By using transvaginal sonography, the bladder can be seen as early as 11 weeks of gestation. By 12 to 13 weeks, the bladder is visualized in 98% of cases using both transabdominal and transvaginal sonography.

1. Fetal Urogenital
Presented by Dr Vrishit Saraswat
Guided By Prof Dr. Dharmraj Meena

6. The often-quoted rule of thumb that
renal length in millimeters approximates
gestational age in weeks only applies to a
narrow gestational age range of 18 to 21
weeks.
The renal/abdominal circumference ratio
remains constant at 0.27 to 0.30 throughout
pregnancy

8. By using transvaginal sonography, the bladder can
be seen as early as 11 weeks of gestation. By 12
to 13 weeks, the bladder is visualized in 98% of
cases using both transabdominal and transvaginal
sonography.
The normal bladder fills and empties (either
partially or completely) approximately every 25
minutes (range, 7-43 min). Therefore, changes in
bladder volume should be observed during the
course of the obstetric sonogram.

9. The umbilical (superior vesical) arteries run
lateral to the bladder as they course toward
the umbilicus

10. PRENATAL DIAGNOSIS OF URINARY
TRACT ABNORMALITIES
Assessment of amniotic fluid volume
Localization and characterization of urinary tract
abnormalities
Search for associated abnormalities

11. EVALUATION OF THE FETAL
URINARY TRACT
Kidneys :-
Presence
Number
Position
Appearance (echogenicity, cysts)
Unilateral or bilateral
Bladder
Presence
Appearance and size

12. Collecting System
Dilation
Level of obstruction
Cause of obstruction
Unilateral or bilateral
• It is important to perform a detailed anatomic scan to
search for associated abnormalities, which may indicate
the presence of a syndrome or chromosomal abnormality.
Renal anomalies may be part of the VATER association
(vertebral defects, anal atresia, tracheoesophageal
fistula, radial defects and renal anomalies). An expansion
of this syndrome, VACTERL, includes cardiac and nonradial
limb defects.

13. Bilateral Renal Agenesis
The ureteric bud fails to develop; nephrons do not
form; no urine is produced; and severe
oligohydramnios results. Pulmonary hypoplasia is the
major cause of neonatal death. Other features of
“Potter’s sequence” include typical facies (beaked
nose, low-set ears, prominent epicanthic folds,
hypertelorism), limb deformities, and IUGR.

14. The ultrasound findings include severe oligohydramnios and nonvisualization
of the kidneys and bladder. Before 16 weeks’ gestation, AFV is not
dependent on urine production and may be normal despite absent renal
function. The absence of fetal kidneys should be the most specific finding,
but this may be difficult to document because of poor image quality
associated with oligohydramnios. In addition, bowel or adrenal glands in
the renal fossae may be mistaken for kidneys. However, recognition of the
distinctive, flattened appearance of the adrenal gland on longitudinal
sonogram (“lying down” adrenal sign) helps to confirm that the kidney
did not develop in the flank. Repeated and consistent nonvisualization of
the urinary bladder (over 1 hour) is a secondary sign of bilateral renal
agenesis.

18. A horseshoe kidney is frequently associated with
other anomalies (e.g., urogenital, cardiac,
skeletal, CNS) and chromosomal abnormalities
such as Turner syndrome, trisomy 18, and
trisomy 9. Isolated horseshoe kidney is a relatively
benign disorder that requires postnatal urologic
followup because of higher prevalence of VUR,
renal calculi, urinary tract infections (UTIs), and
hydronephrosis.

21. Multicystic Dysplastic Kidney
A multicystic dysplastic kidney (MCDK) is the most
common form of renal cystic disease in childhood and
represents one of the most common abdominal masses
in the neonate. The majority of cases are associated with
an atretic ureter and pelvoinfundibular atresia. The
kidney is replaced by multiple cysts of varying sizes.
Between the cysts is a dense stroma, but usually no
normal renal parenchyma. MCDK is almost always
nonfunctional, so the prognosis depends entirely on the
contralateral kidney. Multicystic renal dysplasia usually
affects the whole kidney.

23. In a fetus with obstructive uropathy, the sonographic
identification of cortical cysts is indicative of renal
dysplasia (i.e., irreversible renal damage)

24. Obstructive Cystic Renal Dysplasia
Unilateral disease can be caused by ureteropelvic or
vesicoureteral junction obstruction. Bilateral disease is
caused by severe bladder outlet obstruction, usually
urethral atresia or posterior urethral valves.
Sonographic distinction between MCDK and
obstructive cystic renal dysplasia may be difficult, especially
in the absence of hydronephrosis. In obstructive
cystic renal dysplasia, recognizable parenchyma surrounds
the relatively small cysts, whereas in MCDK, no
normal renal parenchyma can be identified between
cysts. Obstructive cystic renal dysplasia most often occurs
with urethral obstruction.

25. Echogenic dysplastic kidney. Longitudinal
scan of fetus at 32 weeks with urethral obstruction. The
kidney (calipers) demonstrates increased echogenicity, with no
visible cysts. There is loss of corticomedullary differentiation.
With severe chronic obstruction, the kidney becomes dysplastic
and ceases to function. Note lack of pelvicaliectasis. S, Stomach.

30. • Autosomal dominant PKD typically is not recognized
in the fetal period because the kidneys typically appear
normal. In rare cases, ADPKD can present during
the fetal or neonatal period with symmetrically enlarged
hyperechogenic kidneys, within which small cysts
may be identified AFV is often normal.
• Of 83 reported cases of ADPKD presenting in utero
(excluding termination of pregnancy) or in the first few
months of life, 43% died before 1 year.

