0022-534 7/90/1441-0122$02.00/0 THE JOURNAL OF UROLOGY Copyright© 1990 by AMERICAN UROLOGICAL ASSOCIATION, INC.

Vol. 144, July

Printed in U.S.A.

THE URODYNAMIC CONSEQUENCES OF POSTERIOR URETHRAL VALVES CRAIG A. PETERS, MOSHE BOLKIER, STUART B. BAUER, W. HARDY HENDREN, ARNOLD H. COLODNY, JAMES MANDELL AND ALAN B. RETIK From the Division of Urology, Department of Surgery, The Children's Hospital and Harvard Medical School, Boston, Massachusetts

ABSTRACT

We evaluated urodynamically 41 patients with posterior urethral valves because of signs or symptoms of incontinence (35), frequency (3), hydronephrosis (2) and infection (1). Findings included normal urodynamic evaluations in 3 patients, 2 had high voiding pressures secondary to outlet resistance and 1 had incontinence on the basis of external urethral sphincter damage. In the remainder 3 patterns of bladder dysfunction were identified. Myogenic failure with overflow incontinence occurred in 14 patients. In this group clean intermittent catheterization or Valsalva's voiding was used for emptying. Hyperreflexic bladders were seen in 10 patients. Pharmacological suppression of instability was effective in 5 of 7 patients treated; 1 required bladder augmentation. Eleven children had a small capacity bladder and poor compliance. Post-void residuals were low and these bladders were generally but not always stable. Pharmacological bladder relaxation was successful in 3 patients, 3 underwent augmentation, 1 did well with a-agonists and followup is unavailable on the other 4. These 3 patterns of bladder dysfunction represent an overlapping constellation of residual urodynamic abnormalities due to previous bladder outlet obstruction. Individual patients may show facets of several types of dysfunction associated with 1 predominant pattern. (J. Urol., 144: 122126, 1990) Significant voiding dysfunction in boys following treatment of posterior urethral valves remains a challenging clinical problem.1-4 Bauer and associates previously demonstrated that urinary incontinence in a boy with treated posterior urethral valves is seldom due to sphincteric damage. 5 In a small group of such patients several patterns of voiding dysfunction were identified. We extend the findings of the earlier study to define more fully the variable nature of bladder dysfunction associated with posterior urethral valves. In our report less emphasis is placed upon results of therapy, since treatment recommendations were not always followed by the referring physician nor complied with by the patient. MATERIAL AND METHODS

All patients referred for urodynamic evaluation because of suspected lower urinary tract dysfunction during the previous 10 years who had a diagnosis of posterior urethral valves were reviewed. During this period more than 200 patients were evaluated or treated for posterior urethral valves at our hospital. Of the patients 41 (approximately 16%) comprised this study. Any boy with a previous bladder augmentation, evidence of neurogenic bladder dysfunction or insufficient study data (5) was excluded. All patients underwent urodynamic evaluation to delineate the nature of the voiding dysfunction. Urodynamic evaluation consisted of uroflowmetry, water cystometry, urethral pressure profilometry and sphincter electromyography. Before catheterization a urinary flow rate was recorded, followed by a postvoid residual urine volume determination. Water cystometry was performed with a 7 or llF triple-lumen urodynamic catheter. The smaller catheter was used in prepubertal boys. The initial filling rate was set at 20% of expected capacity per minute and decreased if hyperreflexia was noted. Intravesical pressure was measured during filling and voiding. Dynamic urethral pressure profilometry was done through a third chan nel on the urodynamic catheter initially with the bladder empty, Accepted for publication January 26, 1990.

