Bladder dysfunction in children with refractory monosymptomatic primary nocturnal enuresis.J Urol. 1999 Sep; 162(3 Pt 2):1049-54; discussion 1054-5.JU
We studied bladder dysfunction in children with significant primary nocturnal enuresis refractory to treatment.
MATERIALS AND METHODS
We evaluated 33 Chinese boys and 8 girls with a mean age of 10.4 years, who had significant monosymptomatic primary nocturnal enuresis (3 or more wet nights weekly) after desmopressin treatment with or without an enuretic alarm failed. Daytime cystometry, continuous nighttime cystometry and electroencephalography monitoring during sleep, and detailed recording of daytime and nighttime urinary output were performed.
We recognized 5 patterns of bladder dysfunction and its association with sleep-arousal status. Pattern 1 was normal daytime urodynamics with significant bladder instability at night with normal volume voiding precipitated by unstable detrusor contractions in 14 boys (34%). Pattern 2 was normal daytime urodynamics with frequent small volume voiding at night, probably representing latent bladder instability, in 4 boys (10%). Pattern 3 involved abnormal daytime urodynamics with small bladder capacity, a discoordinated daytime voiding pattern and marked nighttime bladder instability associated with poor sleep in 6 boys (15%). Pattern 4 was abnormal daytime urodynamics with an obstructive pattern, and marked daytime and nighttime detrusor hypercontractility (mean maximum detrusor pressure 178 cm. water) in 8 boys (20%). Pattern 5 was abnormal daytime urodynamics with a dysfunctional daytime voiding pattern and frequent small volume nighttime voiding in 8 girls and 1 boy (22%). In all patients functional bladder capacity was smaller than expected for age and the majority had no nocturnal polyuria. Despite underlying bladder dysfunction a 4-week course of 400 microg. desmopressin orally at bedtime still produced a significant response with a greater than 50% decrease in the number of wet nights during treatment in 47% of the patients, although enuretic symptoms immediately relapsed on cessation of therapy in all. Notably cystourethroscopy in 7 of the 8 boys with pattern 4 dysfunction revealed bladder trabeculations and abnormal urethral lesions, including congenital obstructive posterior urethral membranes in 4, Moormann's ring in 2 and irregular scarring at the bulbous urethra in 1.
Abnormal bladder function, including small functional capacity, instability during sleep and marked detrusor hypercontractility, was common in our enuretic children in whom treatment failed. More importantly, nocturnal enuresis may be the only presenting symptom and there may be a response to desmopressin with a decreased number of wet nights even in cases of significant underlying bladder dysfunction. These findings may have important implications for our management strategy for monosymptomatic primary nocturnal enuresis.