Persistent Urinary Ascites Following Bladder Dome Perforation in a Premature Neonate

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Description

A premature male neonate born at thirty-one weeks of gestation was transferred to a neonatal intensive care unit because of progressive abdominal distension, respiratory difficulty, and reduced urine output during the second week of life. The infant had required ventilatory support after birth because of respiratory distress syndrome and remained under intensive monitoring. Umbilical arterial and venous catheters had been inserted shortly after delivery, and intermittent bladder catheterization had been performed several times during treatment for suspected sepsis.

At thirteen days of life, nursing staff observed gradual abdominal enlargement associated with worsening oxygen requirement. Enteral feeding intolerance developed, and the infant became increasingly lethargic. Physical examination revealed tense abdominal distension with visible abdominal wall veins and generalized edema. The scrotum also appeared enlarged and translucent. Blood pressure remained stable, although tachycardia was present. Laboratory evaluation demonstrated elevated serum creatinine and urea levels compared with earlier measurements. Hyponatremia and metabolic acidosis were also identified. Urine output declined substantially over twenty-four hours despite adequate fluid administration. Blood culture results remained negative. Initial abdominal radiography demonstrated diffuse bowel displacement without pneumoperitoneum.

Both kidneys appeared structurally normal without hydronephrosis. Diagnostic paracentesis produced clear straw-colored fluid. Biochemical analysis of the ascitic fluid demonstrated creatinine concentration significantly higher than serum values, strongly suggesting urinary ascites. A voiding cystourethrogram was subsequently performed using minimal contrast volume because of the infant’s fragile condition. Contrast extravasation from the superior bladder wall into the peritoneal cavity confirmed bladder perforation at the dome region. No evidence of posterior urethral obstruction or vesicoureteral reflux was identified.

Emergency operative management was undertaken because of persistent urinary leakage and progressive respiratory compromise from abdominal pressure. Through a small infraumbilical incision, exploration identified a 1 cm perforation at the bladder dome surrounded by inflamed but viable tissue. No intestinal injury or necrosis was present. The perforation was repaired in two layers using fine absorbable sutures. A suprapubic catheter and urethral catheter were inserted simultaneously to provide continuous urinary drainage during healing. Postoperatively, abdominal distension decreased gradually over several days. Respiratory status improved significantly, permitting reduction in ventilatory support. Repeat ultrasonography one week later demonstrated complete disappearance of ascites.

Catheters were maintained for ten days before cystographic reassessment confirmed intact bladder healing without further extravasation. At discharge six weeks later, renal function remained normal and no urinary symptoms were evident. Urinary ascites in neonates represents an uncommon but clinically significant condition that may lead to severe metabolic disturbance and respiratory compromise. Bladder perforation accounts for one of the major causes of neonatal urinary ascites, particularly among premature infants receiving intensive care interventions. The bladder dome remains especially vulnerable because it constitutes the weakest and most mobile portion of the neonatal bladder wall.

Several contributing factors likely participated in perforation development in this patient. Prematurity itself results in reduced tissue strength and limited bladder capacity. Repeated catheterization may additionally injure delicate mucosa and muscular layers. Episodes of bladder overdistension related to urinary retention or catheter malfunction can further increase intravesical pressure and predispose to rupture. Clinical presentation may initially resemble gastrointestinal or septic conditions because abdominal distension, feeding intolerance, and respiratory deterioration occur commonly in critically ill neonates. Declining urine output despite fluid accumulation should raise suspicion for urinary leakage, especially when renal function deteriorates rapidly without intrinsic renal disease.

Management depends on perforation size, clinical stability, and persistence of leakage. Small extraperitoneal perforations may occasionally heal with catheter drainage alone. In contrast, intraperitoneal rupture involving ongoing urinary extravasation generally requires operative repair because continuous leakage may produce severe respiratory and metabolic complications. The favorable outcome in this infant reflected rapid recognition and surgical correction before irreversible renal or pulmonary injury occurred. Continuous postoperative bladder drainage reduced pressure on the repair site and promoted healing.

Premature neonates possess increased susceptibility to postoperative infection and electrolyte instability, necessitating close intensive care monitoring throughout recovery. Long-term prognosis after successful bladder repair in neonates is generally satisfactory when diagnosis occurs early. Follow-up assessment should include monitoring of bladder function, renal growth, and urinary tract anatomy during infancy. Although recurrent perforation remains uncommon, children with previous neonatal bladder injury warrant periodic surveillance.

Conclusion

Prevention of iatrogenic bladder injury in neonatal intensive care units remains clinically important. Gentle catheterization technique, avoidance of excessive bladder distension, and careful monitoring of urinary output may reduce risk in vulnerable premature infants. Prompt investigation of unexplained abdominal distension and oliguria can facilitate earlier diagnosis of urinary leakage. Persistent urinary ascites resulting from bladder dome perforation in a premature neonate. The case demonstrates how urinary leakage may mimic gastrointestinal or septic conditions in critically ill newborns and emphasizes the importance of biochemical ascitic fluid analysis for diagnosis.