and then during bladder filling and voiding. Sphincter electromyography was performed with a 24 gauge concentric needle electrode (Teca) placed at the level of the external urethral sphincter and recorded on a Teca TE-4 electromyograph. The electrode was inserted in the midline of the perineum and advanced toward the striated muscle component of the external urethral sphincter. The appearance of individual action potentials on the audio and oscilloscope channels of the electromyograph indicated satisfactory placement within the external urethral sphincter. Electrode placement was facilitated by transrectal palpation of the urethral catheter. Electromyographic responses to bladder filling, voiding, abdominal straining and the bulbocavernosus reflex were tested. The history was reviewed to assess patient age and mode of presentation, uremia at presentation, presence of hydronephrosis, initial surgical treatment and total number of operations, presence of a unilateral nonfunctioning kidney, development of renal failure or nephrogenic diabetes insipidus and recurrent urinary infections. Sufficient followup data were available in 23 patients to permit assessment of the recommended treatment program. Inadequate patient compliance frequently was the reason for this loss of followup information. The indications for urodynamic evaluation in the 41 boys included persistent day and night wetting in 33, severe urinary frequency in 3, nocturnal enuresis in 2, persistent hydronephrosis in 2 and recurrent urinary infections in 1. Patient age ranged from 3 to 24 years. In the few boys younger than the age of toilet training evaluation was prompted by continuous wetting or in 1 by hydronephrosis. The interval between diagnosis of posterior urethral valves and initial urodynamic evaluation ranged from 2 to 24 years, with a mean of 6.8 years. Patient age at presentation of posterior urethral valves in the 41 patients ranged from the newborn period (21 were less than 4 months old) to 9 years. Sixteen patients presented with uremia, 31 had hydronephrosis and 7 required nephrectomy or had a nonfunctioning kidney. The initial treatment was variable; 17 boys underwent transurethral ablation of posterior

122

URODYNAMIC CONSEQUENCES OF POSTERIOR URETHRAL VALVES

urethral valves alone, 1 underwent open resection, 7 underwent transurethral ablation with delayed reconstruction and 10 underwent initial diversion with subsequent transurethral ablation. Six boys were treated by simultaneous posterior urethral valve ablation with diversion (3) and with immediate reconstruction (3). Six boys suffer from chronic renal failure or have undergone transplantation. Nephrogenic diabetes insipidus was a clinical problem in 9 boys (22%).

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u.

RESULTS

The urodynamic findings in 3 boys were entirely normal. One boy in this group was evaluated for hydronephrosis 3 years after initial therapy for valves. This condition resolved spontaneously without specific treatment. In the other 2 patients voiding dysfunction was considered to be due to developmental delays and they were managed expectantly. Followup is unavailable in these 2 patients. Two patients demonstrated high voiding pressures, reaching at least llO cm. water each. One patient had a urethral stricture 6 years after ablation of posterior urethral valves and multiple reconstructions, and he was treated surgically. One boy seen 2 years after ablation of the valves had no evidence of anatomical obstruction of the urethra or bladder neck and was believed to have a functional bladder outlet obstruction with elevated resistances at the bladder neck and external urethral sphincter region. He responded to oxybutynin and dibenzyline, and eventually was weaned from medication. He has remained well with satisfactory voiding pressures. Presently, we would use an alternative a-antagonist in place of dibenzyline. It is unclear whether the condition was related directly to the posterior urethral valves. One boy had persistent stress urinary incontinence on the basis of external urethral sphincteric insufficiency, presumably due to his having undergone open resection of posterior urethral valves in 1970. Sphincter electromyography demonstrated mild denervation, considered to be due to local injury in the absence of any neurological abnormality. The bladder neck pressures were elevated at 85 cm. water but over-all posterior urethral resistance was inadequate to maintain dryness. He was treated with a-agonists with some benefit. All of the other patients manifested significant bladder dysfunction that led to the voiding dysfunction. Three major categories of bladder dysfunction were evident on review of these patients; myogenic bladder failure, bladder hyperreflexia and bladder hypertonia with small capacity. Boys were allocated to a specific modynamic category on the basis of the most significant underlying cause of the lower urinary tract dysfunction. Overlap of the categories was seen in several boys as shown in table 1, since other forms of bladder dysfunction contributed to the clinical picture, A total of 14 patients had evidence of myogenic failure with inability to generate a sustained bladder contraction. Some boys had bladder atony (fig, 1) while others could only generate bladder contractions that were weak and unsustained. Postvoid residual urine was elevated (average 218 cc). The postvoid residual urine volume could not be determined accurately in 1 boy with hydronephrosis. Bladder capacity often was large but 4 of these patients had a smaller than expected bladder capacity (fig. 2). Voiding usually was by Valsalva's maneuver TABLE

