Posterior Urethral Valves
Posterior urethral valves are the commonest congenital cause of bladder outlet obstruction in male infants — suspected from antenatal hydronephrosis and a thick-walled bladder, confirmed by VCUG, treated by catheter drainage then valve ablation, with the crucial caveat that ablation does not cure the long-term bladder dysfunction or renal damage.
The big picture
Obstructing membranous valves in the posterior urethra (only in males) impede bladder emptying from fetal life. The bladder hypertrophies (thick-walled, trabeculated), pressures rise and transmit back to the upper tracts, causing hydroureteronephrosis and renal dysplasia/damage; severe cases have antenatal oligohydramnios and pulmonary hypoplasia. After birth, a poor urinary stream, palpable bladder, failure to thrive, sepsis or renal impairment may be seen.
Male infant + antenatal bilateral hydronephrosis + thick bladder → suspect PUV; confirm on VCUG, drain then ablate — but remember ablation does not cure the bladder dysfunction or renal damage.
Mechanism pathway
Tap any step to see why it happens.
Symptom sorter
The common presentation.
Diagnostic algorithm
Each step answers one question. Tap to expand.
Treatment ladder
Relieve obstruction in steps (drain, then ablate) while protecting the kidneys, then manage the persistent bladder dysfunction and renal impairment for life.
Complications
- Chronic kidney disease/renal failure
- Valve bladder dysfunction, incontinence
- Recurrent UTI; pulmonary hypoplasia (severe antenatal cases)
- Residual valves after ablation, urethral stricture
- Complications of diversion/augmentation
- Early diagnosis, drainage and ablation; lifelong surveillance of bladder/kidneys
- Re-ablation, bladder management, nephrology care/transplantation
Follow-up
- Renal function and growth
- Bladder function (compliance, emptying, continence)
- UTIs, electrolytes/concentrating ability
- Lifelong, shared urology/nephrology follow-up
- Relieved obstruction with preserved/optimised renal and bladder function
- Progressive renal impairment, refractory valve bladder, incontinence, end-stage renal disease
- Surveillance and on clinical change (function, infections)
- Valve bladder dysfunction, chronic kidney disease/renal failure (a leading congenital cause), incontinence, fertility considerations
Memory hooks
PUV = male infant bladder outlet obstruction.
Antenatal bilateral hydronephrosis + thick bladder.
VCUG confirms.
Drain, then ablate.
Ablation ≠ cure (valve bladder + renal damage remain).
Board traps
Valve ablation does not cure the bladder dysfunction or renal damage.
Bilateral hydronephrosis + thick bladder in a male → PUV (confirm with VCUG).
Forgetting lifelong renal/bladder follow-up.
Clinical cases
A male neonate with antenatal bilateral hydronephrosis has a poor urinary stream, a palpable bladder and a raised creatinine. After diagnosis and successful endoscopic valve ablation, the parents are told he is 'cured'.
Why is that reassurance inaccurate, and what is needed?