33. Meckel-Gruber syndrome
Meckel-Gruber syndrome is a lethal autosomal
recessive disorder that carries a 25% risk of
recurrence. It can be detected by sonography at
11 to 14 weeks’ gestation, particularly in families
with prior affected pregnancies.75 Sonographic
diagnosis requires identification of at least two
features of the classic triad: cystic dysplastic
kidneys (present in almost 100% of cases),
occipital encephalocele (60%-85%), and
postaxial polydactyly(55%)

34. Hyperechogenic kidneys
Small kidney Normal size Enlarged kidneys Enlarged kidneys
with
associated
anomalies
Obstructive
dysplasia
Normal variant
or obstructive
dysplasia
Autosomal recessive
and autosomal
dominant
polycystic kidney disease
Trisomy 13
Meckel-Gruber
syndrome
Beckwith-
Wiedemann
syndrome

36. Congenital mesoblastic nephroma is the most
common renal neoplasm in the fetus and newborn.84
It is a benign hamartoma composed of mesenchymal
tissue (spindle cells), as opposed to the epithelial tissue
of Wilms’ tumor. Wilms’ tumor is a malignant lesion
that is extremely rare in the fetus. Sonographically,
mesoblastic nephroma is indistinguishable from Wilms’
tumor. Mesoblastic nephroma is usually seen as a
moderately echogenic, solid mass completely replacing
the kidney or localized to part of the kidney85
(Fig. 39-18). The mass may demonstrate increased vascularity
and cystic components. Polyhydramnios is a
frequent association84 and may lead to preterm labor
and preterm birth.

39. Neuroblastoma is the most common abdominal
malignancy in neonates, and the adrenal gland is the
most common primary site. On prenatal sonography,
the retroperitoneal mass can be cystic, solid, or of
mixed echogenicity. Adrenal hemorrhage, which is
much more common in the neonate, can have a
sonographic appearance similar to that of an adrenal
or renal neoplasm.

40. Color Doppler ultrasound may be helpful in
differentiation. The key to the diagnosis of
adrenal hemorrhage is evolution of the lesion
over time; serial sonograms demonstrate a
change in echogenicity (from solid to cystic)
and a decrease in size of the mass.94,95
Because neuroblastomas may also regress,
however, it is important to obtain postnatal
follow-up in fetuses with presumed

42. • The size of the renal pelvis increases
throughout gestation and there are published
nomograms for RPD. In general, the cutoff
values for RPD vary between 4 mm and 5 mm
in the second trimester and between 7 and 10
mm in the third trimester. Pyelectasis is
usually an isolated finding, but a detailed
ultrasound examination should be performed
to detect other urinary tract pathologic
processes and nonrenal anomalies.

43. Urinary tract obstruction produces a varied response from the
kidneys. A, Normal kidney. B, Pelvicaliectasis, with or without
parenchymal atrophy.
C, Renal cystic dysplasia, with parenchymal cysts.
D, The dysplastic
kidney may cease to function (lack of pelvicaliectasis).
E and F, Alternatively, the kidney may show increased echogenicity,
with no visible cysts but with pelvicaliectasis (E)
or without pelvicaliectasis (F)

44. PUJ Obstruction

45. •DETECTION OF A URETEROCELE
DETECTION OF A URETEROCELE
Thin-walled cystlike structure in bladder.
Overlooked if bladder is empty.
Full bladder can compress ureterocele.
May cause bladder outlet obstruction

46. Longitudinal scan shows two separate collecting
systems. The hydronephrotic, upperpole
renal pelvis (U) is continuous with the dilated
ureter (arrow). The lower-pole collecting system
(L) is dilated because of reflux

47. CAUSES OF FETAL MEGACYSTIS
• Posterior urethral valves
• Urethral atresia/stricture
• Prune belly syndrome
• Megalourethra
• Cloacal malformation
• Megacystis-microcolon–intestinal
hypoperistalsis

48. MMIHS
Megacystis-microcolon–intestinal hypoperistalsis
syndrome (MMIHS) is a rare, nonobstructive cause of
megacystis, with a 4 : 1 female predominance. The syndrome
involves not only a distended bladder but also
functional small bowel obstruction and microcolon. It
is important to differentiate this syndrome from the
more common posterior urethral valves because it
carries a dismal prognosis, and fetal bladder shunting is
not indicated. The key features of MMIHS are (1) the amniotic fluid
is usually normal or increased; (2) the fetus is usually
female; and (3) rarely a dilated small bowel may be
present.
Advice fetal MRI in suspected cases.

49. Dilated urinary bladder (B) and
proximal urethra (*) give the appearance of a
keyhole, characteristic of urethral obstruction in a
21-week fetus.

50. Coronal scan shows
dilated tortuous ureters (arrows).

51. Urinary ascites
Longitudinal scan of a
22-week fetus shows a thick-walled bladder (B) and
urinary ascites
(*) caused by spontaneous rupture of severe megacystis

53. Urethral atresia causes the most severe form of
obstructive uropathy. The sonographic features include
a greatly distended bladder and anhydramnios after the
first trimester . In the absence of antenatal
treatment, urethral atresia is almost always fatal, because
of associated renal dysplasia and pulmonary hypoplasia.
A small number of survivors have been reported
after antenatal intervention

54. To be continued…..
Thank you