Urinary Tract dilatation (UTD) is one of the most common anomalies that can be picked up prenatally. It occurs in 1–2% of all pregnancies. Its prenatal detection helps to manage the condition prior to the development of complications such as urinary tract infection (UTI), calculus formation or renal dys­function postnatally. In most of the cases (50–70%), the uri­nary tract dilatation is transient or physiologic without any clinical signicance. In the rest, it may be due to obstructive pathology like pelviureteric junction obstruction (10–30%), primary obstructive megaureter (5–15%), posterior urethral valves (1–5%) or vesicoureteric reux (10–40%). The less common causes can be ectopic ureter, duplex collecting sys­tem, and urethral atresia or prune belly syndrome. The etiology may not be dened before birth in all cases and is diagnosed postnatally with imaging which includes ultrasound and mic­turating cystourethrogram (MCUG). Urinary tract dilatation is a dynamic process uctuating over time and with varying con­ditions like degree of distension of urinary bladder prenatally and hydration and patient position postnatally. Hence, urinary tract dilatation can present as a spectrum of severity—for example, not all cases of posterior urethral valves present with severe urinary tract dilatation (Figs.3.49–3.53).

In fetuses of UTD A1, the APRPD is 4 to <7 mm at <28 weeks (Fig. 3.10a, b) and 7 to <10mm at ≥28 weeks (Fig.3.10c, d) with normal renal parenchyma, nonvisualized or undilated ureter, normal urinary bladder with normal amni­otic uid volume. They may have central calyceal dilatation. In fetuses with UTD A2–3, the APRPD is ≥7mm at <28weeks (Fig.3.11a, b) and ≥10mm at ≥28weeks (Fig.3.11c, d) or any one of the following ndings: dilatation of peripheral calyces (Fig. 3.11e, f), abnormal parenchymal thickness or appearance (Fig.3.11g, h), dilated ureter (Fig.3.11i) an abnor- mal urinary bladder or oligohydramnios.

Based on the UTD classication system, a follow up management scheme has been proposed. For UTD A1 diag­nosed before 32weeks, a follow up prenatal ultrasound is recommended at ≥32weeks. If the ultrasound at ≥32weeks reveals resolution of the UTD with normal renal paren­chyma, bladder and ureters, no further prenatal or postnatal follow up is necessary. If there is persistent UTD A1 or UTD A2–3, evaluation after birth is recommended. Postnatal evaluation should include two ultrasound evaluations: the rst at >48h but less than 1month after birth; and the sec­ond 1–6months later. In fetuses considered at increased risk for postnatal uropathy (UTD A2–3), a follow up prenatal ultrasound is recommended within 4–6weeks of the initial diagnosis of urinary tract dilatation. Where there is substan­tial risk for surgery or renal dysfunction, prenatal consulta­tion with a specialist is recommended. After birth, a follow up ultrasound is recommended at >48h of life to avoid a false negative appearance due to neonatal dehydration. Follow up should be performed earlier for obstructive urop­athy, such as suspected posterior urethral valve (as sug­gested by the nding of a thick walled bladder with persistent dilatation and a fusiform appearance and/or posterior ure­thral dilatation on prenatal ultrasound) or for bilateral con­ditions. Worsening ndings on serial prenatal or postnatal ultrasound are associated with increased risk for genitouri­nary pathology. UTD is most often transient and associated with an increased risk of Trisomy 21 anomaly warranting a detailed ultrasound and correlation with aneuploidy screen­ing protocols.