1. Coexistence of bladder dysfunction Secondary Diagnosis

Principal Diagnosis Myogenic failure Hyperreflexic bladder Hypertonic bladder

Myogenic Failure

Hyperreflexic Bladder

1* * One patient with minimal uninhibited contractions.

Hypertonic Bladder 5 5

FIG. 1. Cystometrogram (CMG) of boy with urinary frequency 18 years after treatment of severe posterior urethral valves. No bladder contractions are seen, capacity is 150% of expected and voiding was by Valsalva's maneuver with post-void residuals of 125 cc. Patient became asymptomatic on regimen of double voiding at scheduled times.

100cc 250cc FIG. 2. Cystometrogram (CMG) in 13-year-old boy with severe valves, day and night wetting and no sensation of fullness. No bladder contractions were seen yet high filling pressure was evident in noncompliant bladder. Capacity was 60% of expected.

U~inhibi!ed conlraclions FIG. 3. Uninhibited contractions occur throughout filling in cysto-

metrogram ( CMG) of 5-year-old boy with day and night wetting.

Capacity 20lk«: FIG. 4. Cystometrogram ( CMG) shows hypertonic bladder with noncompliant filling phase and elevated pressures at capacity (50 cm. water). Capacity is 80% of normal. Boy also has component of myogenic failure and voids by abdominal straining.

and urinary flow rates were often low, although normal flow rates were seen in 3 boys. In patients with impaired bladder emptying incontinence was presumably on the basis of overflow because unless specifically encouraged to do so these boys would

124

PETERS AND ASSOCIATES M.C.

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FIG. 5. Cystometrograms ( CMG) in boy with bladder hypertonia due to posterior urethral valves initially evaluated when he was 7 years old with capacity 52% of expected for age and elevated pressure at capacity of 55 cm. water. Followup study when he was 12 years old on oxybutynin shows compliant filling phase and capacity 85% of expected. Pressure at capacity has been reduced to acceptable level (25 cm. water) and he was dry. TABLE

2. Clinical features associated with the urodynamic categories

No. pts. Pt. age at diagnosis Pt. age at urodynamic studies Clinical indicators of severity of valves at presentation: Uremia Hydronephrosis Nephrectomy Multiple operations Chronic renal failure Diabetes insipidus Mean %t

Myogenic Failure

Hyperreflexic Bladder

Hypertonic Bladder

14 1.7* 12

10 3.1 8.4

11 2.1 7.3

5 12 2 5 0 4 33

3 7 1 1 1 1 23

7 7 2 4 4 3 41

* Mean age at diagnosis of boys with myogenic failure without hypertonia was 0.4 years in contrast to those with hypertonia who were diagnosed at a mean age of 4 years. t Mean percentage calculated as the number of clinical indicators of severity as a percentage of the total number possible (6 per patient).

rarely empty completely. One boy had recurrent infections due to failure to empty completely. Clean intermittent catheterization permitted complete emptying and continence in 2 patients. Behavioral therapy with double or triple voiding regimens was successful in 4 boys. Pharmacological therapy with bethanechol chloride and a-blockade was used in 1 boy who became dry but did not adequately empty the bladder. Two boys with a small bladder capacity underwent bladder augmentation; 1 is dry and voiding. Bladder neck reconstruction also was performed in the other boy because of low urethral pressures (25 to 35 cm. water) and he is dry on clean intermittent catheterization. Specific followup is unavailable in 5 others of this subgroup. A hyperreflexic bladder was the basis of voiding dysfunction in 10 boys, characterized by uninhibited contractions early in bladder filling (fig. 3). The mean bladder capacity was normal for patient age (98%) 6 but ranged from 28 to 240% of capacity expected for age. Bladder emptying was usually complete. Urinary incontinence and urgency were due to the uninhibited contractions that were managed successfully by anticholinergic medications in 5 of 7 patients. One of the 2 boys who failed this approach became dry with clean intermittent catheterization alone while 1 became dry with an a-agonist. It appears in these boys that the bladder hyperreflexia improved with time. One boy underwent bladder augmentation and bladder neck reconstruction to become continent. Two boys were unavailable for followup. Eleven boys had a hypertonic, poorly compliant, small ca-

