Urinary ascites secondary to posterior urethral valves

Abstract

Neonatal urinary ascites demands prompt diagnostic and therapeutic medical attention. Obstructing posterior urethral valves are a major cause (70 per cent) of this entity. Survival in these children can be directly related to age, selection of therapeutic modality and the presence or absence of associated pulmonary and electrolyte abnormalities. Oligohydramnios is implicated in the production of pulmonary hypoplasia leading to respiratory distress in these patients. Other manifestations of prolonged, increased fetal compression, that is the non-renal features of Potter's syndrome, include altered facies, aberrant hand and foot development and late fetal growth deficiency. Aberrant pulmonary development seems to be related to increased intrauterine pressure (oligohydramnios alone) as well as increased fetal intra-abdominal pressure (oligohydramnios plus urinary ascites). The best therapeutic results were achieved in those children treated by early, high urinary diversion. The mortality rate for newborns less than 72 hours old was significantly higher (66 per cent) than for those more than 72 hours old (15 per cent).