Yeung C K, Chiu H N, Sit F K
Department of Surgery, Chinese University of Hong Kong, Prince of Wales Hospital.
J Urol. 1999 Sep;162(3 Pt 2):1049-54; discussion 1054-5. doi: 10.1016/S0022-5347(01)68062-5.
We studied bladder dysfunction in children with significant primary nocturnal enuresis refractory to treatment.
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.
我们研究了难治性原发性夜间遗尿症患儿的膀胱功能障碍。
我们评估了33名中国男孩和8名女孩，平均年龄10.4岁，这些患儿在用或不用遗尿警报器的情况下接受去氨加压素治疗后仍有严重的单症状原发性夜间遗尿症（每周尿床3个或更多夜晚）。进行了日间膀胱测压、夜间连续膀胱测压以及睡眠期间的脑电图监测，并详细记录了日间和夜间尿量。
我们识别出5种膀胱功能障碍模式及其与睡眠-觉醒状态的关联。模式1为日间尿动力学正常，夜间膀胱明显不稳定，在不稳定逼尿肌收缩诱发正常容量排尿的情况下，有14名男孩（34%）。模式2为日间尿动力学正常，夜间频繁少量排尿，可能代表潜在的膀胱不稳定，有4名男孩（10%）。模式3涉及日间尿动力学异常，膀胱容量小，日间排尿模式不协调，夜间膀胱明显不稳定且睡眠不佳，有6名男孩（15%）。模式4为日间尿动力学异常，呈梗阻模式，日间和夜间逼尿肌明显过度收缩（平均最大逼尿肌压力178 cm水柱），有8名男孩（20%）。模式5为日间尿动力学异常，日间排尿模式功能失调，夜间频繁少量排尿，有8名女孩和1名男孩（22%）。在所有患者中，功能性膀胱容量均小于预期年龄，且大多数患者无夜间多尿。尽管存在潜在的膀胱功能障碍，但400微克去氨加压素每晚口服4周的疗程仍产生了显著反应，47%的患者治疗期间尿床次数减少超过50%，尽管停药后遗尿症状立即复发。值得注意的是，8名模式4功能障碍男孩中的7名进行膀胱尿道镜检查发现膀胱小梁形成和尿道异常病变，包括4例先天性梗阻性后尿道瓣膜、2例莫尔曼环和1例球部尿道不规则瘢痕形成。
膀胱功能异常，包括功能性容量小、睡眠期间不稳定和逼尿肌明显过度收缩，在我们治疗失败的遗尿症患儿中很常见。更重要的是，夜间遗尿可能是唯一的表现症状，即使在存在严重潜在膀胱功能障碍的情况下，去氨加压素治疗也可能使尿床次数减少。这些发现可能对我们单症状原发性夜间遗尿症的管理策略具有重要意义。