pacity bladder. The mean bladder capacity was 61 % of normal for patient age (range 33 to 78 %) and filling pressures were elevated, up to 95 cm. water (fig. 4). Bladder emptying usually was complete. One boy with persistent hydronephrosis was noted to have high post-void residual urine volumes that may reflect post-void upper tract drainage. No bladder instability was noted in these boys. Urinary incontinence was due to the small functional bladder capacity and high bladder pressures overcoming sphincteric resistance. One boy had low normal external urethral sphincter resistance that did not increase sufficiently with increases in intravesical pressures. Bladder relaxation using anticholinergic medication was used in only 3 boys but was effective (fig. 5). Two of these 3 patients required clean intermittent catheterization for bladder emptying. Bladder augmentation was performed in 3 boys, 2 of whom are dry and voiding satisfactorily, while 1 requires clean intermittent catheterization to empty. One boy became continent after renal transplantation on low doses of an a-agonist. The bladder had not been defunctionalized before transplantation. Followup is unavailable in the other 4 boys with a hypertonic bladder. The clinical features of the boys with the 3 categories of bladder dysfunction were compared (table 2), yet they failed to yield any specific indicators of the causes for the ultimate bladder function. Indicators of more severe congenital obstruction (uremia, hydronephrosis, chronic renal failure, diabetes insipidus and multiple operations) occurred more frequently in the group with a small capacity, hypertonic bladder, less so in those with myogenic failure and least in those with a hyperreflexic bladder. Multiple operations might contribute to bladder dysfunction but may also reflect the original severity of the valves. Recurrent infection was noted with equal frequency in all 3 bladder categories. Elevated bladder neck resistance on either static or dynamic urethral pressure profilometry was noted in only 3 boys; 1 as the principal cause of wetting, 1 with myogenic failure and 1 with a hyperreflexic bladder. It did not appear to be a significant causative factor of bladder dysfunction. The association of persistent hydronephrosis or vesicoureteral reflux with the hypertonic bladder in valves has been recognized. 4 • 7 Of the 11 boys with a hypertonic bladder 5 (45%) also had continuing hydronephrosis. Of 10 boys with hyperreflexia 4 (40%) demonstrated continued hydronephrosis (3) or persistent bilateral vesicoureteral reflux (1) but only 2 of 14 (14%) with myogenic failure had continuing hydronephrosis. A component of bladder hypertonia was found in 9 of the 11 boys with persistent hydronephrosis or reflux. DISCUSSION

Symptomatic voiding dysfunction after an operation for posterior urethral valves has been reported to occur in 13 to 38% of all boys. 8 - 16 These rates reflect varying historical periods and surgical techniques as well as different definitions of voiding dysfunction. Voiding disturbances in boys who have had posterior urethral valves may be due to a variety of causes. Incontinence secondary to sphincteric incompetence is unusual as shown by Bauer and associates in 19795 and this review emphasizes that finding. Severe bladder dysfunction may be present in well over 80% of the boys with voiding abnormalities after surgery for posterior urethral valves. An understanding of the various forms of bladder dysfunction associated with posterior urethral valves will serve as a guide to selecting and evaluating therapy. Not all patients with a voiding disturbance and a history of posterior urethral valves have clinically evident bladder dysfunction. A normal urodynamic evaluation would indicate that expectant or behavioral therapy will be more appropriate for the child. For those boys with evidence of symptomatic bladder dysfunction identification of the specific nature of the bladder disorder will direct therapeutic efforts. Three primary cate-

