 Good evening. Before starting the second part of the fetal urogenital system, let's have a short recap of what we discussed in the first part. So, in the first part, we discussed about the urinary tract dilatation, how to format the report of the UTD so that it will include the description of calluses, cortical thickness and echogenicity, ureter bladder and the bladder outlet. Then we also discussed about the abnormalities of the renal number, position as well as the hyperacoic kidneys and its etiologies. So, in part 2, we will discuss about the anomalies of bladder, the ambiguous genitalia, the adrenal clearance and the ovarian pathologies. So, bladder can be enlarged or bladder can be not at all visualized. So, now coming to dilative bladder. When longitudinal diameter of the bladder is more than or equal to 7 millimeters in the first trimester, then it is called mega cystis. No such cutoff exists in the second or the third trimester. When the bladder diameter is between 7 to 15 millimeter, it is mild to moderate mega cystis. And in this group, 20% cases are associated with chromosomal abnormalities. While in the chromosomal normal group, more than 90% of the cases of this mega cystis resolved to normal. When the bladder diameter is more than 15 millimeters, it is a severe form of mega cystis. In this group, hardly 10% are chromosomally abnormal, but in the chromosomal in normal group, the mega cystis leads to progressive obstructive neuropathy. So, in mega cystis, the chromosomal evaluation is indicated. So, this is around the 13 weeks fetus, where you can see a very prominent bladder. When the bladder diameter was measured, it was around 9.3 millimeters. And here, you can see the kidneys, which are very prominent, the pervecalation system is very prominent, the dental cortex is ecogenic. And then if you see here, you can see the dilated ureter also. While this is another fetus of around 13 weeks, where you can see this hugely dilated distended urinary bladder. See, this large bladder is senior, the bladder can be identified by the uterine artist. And again in this video, you can see the dilated pervecalation system and then the hyper-equity nal cortex. And what are the causes of bladder dilatation? It could be a transient dilatation or it could be an obstructive abnormality caused by posterior urethral valves or urethral stenosis or atrophy or colloidal degeneracies. Or it can be non-obstructive anomalies like the VU reflux, the vesicle atonia, the mega cystis micro colon intestinal hypoperestalsis that is the NMIS syndrome and mega cystis mega urector syndrome. Both these syndromes are quite rare. There are ultrasound, there are certain specific characteristics of the bladder along with the ureter kidney and amniotic fluid, which can help us to reach the specific diagnosis for the distended bladder. In posterior urethral valve, we get a distended thick bald bladder. We can get the keyhole sign. Nearly ureters are dilated. There can be hydronephrosis and depending on the degree of hydronephrosis, the ringal cortex can be ekozine and there can be even presence of small cysts. The amniotic fluid can be normal or can be reduced. When in urethral atresia, the bladder is grossly distended with very thin walls. The kidneys and the kidneys are small and ekozidic. They are basically because of the obstructive cystic dysplasia and here the lycra amount the amniotic fluid is markedly reduced or it can be absent. When in primary reflux, the bladder wall is apparently normal. The bladder is distended. The ureters depending on which stage of reflux it is, it can be dilated or normal. The hydronephrosis is definitely there and the amniotic fluid is normal in primary reflux. When in cloacal dysgenesis or persistent cloaca, the distended bladder has a normal or a thick wall and we can see the presence of hydrocolpus behind posterior to the bladder. Here because of the compression of the bladder outlet because of the hydrocolpus, the bladder is dilated. The ureters are dilated. Here we can get hydronephrosis and depending on the degree of obstruction, the amniotic fluid may be normal or can be reduced. So, here is a case of posterior refill valve where you can see a thick wall bladder with a typical keyhole sign and then the kidneys are highly ekozidic and you can see the central carisal dilatation also. With recent advances, fetal intervention is possible in the luto. So, fetal interventions like the vesicle amniotic shunt, which is a percutaneously done under the ultrasound guidance or a fetal systoscopic laser ablation of the posterior urethral valve can be done. So, now in which fetuses should we go for the interventions? So, a classification of the luto according to the severity was proposed in which luto was divided into three stages. The criteria used for this staging are amniotic fluid volume, the ekozidicity of the fetal kidneys, the renal cortical cyst, the renal dysplasia and the fetal urinary biochemistry. The fetal urinary biochemistry tells us about the renal function. The renal ekozidicity, the presence of the cortical cyst or the renal dysplasia indicate that the kidneys definitely damaged. So, in stage when everything is normal, the fetal urinary biochemistry is also favorable and therefore in such cases the interventions are not indicated. In stage 2, there is severe luto, but the prenatal findings, the parameters like amniotic fluid ekozidicity, etc, suggest that the renal function is preserved and in this way if you go for fetal intervention, then there is a high chance that the severe renal impairment can be avoided. While in stage 3, the parameters already suggested that there is significant fetal abnormal renal function and that the intervention can be indicated basically to prevent the pulmonary hypoplasia, but not the postnatal renal impairment. Now, coming to the non-visualization of the bladder. Whenever the bladder is not visualized, first we have to look at the kidneys and see for the presence. If the kidneys are not present and the amniotic fluid is totally absent, then it is bilateral renal urgenesis, which can be diagnosed or confirmed on the color Doppler examination by showing the absence of the renal arteries. And