocele, dilated, thick-walled urinary bladder or posterior urethral dilatation . If the contralateral kidney is normal, the amount of amniotic fluid is normal. Bilateral UPJ obstruction occurs in about 30% of cases. Involvement is usually asymmetrical. In cases of severe bilateral UPJ obstruction, oligohydramnios is present and the urinary bladder remains empty. Unilateral obstruction may be associated with contralateral multi-cystic dysplastic kidney or renal agenesis. The correct diagnosis of hydronephrosis due to UPJ obstruction is important because reconstructive surgery may salvage a hydronephrotic kidney even when there appears to be a thin rim of renal parenchyma . UPJ obstruction may be associated with central nervous system (CNS), cardiovascular system (CVS), gastro-intestinal (GIT), skeletal [Figure 6] malformations and chromosomal anomalies. 
Ureterovesical Junction Obstruction
It is the second most common cause of hydronephrosis. US visualises varying degrees of ureterectasis and caliectasis [Figure 7] In uniteral cases the bladder fills and empties normally and there is no evidence of bladder wall thickening or posterior urethral dilatation. Normal fetal ureters are never visualised on ultrasound. The dilated ureter appears as an echo-free intra-abdominal tubular structure, which touches the spine and can be traced back to the renal pelvis [Figure 7]. Sometimes, in severe bilateral obstruction (in which the bladder is small), the ureters are convoluted and are so dilated that they may be falsely assumed to be the bladder. In such situations, differentiating a `ureterovesical obstruction' is difficult. The presence of a dilated posterior urethra helps in differentiating these two entities. The most common cause of ureterovesical obstruction is ureteric duplication and obstruction of the upper pole moiety. US visualises dilatation of the obstructed ureter leading to a hydronephrotic upper pole. The ureterocele may rarely be seen as a cystic structure within or adjacent to the urinary bladder .
It is difficult or impossible to differentiate between ureterovesical junction obstruction and other causes of mega-ureter. However, if obstruction is the cause, the ureter lengthens and so is more serpiginous than in primary mega-ureter where the course is much straighter . Furthermore, in primary refluxing ureter, hydronephrosis is usually mild and non-progressive and there may be evidence of peripheral cortical dysplasia. In the presence of a duplex system, ectopic or horseshoe kidney, obstruction is most likely .
Posterior urethral valves, anterior urethral valves, diverticula, urethral strictures, urethral atresia and ectopic ureterocele cause bladder outflow obstruction. Functional bladder neck obstruction can also result from non-relaxation of the bladder neck in neurogenic bladder dysfunction.
Although the antenatal sonographic signs of urethral obstruction vary, the cardinal signs include dilatation of the fetal urinary bladder and proximal urethra with hypertrophy if it is thick enough to be measured . A dilated posterior urethra (seen in upto 50% of patients) appears as a focal outpouching of the urinary bladder extending towards the perineum. Such an appearance is described as a `key-hole appearance'. The presence of ureterectasis, caliectasis and oligohydramnios augments the diagnosis of urethral obstruction. However, their absence should not preclude the diagnosis .
Posterior urethral valves [Figure 3],[Figure 4],[Figure 5],[Figure 8]a,b are the most common cause of bladder outflow obstruction. The condition exclusively occurs in the male fetus. It can be diagnosed as early as 12 weeks of gestation  [Figure 8]A,B. Early detection is important because posterior urethral valves are one of the few malformations amenable to fetal surgery. The condition usually occurs as a sporadic disorder but familial cases have been reported too . It may be associated with abnormal karyotype, including Trisomy 13 and 18 . Associated abnormalities reported are tracheo-esophageal fistula, total anomalous pulmonary drainage, mitral stenosis, skeletal abnormalities and imperforate anus ,,.
Fetal urethral atresia (common in female fetuses) is characterised by anhydramnios. The completely obstructed bladder appears as a massive centrally placed cystic structure  [Figure 9]a,b. The chest circumference is extremely small in relation to the abdominal circumference . If the atresia is due to persistent cloaca, the cystic structure may be more complex with two or three `loculations' . In urethral atresia the appearance of the kidneys may be identical to multi-cystic dysplastic kidney or the adult polycystic kidney disease, whereas, early urethral obstruction due to posterior urethral valves leads to peripheral cortical cystic dysplasia of the kidneys [Figure 3],[Figure 4]. Urethral agenesis may be associated with the rare MURCS association . Ruling out other causes of bladder outflow obstruction, such as urethral strictures (rare in boys) and anterior urethral valves (exclusively occurs in boys), may be difficult or impossible, but such cases are rare.
