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The P.A.D.U.A. technique is a method of addressing congenital urethral narrowing.
It involves passive dilation with a series of progressively larger indwelling catheters.
Utilization is limited by scant literature, particularly regarding technical details
and long-term durability. Tools for achieving safe and reliable urinary drainage are
critical in these patients, who require careful stewardship of their kidney and bladder
To describe long-term urethral patency and urinary function following P.A.D.U.A.,
and to provide sufficient technical detail to reproduce the technique.
Patients with congenital urethral narrowing managed with P.A.D.U.A. were identified
and chart review was performed. Details of catheter exchange sequences were compiled
and described. The primary outcome was the attainment of adequate urethral caliber
by successful completion of P.A.D.U.A., and the secondary outcome was voiding per
urethra at most recent follow-up.
P.A.D.U.A. achieved adequate urethral caliber in 9/11 (82%) of patients. This included
seven patients with Prune Belly Syndrome, one with isolated urethral atresia, and
one with a cloacal anomaly. P.A.D.U.A. failed to achieve urethral patency in one patient
with urethral duplication, who was unable to progress through the catheter sequence,
and one patient with Prune Belly Syndrome, who completed P.A.D.U.A. but developed
recurrent narrowing one week later. There were no delayed failures of urethral patency.
Patients who achieved patency underwent a median of seven catheter placements over
92 days. Median (range) initial and final catheter sizes were 3.5F (1.9–8F) and 14F
(8–16F). While 82% achieved patency, only 3/11 (27%) were voiding spontaneously per
native urethra at most recent follow-up.
This series of patients undergoing P.A.D.U.A. for primary treatment of congenital
urethral narrowing is the largest to date and provides granular technical details.
It aligns with prior reports suggesting that P.A.D.U.A. achieves urethral patency
in most patients with Prune Belly Syndrome or isolated urethral atresia, but has limited
application in the hypoplastic duplicated urethra. Despite high rates of urethral
patency in this select population, many patients will not achieve and maintain spontaneous
voiding without catheterization. This is likely due to ongoing deterioration of bladder
function caused by the prenatal developmental insult, paralleling the phenomenon seen
in posterior urethral valves.