Enuresis is subclassified into two subtypes, primary and secondary. Primary enuresis encompasses children who have never achieved continence, whereas secondary enuresis refers to those children who maintain continence for at least one year, only to lose it at some point after that. The term itself is derived from the Greek enourein, “to void urine” and has come to imply nocturnal events, although that connotation is not inherent in the derivation of the word itself.

There is a rich literature concerning enuresis and its treatment over the centuries. In retrospect, many of these treatment approaches now appear to have been quite sadistic. This history has been summarized in an excellent review in 1951 by Glicklich (1), which covers material dating back to the Ebers Papyrus of 1550 B.C.

There has been substantial progress in the treatment of enuresis, which in turn has contributed to a greater understanding of the fundamental pathophysiologic processes involved. These advances are reviewed in this chapter.

Statistics concerning the prevalence of enuresis also must take into account the severity of the disorder. For example, in the Isle of Wight Study, Rutter and colleagues (1989) (2) found that 15.2% of boys were wet less often than once a week, whereas only 6.7% wet at least once a week. The corresponding figures for girls were 12.2% and 3.3%, respectively. By age 14 years, only 1.9% of boys were wet less often than once a week, and 1.1% were wetting at least once a week, with the corresponding figures for girls being 1.2% and 0.5%, respectively (Rutter et al., 1973) (3). Longitudinal data from the Isle of Wight Study have illustrated that wetting develops in
many children between the ages of 5 and 7 years. Enuresis also was found in greater frequency in children undergoing psychosocial stress and in those living in socially disadvantaged circumstances (2).

A Scandinavian study of 3,206 7-year-old children found an overall prevalence of 9.8%; 6.4% of this group was accounted for by children with night wetting, 1.8% by day wetters, and 1.6% by those with mixed day and night wetting. This study also showed a strong genetic influence in that the risk of a child having enuresis was 7.1 times greater if the father manifested enuresis after 4 years of age, and 5.2 times greater if the mother did (4).

An 8-year longitudinal study in New Zealand found a prevalence of 7.4% for nocturnal enuresis in 8 year olds. This figure was accounted for by 3.3% with primary enuresis and 4.1% with secondary enuresis (5).

More recent studies have found remarkably similar results. In a group of 392 7-year-old children from the west coast of Sweden, Wille (6) reported a prevalence of 7.3% for monosymptomatic primary enuresis. A questionnaire study involving a large cohort of Australian children in the 5- to 12-year-old range reported an overall incidence of 5.1% for nocturnal enuresis of at least weekly frequency and 1.4% for daytime wetting of similar frequency (7). In a population-based questionnaire study, Soderstrom et al. (8) reported bedwetting at a frequency of at least once per month in 7.1% of first-graders, and 2.7% of fourth-graders.

As noted, the term enuresis itself denotes only the voiding of urine, but over the years, it has acquired both a pathologic and a nocturnal connotation. Daytime wetting is correctly referred to as diurnal enuresis, whereas nighttime wetting is referred to as nocturnal enuresis.

In the text revision of the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), the American Psychiatric Association (2000) defines functional enuresis as “repeated voiding of urine during the day or at night into bed or clothes, whether involuntarily or intentionally.” DSM-IV-TR goes on to specify that “the behavior is clinically significant as manifested by either a frequency of at least twice per week for at least three consecutive months or impairment in social, academic (occupational) or other important areas of functioning.” The child must also have reached an age at which continence could reasonably be expected. The DSM-IV-TR uses a chronologic age of 5 years as a cutoff or a mental age of 5 years for those children with developmental delays. The DSM-IV-TR also stipulates that the wetting not be the result of “the direct physiological effects of a substance (e.g., diuretics) or a general medical condition (e.g., diabetes, spina bifida, a seizure disorder).” Three subtypes of enuresis are defined: nocturnal only (nighttime wetting), diurnal only (daytime wetting), and nocturnal and diurnal (mixed day and night wetting). A distinction also is made between primary and secondary enuresis. Primary enuresis refers to those children who have never achieved urinary continence, whereas secondary enuresis refers to those children who have achieved continence and then lost it. The period of continence necessary to differentiate between primary and secondary enuresis had variously been proposed to be 6 months to 1 year. The DSM-IV-TR does not specify a precise period of time for the distinction, but instead makes reference to “a secondary type in which the disturbance develops after a period of established urinary continence.” A child is not considered to have primary functional enuresis until 5 years of age. Secondary enuresis can begin at any time, once the criterion of initial continence has been fulfilled, but the usual onset is between 5 and 7 years of age (2).

