PubMed1975
Infants with posterior urethral valves may seem to have diverse and unrelated symptoms when, in fact, the clinical findings are all related to the primary effect of the valves during various stages of early growth. In some, prenatal urinary obstruction leads to such severe oligohydramnios that the fetus is stillborn. Others, somewhat less affected, are born alive but have severe respiratory distress from hypoplastic (stiff) lungs and die of respiratory problems. Still others can be associated with massive ascites and urinomas, and be stillborn or die soon after birth. In less severe cases the neonates may have unexplained respiratory distress with pneumomediastinum or pneumothorax as the only indication of obstructive urologic disease with deficient urinary output. Urinomas or ascites may later develop beyond the neonatal period as the post-natal obstructive effects of the valves accumulate and the urinary system ruptures and decompresses itself. Finally when the urinary system does not decompress itself, the back pressure can lead to rapid and progressive renal damage until the kidneys can no longer concentrate urine and lose water. The infant becomes dry, acidotic and paradoxically at this stage, puts out large quantities of dilute urine. Physicians caring for infants should be highly suspicious of posterior urethral valves in any male infant with unexplained respiratory distress or metabolic derangements, abdominal distension or flank masses.