Paeds Vivas · nephrology-urology-fluids-and-electrolytes
Oliguria, anuria and urinary obstruction: Viva
Branching clinical structured oral on paediatric oliguria, anuria and urinary obstruction: defining oliguria and anuria by urine output thresholds, the pre-renal, renal and post-renal classification, the emergency catheter decompression of a lower tract obstruction, the pathophysiology of obstructive nephropathy, and the recognition and fluid management of post-obstructive diuresis.
On this page & tools
Target exams
Branch 1: Definition and classification
The candidate should recognise that this infant has true anuria with a lower tract obstruction, the classic presentation of posterior urethral valves in a male infant. A strong candidate states the urine output thresholds precisely: oliguria is a urine output below 0.5 mL per kg per hour for six hours or more, and anuria is below 0.3 mL per kg per hour for 24 hours or more, or complete absence for 12 hours or more, by the KDIGO criteria. The candidate should note the stricter bedside convention of anuria as below 0.1 mL per kg per hour or below 1 mL per kg per day, and that the absence of any urine on catheterisation distinguishes true anuria from retention or a missed collection. [1]
If the examiner presses on the classification, the candidate should describe the three anatomical levels: pre-renal, where reduced perfusion lowers the filtration pressure in a structurally intact kidney; renal or intrinsic, where the nephron is structurally damaged; and post-renal or obstructive, where a block in the outflow tract raises the hydrostatic pressure upstream. The candidate should identify this infant as a post-renal cause, and should name posterior urethral valves as the most common cause of lower tract obstruction in male infants, presenting with a palpable distended bladder, a poor stream, and antenatal bilateral hydronephrosis. [6]
Branch 2: Immediate and definitive management
If asked about the immediate management, the candidate should treat the anuria with a palpable bladder as an obstruction until proven otherwise, and the first action is a urinary catheter, not a fluid bolus. A paediatric Foley catheter, 6 to 8 French for an infant, is passed to relieve the obstruction and to measure the retained volume, and the drainage of a large retained volume confirms the diagnosis. If the urethral catheter will not pass, the candidate should not persist traumatically but should escalate to a suprapubic catheter or urgent urology, because the decompression must be achieved by whatever route reaches the bladder. [6]
The candidate should run the hyperkalaemia management in parallel. A 12-lead ECG is checked, and if there are ECG changes, intravenous calcium gluconate at 0.5 mL per kg of the 10 percent solution is given for myocardial membrane stabilisation, followed by the agents that shift potassium into the cells. The candidate should state that the decompression addresses the underlying cause of the potassium retention. The definitive management is the primary valve ablation by a paediatric urologist, or a temporary vesicostomy in the small or unstable infant, and a voiding cystourethrogram confirms the diagnosis. The candidate should involve the nephrologist and the urologist early and arrange the life-long nephrology follow-up. [6]
Branch 3: Pathophysiology and post-obstructive diuresis
If the examiner moves to the pathophysiology, the candidate should explain the pressure-driven mechanism. A block in the outflow tract raises the hydrostatic pressure upstream, and that pressure transmits backwards into the tubules and the Bowman capsule, narrowing the filtration gradient and lowering the glomerular filtration rate. The kidney is structurally intact at this early stage, so the relief of the obstruction restores the gradient within hours. If the obstruction persists, the pressure-driven fall progresses to the tubular atrophy and the interstitial fibrosis that Nørregaard and colleagues charted at the molecular level, and the duration of the obstruction determines the recovery. [3]
The candidate should describe the post-obstructive diuresis that follows the relief. The obstructed kidney loses its concentrating ability and its sodium-retaining capacity, so on decompression it excretes a high volume of dilute, sodium-rich urine. A physiological diuresis lasts hours, but a pathological post-obstructive diuresis persists beyond 24 hours with a urine output above 3 mL per kg per hour, and it can deplete the intravascular volume and the electrolytes to the point of hypovolaemic shock. The management replaces approximately 50 to 75 percent of the previous hour's urine output with an isotonic fluid, because the full replacement perpetuates the diuresis. The candidate should stress that the child who is making urine after the decompression is not necessarily safe, and the diuresis must be actively monitored. [7]
References
- [1]Kellum JA, Lameire N, KDIGO AKI Guideline Work Group Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Crit Care, 2013.PMID 23394211
- [3]Nørregaard R, Mutsaers HAM, Frøkiær J, Kwon TH Obstructive nephropathy and molecular pathophysiology of renal interstitial fibrosis. Physiol Rev, 2023.PMID 37440209
- [6]López Pereira P, Martinez Urrutia MJ, Jaureguizar E Initial and long-term management of posterior urethral valves. World J Urol, 2004.PMID 15558286
- [7]Leinum LR, Berthelsen C, Azawi N Post-obstructive diuresis; underlying causes and hospitalization. Scand J Urol, 2020.PMID 32449436