Oliguria, anuria and urinary obstruction: SAQ

This male infant presents anuria with a palpable distended bladder, which is a lower urinary tract obstruction until proven otherwise, and the most likely diagnosis in a male infant is posterior urethral valves. The palpable suprapubic mass that does not empty with gentle pressure is a distended bladder, and the absence of any urine today is true anuria rather than a missed collection. The creatinine of 145 micromoles per litre and the potassium of 6.6 mmol per litre confirm an acute kidney injury with hyperkalaemia complicating the obstruction, and the metabolic acidosis with a pH of 7.24 reflects the accumulating acid from the failing kidney. The immediate priority is to relieve the obstruction by catheterisation and to treat the hyperkalaemia in parallel. ^[6]

Question 1 (10 marks)

Outline the immediate management of this infant, including the relief of the obstruction and the management of his hyperkalaemia. ^[6]

The first action is to pass a urethral catheter, because anuria with a palpable bladder is a lower tract obstruction until proven otherwise. An appropriately sized paediatric Foley catheter, 6 to 8 French for an infant, is passed with aseptic technique, and the drainage of a large retained volume confirms the diagnosis and begins the decompression. If the urethral catheter will not pass, as it may in posterior urethral valves where the catheter coils at the obstruction, I would not persist traumatically but would escalate to a suprapubic catheter or to urgent paediatric urology referral. The decompression must be achieved by whatever route reaches the bladder, because the relief of the obstruction is the single most important intervention for preserving renal function. ^[6]

In parallel I would treat the hyperkalaemia as an emergency. I would check a 12-lead ECG, and if there were ECG changes of hyperkalaemia, I would give intravenous calcium gluconate at 0.5 mL per kg of the 10 percent solution over 5 to 10 minutes with cardiac monitoring to stabilise the myocardial cell membrane. Calcium does not lower the potassium, so I would follow it immediately with the agents that shift potassium into the cells, including intravenous insulin with glucose, nebulised salbutamol, and sodium bicarbonate given his acidosis. I would recheck the potassium after each intervention because the effect is transient, and the decompression of the obstruction addresses the underlying cause of the potassium retention. ^[1]

I would establish the intravenous access, check a bedside glucose, send the bloods for creatinine, electrolytes, full blood count, and a venous gas, and send a urine specimen for culture once the catheter is draining. I would request an urgent renal tract ultrasound to confirm the bilateral hydronephrosis, the dilated posterior urethra, and the thick-walled bladder of posterior urethral valves, and I would involve the paediatric nephrologist and the paediatric urologist early for the definitive diagnosis by voiding cystourethrogram and the primary valve ablation. I would monitor the infant in a neonatal or paediatric intensive care setting with hourly urine output, continuous cardiac monitoring, and serial creatinine and electrolytes. ^[6]