Urinary bladder dilatation and thickening of the muscle wall are found usually with bladder outflow obstruction. However, similar findings may be associated with neurogenic bladder dysfunction. US recognition of the dilated posterior urethra helps in differentiating bladder outflow obstruction from neurogenic bladder. Furthermore, a normal spinal evaluation makes a neuraxis abnormality less likely. Megacystis-microcolon syndrome predominantly affects girls and is associated with a large urinary bladder, dilated small bowel and polyhydramnios. Massive vesicoureteric reflux is difficult to differentiate from bladder outlet obstruction . However, in such situations, posterior urethral dilatation is never visualised.
Urethral obstruction from valves is the most common cause of the Prune-belly syndrome. The condition is characterised by a hypotonic abdominal wall, a large distended urinary bladder with ureterectasis and caliectasis and cryptorchidism.
Renal dysplasia, defined as abnormal parenchymal development from anomalous differentiation of metanephric tissue, implies irreversible damage . About 90% of renal dysplasia is associated with urinary tract obstruction during nephrogenesis . The severity of obstruction and also its site correspond well with the pattern of dysplasia ,. Bernstein  classified renal dysplasia into four categories;
Multicystic dysplasia _ MCDK (unilateral multicystic dysplasia is invariably due to ureteric atresia while bilateral malformation is accompanied by bilateral ureteric or urethral atresia). Focal or segmental dysplasia (associated with renal or ureteric duplication with an ectopic ureterocele and ureteric reflux). This pattern of dysplasia resembles MCDK or peripheral cortical cystic dysplasia. Bilateral peripheral cortical cystic dysplasia (commonly caused by posterior urethral valves). Heredofamilial cystic dysplasia (occurs in a number of rare inherited syndromes and is nonobstructive in origin).
Multicystic Dysplastic Kidney
Many reported cases were diagnosed during the late second and third trimester. However, the condition can be detected by transvaginal ultrasound (TVS), as early as in the 12th week of gestation. MCDK is characterised by an un-capsulated, paraspinal mass with multiple, randomly arranged, non-communicating cysts of variable sizes, resembling a bunch of grapes, with total loss of the reniform shape of the kidney [Figure 10]a,b. Rare segmental MCDK may occur in one pole of a duplex kidney or within a crossed fused ectopic kidney . In unilateral cases, there is no oligohydramnios and the bladder appears normal. In bilateral cases [Figure 10]c there is severe oligo-hydramnios and the fetal urinary bladder remains empty. Bilateral cases always lead to Potter's sequence. The MCDK may change substantially in appearance with the progression of pregnancy . The kidney may enlarge or may diminish in size. Spontaneous involution has been noted to occur before birth ,.
Correct distinction between MCDK and hydronephrosis (due to UPJ obstruction) is important because MCDK is almost a functionless kidney and there is a low incidence of complications and a high incidence of spontaneous regression and involution , whereas reconstructive surgery may salvage a hydronephrotic kidney.
In up to 40% of patients there will be a contralateral renal tract anomaly, which may include malrotation, UPJ obstruction or horseshoe kidney. Other associated anomalies include CVS, CNS (anencephaly, hydrocephalus, spina bi fida), GIT (diaphragmatic hernia, duodenal stenosis, tracheo-esophageal fistula, imperforate anus) anomalies, cleft palate and bilateral absence of radius and thumb. MCDK may occur in association with many syndromes such as Dandy-Walker and Apert's syndrome.
Peripheral Cortical Cystic Dysplasia
It is associated with non-atretic urinary tract abnormalities, most commonly posterior urethral valves  [Figure 3],[Figure 4]. Sonographically the kidneys may appear abnormally reflective. The increased reflectivity of the kidney is due to the multiple microscopic cysts and the increased fibrous tissue within the dysplastic kidney . The degree of reflectivity of the renal substance can predict moderate to severe dysplasia  but assessment of fetal renal echogenecity offers only limited predictive value (specificity = 80% and accuracy of positive prediction = 89%) for cortical dysplasia . Visualisation of renal cortical cysts in a fetus with known obstructive uropathy accurately predicts (specificity = 100% and accuracy of a positive prediction = 100%) the presence of severe and irreversible dysplasia . However, it may be difficult to demonstrate cysts in all cases of dysplasia because the cysts are too small to be imaged clearly by ultrasound . Rarely, the APCKD (autosomal dominant) may present prenatally ,,. The appearance of the kidneys may be identical to peripheral cortical cystic dysplasia. However, in such situations, there is no dilatation of the upper or lower urinary tracts.