U.RODYNAMlC CONSEQUENCES O'F .POSTERIOR URETHRAL VALVES

gories of bladder dysfunction have been identified in these with posterior urethral valves. Each of these categories was seen in the original report by Bauer and associates although in small numbers. 5 With this larger group of children the frequency of occurrence of these 3 categories appears to be similar. These categories should not be considered as absolutely distinct. Significant overlap may be seen, since each category represents a cluster of urodynamic abnormalities, some of which may also be present in the other categories (table 1). One boy demonstrated evidence of bladder instability without ever having a sustained bladder contraction; he had a noncompliant, small capacity bladder as well as poor sphincter resistance. In any individual patient 1 pattern seems to be predominant and may best serve to guide initial therapy. The coexistence of several patterns of urodynamic dysfunction cannot be ignored, however, and the ultimately successful therapeutic regimen may need to address each of the various patterns present. The most appropriate management of the boys with sphincteric incompetence contributing to the incontinence remains controversial. Pharmacological therapy with an a-agonist may be of occasional benefit and is worth a trial. The best alternative for surgical correction appears to be either a Young-Dees type bladder neck narrowing or the artificial urinary sphincter. Both methods have been reported to provide acceptable rates of continence in experienced hands and the choice presently seems to be one of individual preference. 17•18 In either case the bladder may be the critical feature that determines the ultimate clinical outcome, and its status must be defined and treated in conjunction with increasing outlet resistance. Myogenic failure may be most effectively treated with clean intermittent catheterization but several patients have done well voiding by Valsalva' s maneuver alone, or coupled with a double voiding program. If bladder capacity is inadequate augmentation may be required to achieve continence. The hyperreflexic bladder often will respond to anticholinergic pharmacotherapy, yet clean intermittent catheterization then may be needed to ensure adequate emptying. Augmentation occasionally may be necessary in this group as well. The hypertonic, small capacity bladder probably is less responsive to anticholinergics but an initial trial is of value. Bladder augmentation often is the most effective long-term management option. Bladder capacity clearly is an important constraint in achieving continence. This may be even more critical in the patient with nephrogenic diabetes insipidus whose high urine output decreases the effective bladder capacity. In combination with a smaller than normal bladder, diabetes insipidus is a difficult clinical problem. Thiazide therapy has achieved limited success in some patients by producing a state of relative sodium depletion and ultimate decrease in urine volumes. 19• 20 Such a regimen is not without side effectso Bladder augmentation with a bowel segment may be necessary in this group, yet electrolyte imbalances in boys with renal insufficiency must be anticipated and treated. 21 This group of boys may be particularly well suited for gastrocystoplasty" 22 An important aspect of bladder dysfunction secondary to posterior urethral valves is the association of upper tract damage in the setting of a hypertonic bladder. 4 • 7 A failure of resolution of hydroureteronephrosis after posterior urethral valve resection, progression of upper tract damage or persistent reflux, even after an antireflux operation, may be on the basis of bladder dysfunction. This may occur in the absence of voiding symptoms. Eleven boys in this group had evidence of either hydronephrosis or vesicoureteral reflux associated with bladder dysfunction and 9 of these 11 (82%) had some degree of bladder hypertonia. Four of these 11 boys demonstrated high urine outputs due to nephrogenic diabetes insipidus, which may further contribute to continuing hydronephrosis. Similarly, infrequent voiding may exacerbate upper tract damage. 23 The primary pathological condition is in the bladder, rather than

