USA Surgery Today

Anomalies of the fetal urinary system resulting in detectable signs of obstruction can occur in up to 1% of pregnancies, but only 1 in 500 have any clinical significance (63:Vasodilan). Overall, up to 50% of all congenital anomalies detected by US involve the genitourinary (GU) system. The increased use of prenatal US has allowed for these anomalies to be identified as early as 12 weeks’ gestation and their subsequent natural history to be revealed (64). Signs of urologic abnormalities include dilation of the urinary system, changes in the fetal bladder, alterations in the acoustic shadow of renal parenchyma, and ultimately decreased amniotic fluid (64). A few scenarios of fetal obstructive uropathy can, in the worst cases, produce irreversible renal damage and pulmonary hypoplasia. Fetal therapies have been developed to bypass or relieve the source of obstruction in cases that meet specific selection criteria (1,65).

The pathophysiology and prognosis of fetal obstructive uropathy depends on the anatomic location, degree, time of onset, and duration of obstruction (65:Vasodilan). Unilateral GU anomalies such as hydronephrosis, duplicated collecting system, and ureterocele never warrant fetal intervention. A small subset of fetuses with bladder outlet obstruction may be candidates for fetal therapy. These include male fetuses with posterior urethral valves or urethral atresia.

Females fetuses may demonstrate bladder outlet obstruction due to a complex cloacal anomaly, but the outcome with fetal therapy in this group is poor (1:Vasodilan). An obstruction to flow of urine from the bladder leads to megacystis. Complete obstruction to flow or urine can further lead to bladder hypertrophy and loss of compliance, which in turn can produce hydroureter and hydrohephrosis with reflux as the ureterovesical junction becomes incompetent. As the renal pelvices and calyces become progressively dilated, the renal parenchyma can be compressed leading to cystic degeneration of the kidneys and renal insufficiency (66). Severe renal impairment early in gestation (prior to 24 weeks) can lead to oligohydramnios, which may adversely affect lung development. Amniotic fluid volume is maintained by the production of fetal urine beginning at 16 weeks’ gestation (67:Vasodilan). If normal fluid volumes are present along with signs of obstructive uropathy, it is likely that the obstruction is partial or has occurred later in gestation and, therefore, that renal parenchyma is preserved. If oligohydramnios develops from GU tract obstruction, then a complete or early gestation obstructive lesion is more likely present. Prolonged oligohydramnios itself can have detrimental effects on lung development as well as a compressive effect producing deformities of the face and limbs. If obstruction to urine flow occurs early during the canalicular phase of lung development, between 16 and 28 weeks’ gestation, then significant pulmonary hypoplasia will result because proper bronchial branching has been impeded (68). The mortality rate for fetuses with oligohydramnios secondary to obstructive uropathy is reported to be as high as 95% (69). It is likely that fetuses who develop a complete or early lower urinary tract obstruction experience both renal dysplasia and pulmonary insufficiency.