Heredofamilial Cystic Dysplasia
A number of rare inherited syndromes such as Zellweger's, Meckel-Gruber and Jeune syndrome are associated with nonobstructive cystic dysplasia. The appearance of the kidneys may be identical to peripheral cortical cystic dysplasia, MCDK or APCKD. Prenatal diagnosis can be made by the identification of the associated abnormalities in the syndrome . Zellweger's syndrome is characterised by cerebro-hepato-renal dysplasia. In Meckel-Gruber syndrome, cystic dysplasia is associated with a cranio-spinal defect and post-axial polydactyly while Jeune syndrome is associated with asphyxiating thoracic dystrophy and Trisomy 18 .
A urachal cyst is single and lies in the anterior part of the fetal abdomen extending from the bladder to the umbilicus. Urachal anomalies are more common in boys. A patent urachus may occur as an isolated anomaly or it may be associated with the prune-belly syndrome.
Antenatal detection of ovarian cysts has been reported usually in the second or third trimester. The majority, are benign simple cysts such as follicular, theca lutein, corpus luteum or simple cysts in which the cell lining has been destroyed. The cause of fetal ovarian cysts still remains unclear. It may be related to excessive stimulation from maternal/placental gonadotropins. This would explain an increased incidence of ovarian cysts in infants of mother with diabetes, rhesus isoimmunisation or toxemia ,,. Congenital hypothyroidism may be associated with fetal ovarian cysts .
An uncomplicated cyst appears as a purely cystic mass with an imperceptible cyst wall  [Figure 11]a,b. Though usually unilateral, bilateral cysts have been reported too . These cysts are usually of 3-5 cm size but may grow to very large proportions. Since the fetus has almost no true pelvic cavity, the cyst may lie in the mid or upper abdomen or even on the contralateral side [Figure 11]a,b and because of a long cyst pedicle, it may wander in the abdomen . The cyst may increase in size, decrease or even disappear or undergo complications . Complications include torsion, hemorrhage, necrosis, rupture and intestinal obstruction. A cyst complicated by torsion or hemorrhage invariably contains a fluid-debris level, a retracting clot or septa . Such cysts may also appear solid because of organised hematoma. Development of a fluid-debris level in the cyst appears to be a specific sign of cyst torsion  [Figure 11]c. Complicated cysts also have a definable, thin, echogenic wall due to dystrophic calcification  [Figure 11]d. There may or may not be perceptible color or spectral Doppler flow. A cyst complicated by torsion may show extreme mobility during real time sonography because such a complication leads to the necrosis of the cyst pedicle or fallopian tube, allowing the cyst to break loose and float in the peritoneal cavity. Torsion is common in utero and may occur even when the cyst does not grow to large proportions.
Polyhydramnios has been reported in about 5%-10% of patients. The exact cause of polyhydramnios is not known. Partial obstruction of the small bowel or compression of the umbilical cord are two proposed theories ,.
Precise diagnosis of an ovarian cyst is difficult. Differentiation from mesenteric, omental, retroperitoneal cysts, cystic teratoma, duplication cyst, adrenal cyst, pancreatic cyst and unilateral hydronephrosis due to UPJ obstruction is difficult. However, an ovarian cyst
Hymenal atresia results in a dilated uterus and vagina [Figure 12]. Accumulated secretions in the uterus and vagina present as a cystic mass, which extends low into the pelvis, posterior to the bladder. Hydrometrocolpos may obstruct the bladder and intestines. Bladder obstruction may cause hydronephrosis while intestinal obstruction may lead to meconium peritonitis. The condition may present as a part of a syndrome such as McKusick-Kaufman syndrome, which is an autosomal recessive, multiple malformation syndrome characterised by hydrometrocolpos, MCDK, polydactyly and may be associated with nonimmune hydrops .
GASTROINTESTINAL CYSTIC LESIONS
Approximately 15% of pediatric abdominal masses are gastrointestinal in origin. Fetal abdominal cystic masses related to the GIT may occur due to intestinal obstruction, gastric duplication and omental or mesenteric cysts. Obstructions involving the stomach, duodenum, jejunum or proximal ileum are called high obstructions. Obstructions that involve the distal ileum or colon are called low intestinal obstructions. The diagnosis is usually not made until late in the second or third trimester.
