Lower Urinary Tract Dysfunction and Urodynamics in Children

Contemporary research has shown that bladder problems in most children are due to disturbed or delayed development of the control of lower urinary tract function. As a result, urologists now see increasing numbers of children with bladder dysfunction, which is now viewed as a somatic and treatable disorder. This article starts with an overview of voiding dysfunction in children, discusses the assessment of this dysfunction and reviews the method of natural fill cystometry, which is proposed as the future golden standard in urodynamics. A description of various urotherapy techniques follows and the article ends with a summary of the pharmacological treatment of lower urinary tract dysfunction in children. a child with a normal bladder voids 3–7 times a day. Bladder capacity grows by about 30 ml/year, normal voiding pressure is 100 cm H 2 O and post-void residual is minimal. A postvoid residue of 5 ml is suspect and 20 ml is pathological. The urinary flow rate depends upon the amount voided: [maximum flow rate] volume voided (ml) [11]. Lower Urinary Tract Dysfunction In about 10% of children, an overactive or unstable detrusor produces urge symptoms (urge syndrome). A smaller group has an overactive or dyscoordinated sphincter (dysfunctional voiding or non-neurogenic bladder sphincter dysfunction, NNBSD). The smallest group includes those with underactive or acontractile detrusors (‘lazy bladder’) and this group is the most problematic. In adults, the micturition reflex is inhibited by midbrain and cortical centers. The cortex center switches on the pontine micturition center, which in turn stimulates the sacral micturition center to start detrusor contraction and sphincter relaxation for voluntary voiding. Immaturity (or delayed maturation), trauma or disease affecting the neural tracts between the cortex, pons and sacral center will result in an overactive bladder and sometimes also in dyscoordination between the detrusor and sphincter in NNBSD. Many cases of childhood overactive bladder are believed to have a hereditary predisposition. For example, multigeneration families with nocturnal enuresis show a high rate of day wetting [12]. Currently, investigators are searching for a dominant gene causing urge incontinence [13]. Pathophysiology of NNBSD For the past 20 years, the pathophysiological cascade leading to overactive sphincter was believed to start with detrusor instability, causing frequency, urgency and urge incontinence. Sphincter overactivity was thought to develop as a result of resisting the overactive bladder. Although dry, such children were thought to lose the ability to relax the sphincter and developed dysfunctional voiding with residual urine and gradual distension of the bladder. In Hjälmås/Hoebeke/de Paepe Eur Urol 2000;38/5 (Curric Urol 1.5:1–11) Structural Development The bladder is a separate structure in the fetus by 8 weeks of gestation and fetal development is dependent on its function. In exstrophy, where the anterior part of the bladder is missing, the lack of stretch and contraction results in reduced bladder growth and an abnormal detrusor. When excessive stretch of the bladder occurs due to congenital infravesical obstruction, the connective tissue of the detrusor hypertrophies and compliance is impaired, causing detrusor hyperactivity in the child [1]. Neuromuscular Development At 14 weeks of gestation, the detrusor [2] is already richly innervated and the sphincter is well developed [3, 4]. A large variety of neurotransmitters and receptors, including those for nitric oxide, are present in the lower urinary tract [5, 6]. Integrated detrusor-sphincter activity was previously believed to be due to simple reflex action as the bladder fills, but it is now thought that neural control plays a role in the fetus. Such control is immature and results in frequent ( 30/24 h) and incomplete micturitions (fig. 1). Similarly in the infant, supraspinal control plays more of a role than previously recognized; for example, a sleeping infant will wake to void [7]. Until 6–12 months of age, micturitions are incomplete and occur about once an hour [8]. Development of Urodynamic Variables Increasing supraspinal and cortical control of voiding [9, 10] means that by age 6–7 years Fig. 1. Bladder volume over time in a fetus of 29 weeks of gestation.