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the ureterovesical junction and successful must address that fact. The determinants of ultimate bladder function in the setting of posterior urethral valves remain unclear. No specific factors were identified in these patients. This analysis may be hindered by the difficulty in quantitating the severity of the original obstruction. Using clinical indicators of severity, indirect as they are, it may be suggested that more severe obstruction, evidenced by a higher frequency of the clinical indicators of severity, leads to the small capacity, hypertonic bladder (table 2). Bladders with unsustained contractions (myogenic failure) usually have been considered to be end stage, decompensated bladders. Boys in our report with myogenic failure without evidence of hypertonicity, however, were diagnosed earlier in life (0.4 years) than those with myogenic failure and hypertonicity (4 years). Which of these represents an end stage bladder, if either does, is unclear but perhaps those bladders with myogenic failure and those with hypertonicity represent an end stage condition, the distinction being the product of differing severity and duration of obstruction. High grade obstruction for a short period during early life may affect the bladder differently than a longer period of obstruction. The hyperreflexic bladder is seen in boys who were diagnosed later and with fewer indicators of severe posterior urethral valves. An analogy may be drawn to adult bladder outlet obstruction secondary to benign prostatic hyperplasia where a clinical progression has been described beginning with irritative symptoms of frequency and urgency, ultimately ending in bladder decompensation with myogenic failure. Some authors consider the acquired bladder lesion in men to be entirely distinct from that in the child. 2 It has been stated that congenital bladder outlet obstruction induces changes in neurotransmitter receptors levels as well as hyperplasia and hypertrophy of bladder muscle and collagen. 2 Experimental evidence in the postnatal period has supported this claim. 24- 26 Speakman and associates demonstrated severe and apparently irreversible morphological and neurological changes in the obstructed adult bladder. 26 Controversy remains with regard to the reversibility of these changes in adults and virtually no data exist with regard to children with posterior urethral valves. These findings may help one to understand the cause of bladder hyperreflexia and hypertonia but do not shed light on the differing end points seen in these patients. CONCLUSIONS

Posterior urethral valves have been found to lead to an overlapping constellation of urodynamic abnormalities, often many years after the initial diagnosis and treatment of posterior urethral valves. Voiding dysfunction and urinary incontinence in boys with a history of posterior urethral valves seldom are the result of sphincteric incompetence. Three major categories of bladder dysfunction were identified as leading to voiding symptoms: myogenic failure, hyperreflexia and bladder hypertonia. A careful urodynamic assessment is needed to define the abnormal bladder, and guide the clinician in selecting and evaluating therapy. Therapy should be designed to provide for low pressure urinary storage for an acceptable period and for complete bladder emptying. The interaction of severity and duration of obstruction may be important factors but the determinants of ultimate bladder function in the setting of posterior urethral valves remain unclear. REFERENCES

1. Ruarte, A. C., Rivain, T., Pascal, B. and Cukier, J.: Incontinence des urines persistante apres section endoscopique des valves de l'urethre posterieur chez le gar9on. Etude urodynamique. J. d'Urol., 87: 309, 1981. 2. Glassberg, K. I., Hendren, W. H., McLorie, G. A., Tanagho, E. A., Whitaker, R.H., Weiss, R. M., Koff, S. A. and Mitchell, M. E.: Persistent ureteral dilatation following valve resection. Dial. Ped. Urol., vol. 5, No. 4, p. 2, 1982.