Duodenal Atresia or Stenosis
The duodenum is the most common site of atresia or stenosis. It occurs when the duodenum, which is a solid tube from about three to six weeks of gestation, fails to recanalise partially or completely. About 80% atresias or stenoses are just distal to the ampulla and are frequently accompanied by abnormalities of the bile duct and pancreas. This abnormality is not usually evident at a routine 18 to 20 week scan but is more often detected later in the pregnancy when the patient presents for an anomaly scan because of polyhydramnios. Antenatal diagnosis relies on the US image of the `double bubble' sign in a transverse section of the fetal abdomen . This image results from dilatation of the stomach and duodenum proximal to the atretic area . A connection must be demonstrated at the pylorus  [Figure 13]. On occasion, a coronal scan of the normal stomach can produce an image similar to that of duodenal atresia because of the presence of a proximal incisura angularis . Transverse scans of the fetal abdomen demonstrate the depth of the incisura and solve this diagnostic problem . US cannot diagnose the actual site and type of obstruction. However, it is of little importance because there is no cause of congenital duodenal obstruction, complete or partial, that does not require surgery. Measurement of bile acid concentration in amniotic fluid may differentiate a lesion above the ampulla of Vater (in which bile acids are absent) from those below the ampulla (in which bile acids are present).Duodenal atresia or stenosis may be associated with other congenital anomalies such as other intestinal atresias, congenital heart disease and the VACTERL association. About 30% of cases are associated with Down's syndrome.
Jejunal or Ileal Obstruction
Jejunal atresia or stenosis and ileal atresia or stenosis are less common than duodenal atresia. Unlike duodenal atresia, jejunal atresia and ileal atresia are caused not by failure of recanalization but by ischemic injury to the developing gut. The ischemia may be due to a primary vascular accident or secondary to a mechanical obstruction, such as that which occurs in the case of an in utero volvulus . Inspissated, tenacious, noncalcified meconium in meconium ileus is a major source of increased echogenicity in the fetal abdomen ,,. It is usually associated with cystic fibrosis, which is an autosomal recessive disorder. Rarely, pancreatic duct obstruction may cause meconium ileus. Visualisation of dilated, echogenic bowel with shadowing suggests cystic fibrosis. However, their absence should not preclude the diagnosis. About 30% of neonates with bowel obstruction are associated with cystic fibrosis .
The criteria for dilated bowel loops include both subjective and luminal measurements ,. US visualises at least one or more fluid containing, tubular, sausage-shaped structures  of more than 7 mm internal diameter
[Figure 14]a,b. The loop just proximal to the site of obstruction may be disproportionately dilated with a bulbous end. Peristaltic activity and floating particles can be visualised in the lumen of the dilated loops of the bowel. Dilated fetal bowel is a nonspecific US finding that may indicate the presence of fetal intestinal abnormalities of many etiologies i.e. atresia or stenosis, malrotation with volvulus, meconium ileus, Hirschsprung's disease, congenital bands, enteric duplication and Meckel's diverticulum. The cause of bowel anomaly and level of obstruction cannot be determined accurately in the prenatal period .
Small bowel obstructions are usually associated with polyhydramnios and association with other anomalies and abnormal karyotype is rare .
If the ischemic event that produced the atresia caused a perforation, there may be evidence of meconium peritonitis with peritoneal calcification . Meconium peritonitis may take a variety of forms depending on the time sequence of the perforation . The fibro-adhesive type of meconium peritonitis seals off the perforation and forms a meconium pseudocyst which is characterised by a highly reflective, calcified intra-abdominal mass associated with dilated bowel, ascites and polyhydramnios. In the cystic variety, a cystic mass is visualised at the site of perforation, in which meconium continues to leak. Such meconium peritonitis may not be associated with dilated bowel loops or polyhydramnios. Meconium peritonitis in utero with calcified peritoneal foci, fetal ascites, bowel dilatation and hydramnios is more often due to ischemic bowel than due to cystic fibrosis . The differential diagnosis of meconium pseudocyst includes hemangioma, teratoma, ovarian dermoid, hepatoblastoma and metastatic neuroblastoma .
Large Bowel Obstruction
Colonic obstructions may result from Hirschsprung's disease, meconium plug syndrome or small left colon syndrome and colon atresia. Less frequent causes include anorectal malformations and megacystis-microcolon-intestinal hypoperistalsis syndrome.
