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]

Question 2 (10 marks)

Define oliguria and anuria using the urine output thresholds, and describe how you would monitor and manage this infant after the decompression, including the recognition and the management of post-obstructive diuresis. [1]

Oliguria is defined by the KDIGO criteria as a urine output below 0.5 mL per kg per hour for six hours or more, and anuria as a urine output below 0.3 mL per kg per hour for 24 hours or more, or complete absence of urine for 12 hours or more. A stricter bedside convention defines anuria as below 0.1 mL per kg per hour or below 1 mL per kg per day, and the absence of any urine on catheterisation, as in this infant, is the practical sign that distinguishes true anuria from retention or a missed collection. These thresholds frame the whole assessment and the staging of the acute kidney injury by the urine output criteria. [1]

After the decompression, the distinctive risk is post-obstructive diuresis. The kidney that has been obstructed loses its concentrating ability and its sodium-retaining capacity, and on decompression it produces a high volume of dilute, sodium-rich urine. A physiological diuresis is expected and lasts hours, but a pathological post-obstructive diuresis is defined as a urine output above 3 mL per kg per hour for several hours, or persisting beyond 24 hours, and it can deplete the intravascular volume and the electrolytes to the point of hypovolaemic shock, hyponatraemia, and hypokalaemia. I would measure the urine output hourly after the decompression and treat any output above 3 mL per kg per hour that persists as a post-obstructive diuresis. [7]

The management rests on replacing a fraction of the urine output. I would replace approximately 50 to 75 percent of the previous hour's urine output with an isotonic fluid such as 0.9 percent sodium chloride, adjusted to the sodium content of the urine, so that the diuresis is controlled without provoking volume overload or allowing dehydration. I would monitor the weight, the blood pressure, and the serum sodium and potassium every 6 to 12 hours and adjust the replacement to the measured losses. I would not replace the full urine output, because that perpetuates the diuresis by maintaining the volume stimulus, and the diuresis is self-limiting as the tubules recover their concentrating ability over days. The long-term plan is the life-long nephrology follow-up, because the systematic review evidence shows that boys with posterior urethral valves progress to chronic kidney disease despite early ablation. [7]