then with persistently non-visualized bladder, you see kidneys. How will you proceed? So, here we have to look for the ecogenesis of the kidney and then if the kidneys are hyper-ecoic, we need to look for the volume of the kidneys. We have studied this algorithm last time. If the volume of the kidneys is large, like the kidneys are large hyper-ecoic with absent or reduced amniotic fluid, then it can be ARPKD or ADPKD or it can be bilateral multi-cystic kidney. And then if the renal volume is reduced with decreased amniotic fluid, then it is a prototype for type means it is the obstructive cystic renal dysplasia. Now, if the kidney ecogenesis is normal, how will we proceed? Here we have to look at the amniotic fluid. The amniotic fluid is reduced with the absent or reversed endosteric flow on the umbilical arteries, then it is a severe FGR. And if the amniotic fluid is normal, we have to evaluate the genital area to look for any genital mass which can keep present a bladder extrafie or a cloacal extrafie. The rare cause of bladder non-visualization, which we should know are bladder extrafie and the cloacal extrafie. Bladder extrafie is a very rare condition which occurs in one in 30,000 live birds. Here there is persistently non-visualization of the bladder with a small mass on the lower anterior abdominal vault. It is associated with abdominal genitalia and the amniotic fluid is normal. To differentiate the bladder extrafie from other anterior abdominal masses, the key angle was proposed by Kavita Aneja in IJRI in 2017. So what is this key angle? It is the angle between the umbilical arteries and the aorta. Normally this angle is acute angle by the bladder extrafie. This angle becomes an obtuse or it goes nearly to 90 degrees. These images are from Dr. Aneja's publication where in the lower one you can see the acute angle formed by the umbilical arteries and the aorta tension while in bladder extrafie here you can see that the angle is become obtuse. In the axial section we can see the parallel course of the intraabdominal umbilical arteries instead of the converging course. Cloacal extrafie it's a still rare condition. Here persistent cloaca occurs because of failure of the urorectal septum to divide cloaca into anterior urinary bladder and the posterior rectum. In presence of a lower anterior abdominal vault defect, this persistent cloacal aversion occurs leading to the cloaca extrafie. Here again in ultrasound we cannot see the bladder. There is an infra umbilical mass which is formed by the averted cloaca and also the umphalocene. Spinal renal and clover limb anomalies are associated with cloaca extrafie. And this is a postnatal picture of a typical elephant trunk appearance in the cloaca extrafie where we can see the umphalocene. The bilateral bulges are the amybladders and through which a small bowel herniation occurs which give the appearance of the elephant trunk. So this is the elephant trunk appearance classical of cloaca extrafie. Now coming to ambiguous genitalia the incidence is around 1 in 4500. On ultrasound the accurate diagnosis is very difficult. The micro penis with cryptorchidism cannot always be differentiated on ultrasound from the clitoral hypertrophy with normal labia. So here is a case this primate came for ultrasound between 17 to 18 weeks. The ultrasound findings were that there was there were bilateral CTV. Adrenal glands were enlarged and the the genitalia were abnormal. So here in this clip you can see hypoechoic triangular large areas just above the kidneys. The length of this hypoechoic triangular area is nearly half that of the kidneys. So these are the still images of the left adrenal and the right adrenal gland which are enlarged. And on this clip of the perineal area you can see the labia and in between there are there is a protrusion. So in this case a higher diagnosis of congenital adrenal hyperplasia was suspected. The patient refused any fickle investigations like amnu and the pregnancy was terminated and this is the picture of the abortus showing the abnormal genitalia. And this is the report of the mother which was later done where it shows that the CYP21A2 gene shows a mutation which is associated with congenital adrenal hyperplasia. Though in this case it was of uncertain clinical significance. The other adrenal gland anomalies which we can see in the prenatal period are the adrenal gland cysts where we can see just above the kidney we can see rounded legions which may be an echoic or can have internal echoes. There can be atrial hemorrhage which present as mass and then there can be neuroblastoma which are very rare finding. And ovarian cysts are the common intraabdominal cysts in the female fetus and they are usually seen in the third trimester or third trimester. Presentation is usually an anechoic cyst in the pelvis. At times the cyst can be hemorrhagic and may go in torsion. It can be unilocular or it can be a multi-locular cyst. Rarely there can be polyhydramnus because of bowel obstruction caused by the large cyst. Spontaneous regression is always seen after the birth. On ultrasound we need to show the cysts separate from the bladder. Identification of the bladder can be done by the visualization of the umbilical arteries on the color Doppler. And in our reporting we should mention about the presence of pelvic cysts rather than labelling them as ovarian cysts in the report. So to conclude bladder must be documented in all trimester. A detailed evaluation of the perineal area is indicated in suspected pathologies. And to repeat again GUT evaluation begins from the first trimester and we should remember that the cacod that is the congenital anomalies of kidney and the urinary tract are evolving anomalies. And in the description of the urinary tract dilatation we should include the renal pelvis, scalysis, ureter and the bladder as well as the amniotic fluid. And then we should remember that ultrasound finding can prognosticate the renal outcome and therefore they should be very meticulously evaluated. And a timely antinatal and postnatal therapy can be initiated by our prenatal ultrasound findings which prevent the renal damage and improves the outcome of the affected child. Thank you very much.