In contradistinction to small bowel obstruction, the diagnosis of large bowel obstruction may be difficult in that, as a result of fluid absorption by the colonic mucosa, there may be little or no proximal dilatation and no polyhydramnios. Further, distinguishing abnormally dilated colon from normal colon occasionally may be difficult since the normal fetal colon progressively enlarges during pregnancy and can approach 2 cm in diameter towards term . In addition, prenatal identification of the precise cause and site of obstruction may not be possible.
Hirschsprung's disease is caused by varying lengths of aganglionic bowel leading to functional obstruction. It can be diagnosed in the prenatal stage  [Figure 15]. However, precise diagnosis of the condition is difficult in the absence of a positive family history. Boys are affected more often than girls (4:1) and there is an increased familial incidence in long segment disease. Serious associated anomalies are relatively infrequent. However, the condition may be associated with Down's syndrome (5%), Laurence-Moon-Bardet-Biedl syndrome and Wardenburg syndrome as well as CVS abnormalities.
Meconium plug syndrome is a common cause of colonic obstruction. The exact etiology of the syndrome remains unknown. There is no association with cystic fibrosis.
Colon atresia is rare compared with atresias of the small bowel. The atresia may occur with other intestinal atresias. As is the case with small bowel atresias, association with other anomalies and abnormal karyotype is rare.
Anorectal atresia _ ARA (includes spectrum of malformations such as imperforate anus, anal agenesis and rectal atresia) can be recognized in utero  and has a high frequency of associated malformations. Although colon dilatation does not occur in all cases, discovery of a colon diameter greater than 2 SD above normal diameter is considered abnormal . A `U' or `V' shaped segment of the dilated bowel arising from the perineal region behind the bladder is particularly suggestive of ARA  [Figure 16]. Presence of intraluminal meconium calcification suggests imperforate anus with a rectourinary fistula . Anal atresias are associated with many syndromes . Association with the VACTERL association, sacral agenesis and lower limb hypoplasia as part of the caudal regression syndrome  is common.
Megacystis-microcolon syndrome, as discussed earlier, is characterised by a large size stomach and urinary bladder with polyhydramnios.
Duplication, Mesenteric and Omental cysts.
There is no specific US sign for duplication cysts as well as mesenteric and omental cysts. Therefore, it may prove impossible to make a precise prenatal diagnosis. The cause of intestinal duplication is unknown, but its development has been attributed to defects in recanalization of the intestinal lumen after the solid stage of embryonic development. Localised duplication may occur in any area of the gastrointestinal tract but is most common in the ileum and jejunum. Duplication of the entire colon, rectum, anus and terminal ileum may occur. The defects are thought to be secondary to caudal twinning with duplication of the hind-gut, genital and lower urinary tracts.
Duplication cysts [Figure 17] are elongated, tubular or spherical cystic masses, usually unilocular and anechoic. Multiple septations and sludging levels may be visualised.
Duplication cysts may cause bowel obstruction, which can be diagnosed easily by demonstration of distended peristaltic loops of bowel proximal to the cyst. Localised duplication cysts may be difficult to differentiate from Meckel's diverticulum. Meckel's diverticulum usually communicates with the gastrointestinal tract and has gastric contents.
The cause of mesenteric and omental cysts is unclear but these are generally considered to be lymphatic hamartomas. These cysts are usually single and multilocular and may vary in size from a few millimetres to several centimetres. The fluid they contain may be serous, chylous or hemorrhagic . Differentiation from other cystic masses particularly ovarian cysts and retroperitoneal cysts, is difficult or impossible.
HEPATOBILIARY CYSTIC LESIONS
Cystic hepatic masses are usually biliary in origin. Small hepatic cysts are usually simple and are of little significance. Large hepatic cysts of unknown cause have been reported too . Gallbladder should be visualised separately from the lesion.
Choledochal cyst is a rare disorder. The majority of cases have been reported in Japan. The condition can be diagnosed in the late second or third trimester. It usually presents as a solitary, non-pulsatile cystic mass in the right upper quadrant of the fetal abdomen. Demonstration of dilated bile ducts entering the cyst confirms the diagnosis ,. The cause of bile duct dilatation is controversial and may be due to congenital weakness of the wall of the common bile duct in a specific segment associated with increased intraductal pressure secondary to obstruction of the distal common duct. Choledochal cyst is a sporadic occurrence and no specific associations have been reported.
OTHER CYSTIC LESIONS
Rarely, cystic masses may arise from adrenal glands, pancreas, spleen other abdominal organs and retroperitoneum. Precise antenatal diagnosis of these lesions is almost impossible.
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