Bloom and co-workers dilated the striated sphincter in children with myelodysplasia, elevated detrusor leak point pressures, and upper tract changes.  They did this to decrease outlet resistance, the same change as that effected by a vesicostomy. A vesicostomy simply bypasses the urethra while dilation directly reduces urethral resistance. At the time Bloom and co workers did the dilations, it was known from othe r data that all myelodysplastic children with abnormal upper tracts had a low-compliance bladder. In follow-up of those children treated by urethral dilation, Bloom and co-workers found upper tract changes resolved but there was also a dramatic and sustained improvement in bladder compliance [9, 10 ]. That finding established that the outlet controls the detrusor pressure response to filling. Further, it is clear that that high, fixed outlet resistance related to a functional or structural abnormality, or that achieved surgically, can induce a destructive detrusor response, which leads to altered compliance and can cause upper tract damage. The relationship between the outlet and the bladder governs what is possible to achieve surgically where passive urinary loss is the result of a lack of proximal urethral sphincter function coupled with bladder decentralization. Where very high outlet resistance is achieved, with a procedure like the Kropp buried urethra or some variety of the Mitrofanoff procedure, a method to enlarge the bladder is required to obviate high detrusor (or reservoir) pressures [11, 12]. It is important to emphasize that passive urinary loss related to poor proximal urethral sphincter function can coexist with high detrusor leak point pressures and a risk to upper tract function.
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