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3. Rivain, T., Beurton, D. and Cukier, J.: Troubles de !'accommodation vesicale chez les enfants porteurs de valves de l'urethre posterieur. J. d'Urol., 89: 581, 1983. 4. Campaiola, J. M., Perlmutter, A. D. and Steinhardt, G. F.: Noncompliant bladder resulting from posterior urethral valves. J. Urol., 134: 708, 1985. 5. Bauer, S. B., Dieppa, R. A., Labib, K. K. and Retik, A. B.: The bladder in boys with posterior urethral valves: a urodynamic assessment. J. Urol., 121: 769, 1979. 6. Bauer, S. B., Retik, A. B., Colodny, A.H., Hallett, M., Khoshbin, S. and Dyro, F. M.: The unstable bladder in childhood. Urol. Clin. N. Amer., 7: 321, 1980. · 7. Glassberg, K. I., Schneider, M., Haller, J. 0., Moel, D. and Waterhouse, K.: Observations on persistently dilated ureter after posterior urethral valve ablation. Urology, 20: 20, 1982. 8. Cass, A. S. and Stephens, F. D.: Posterior urethral valves: diagnosis and management. J. Urol., 112: 519, 1974. 9. Egami, K. and Smith, E. D.: A study of the sequelae of posterior urethral valves. J. Urol., 127: 84, 1982. 10. Johnston, J. H. and Kulatilake, A. E.: The sequelae of posterior urethral valves. Brit. J. Urol., 43: 743, 1971. 11. Atwell, J. D.: Posterior urethral valves in the British Isles: a multicenter B.A.P.S. review. J. Ped. Surg., 18: 70, 1983. 12. Kurth, K.-H., Alleman, E. R. J. and Schroder, F. H.: Major and minor complications of posterior urethral valves. J. Urol., 126: 517, 1981. 13. Parkhouse, H. F., Barratt, T. M., Dillon, M. J., Duffy, P. G., Fay, J., Ransley, P. G., Woodhouse, C.R. and Williams, D. I.: Longterm outcome of boys with posterior urethral valves. Brit. J. Urol., 62: 59, 1988. 14. Scott, J. E.: Management of congenital posterior urethral valves. Brit. J. Urol., 57: 71; 1985.

15. Williams, D. I., Whitaker, R. H., Barratt, T. M. and Keeton, J.E.: Urethral valves. Brit. J. Urol., 45: 200, 1973. 16. Churchill, B. M., Krueger, R. P., Fleisher, M. H. and Hardy, B. B.: Complications of posterior urethral valve surgery and their prevention. Urol. Clin. N. Amer., 10: 519, 1983. 17. Sidi, A. A., Sinha, B. and Gonzalez, R.: Treatment of urinary incontinence with an artificial sphincter: further experience with the AS791/792 device. J. Urol., 131: 891, 1984. 18. Rink, R. C. and Mitchell, M. E.: Surgical correction of urinary incontinence. J. Ped Surg., 19: 637, 1984. 19. Alon, U. and Chan, J. C.: Hydrochlorthiazide-amiloride in the treatment of congenital nephrogenic diabetes insipidus. Amer. J. Nephrol., 5: 9, 1985. 20. Niaudet, P., Dechaux, M., Trivin, C., Loirat, C. and Broyer, M.: Nephrogenic diabetes insipidus: clinical and pathophysiological aspects. Adv. Nephrol., 13: 247, 1984. 21. Mitchell, M. E. and Piser, J. A.: Intestinocystoplasty and total bladder replacement in children and young adults: followup in 129 cases. J. Urol., 138: 579, 1987. 22. Adams, M. C., Mitchell, M. E. and Rink, R. C.: Gastrocystoplasty: an alternative solution to the problem of urological reconstruction in the severely compromised patient. J. Urol., 140: 1152, 1988. 23. Allen, T. D.: The non-neurogenic neurogenic bladder. J. Urol., 117: 232, 1977. 24. Elbadawi, A., Meyer, S., Malkowicz, S. B., Wein, A. J., Levin, R. M. and Atta, M. A.: Effects of short-term partial bladder outlet obstruction on the rabbit detrusor: an ultrastructural study. Neurourol. Urodynam., 8: 89, 1989. 25. Kato, K., Wein, A. J., Kitada, S., Haugaard, N. and Levin, R. M.: The functional effect of mild outlet obstruction on the rabbit urinary bladder. J. Urol., 140: 880, 1988. 26. Speakman, M. J., Brading, A. F., Gilpin, C. J., Dixon, J. S., Gilpin, S. A. and Gosling, J. A.: Bladder outflow obstruction-a cause of denervation supersensitivity. J. Urol., 138: 1461, 1987.

The urodynamic consequences of posterior urethral valves.

We evaluated urodynamically 41 patients with posterior urethral valves because of signs or symptoms of incontinence (35), frequency (3), hydronephrosi...
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