The physiologic manifestations of this disorder have led to a wide range of etiologic theories. A primary focus of these studies has naturally been the anatomy of the bladder and urinary tract. Shaffer et al. (9) elegantly combined an investigation of bladder anatomy and physiology with the covariable of behavioral disturbance. It might intuitively be expected that children with dysfunctional or abnormal bladders would be those without a concomitant behavioral disorder to explain their enuresis and that those whose enuresis could be explained on the basis of psychopathology would have normal bladders. The results were counterintuitive in that those children who were behaviorally disturbed also had significantly lower functional bladder volumes and more developmental delays. Thus, although not providing a parsimonious explanation to differentiate the etiology of enuretic events between psychiatrically disturbed and nondisturbed children with enuresis, the study did lend further support to a theory of general developmental delay, which would explain both the enuresis and the high frequency of behavioral disturbance. Another study that investigated bladder capacity in children with primary nocturnal enuresis, former enuretic patients, and control subjects, also failed to find any significant difference in bladder capacity between the groups (10). It also has been demonstrated that fluid loading can produce enuretic events in children who do not have a history of enuresis 11,12. Children with enuresis were found to have developmental delays twice as often as those without in a large longitudinal population study (13) and Touchette et al. (14) have more recently reported an association between bedwetting and related developmental milestones. An investigation of event-related potentials and brain stem auditory-evoked responses found longer latencies in children with enuresis, as compared to controls, which the authors interpreted as evidence of a maturational delay (15). A study that compared 35 otherwise healthy children with enuresis with a control group found that the bone age of the children with enuresis displayed a significant lag behind chronologic age, leading the authors to speculate about delayed maturation of central nervous system regulatory functions (16). However, a more recent investigation found no statistical difference in the bone age of children with enuresis and controls (17).

There is an obvious relationship between enuresis and bladder infection; (18) thus, an infection of the urogenital tract should be ruled out before a diagnosis of functional enuresis is made. This is especially important for girls, who are more prone to urinary tract infections (19). The possibility of urinary tract obstruction as a widespread cause of enuresis has been reported (20) but has been criticized because such a hypothesis can lead to unnecessary surgery (21). After extensively reviewing the literature on this subject, Shaffer (22) concluded, “There is no evidence that urethral dilatation or bladder neck repair are effective treatment for enuresis.” The only exception to this would be if there were very specific pathophysiologic findings.

Other investigations into the role of urodynamic abnormalities in the pathogenesis of primary enuresis support Schaffer’s conclusion (23). In a large study, Kawauchi et al. (24) found an incidence of urologic abnormalities of 1.8% on intravenous pyelography (n = 940), 7.1% on voiding cystourethrography (n = 695), 11.5% on cystometry (n = 487), and no abnormalities on renal ultrasonography (n = 58). Of those who did manifest reflux on voiding cystourethrography, the degree of reflux was assessed as mild in 92.1%.

Yeung et al. (25) utilized noninvasive ultrasound techniques to assess physiological bladder parameters in 514 children with primary enuresis (age 5 to 18 years; mean age 11.2 years), and 339 age-matched controls. Analysis of the data from the entire
study group yielded three subtypes: small-capacity bladder with thick wall; normal-capacity bladder with normal wall thickness; and large-capacity bladder with thin wall. There was also a four-week period of treatment with DDAVP for the children with enuresis. The authors found that “poor response to treatment was significantly associated with pathological bladder conditions, that is, small-capacity bladder with thick bladder wall or large-capacity bladder with thin bladder wall.”

The nature of the enuretic phenomenon has naturally led to speculation concerning a psychodynamic etiology. These hypotheses have in general evolved from case reports or have been derived from theoretical considerations. There has been one rigorous attempt to define the generalizations derived from the literature regarding enuresis and encopresis and then to determine with what frequency these generalizations were borne out by an analysis of the clinical material. This elegant study by Achenbach and Lewis (26) revealed that “only two of the twenty-four generalizations derived from the literature regarding encopresis and enuresis received support at the conventional level (probability = 0.05) of statistical significance.”

Epidemiologic studies have, however, shown a correlation between psychological disturbance and enuresis, which is more pronounced in older children (2). This observation then raises the question of the nature of the relationship: Is it a causal, incidental, or secondary relationship? The aforementioned link between enuresis and developmental delays, which are also linked to psychopathology, would suggest that there is a common underlying maturational factor that predisposes vulnerable children to manifest both behavioral disturbances and enuresis. In further support of this hypothesis are the observations that the nature of the behavioral disturbance in children with enuresis is nonspecific (27) and that no physiologic marker can be found that reliably differentiates psychologically disturbed from nondisturbed children with enuresis 9,28. Biederman et al. (29) have evaluated the possible linkage between enuresis and attention deficit hyperactivity disorder (ADHD). Their findings indicated that enuresis did not increase the risk for psychopathology in children with or without ADHD but was associated with increased risk for learning disability in normal control children, but not in those with ADHD. Baeyens et al. (30) investigated the prevalence of ADHD in 120 children (age 6 to 12 years) with primary enuresis, utilizing parent and teacher questionnaires as well as diagnostic interviews. Their results indicated that 15% met the criteria for ADHD, and a further 22.5% met the criteria for ADHD Inattentive Type. A two-year follow-up study of the same cohort indicated that 73% of those diagnosed with ADHD had the diagnosis reconfirmed at follow-up (31). The authors also noted that the odds of a child with ADHD still having episodes of nocturnal enuresis at 2-year follow-up were 3.2 times higher than those for a child who did not have comorbid ADHD. The association with behavioral disturbance has been reported as being greater for secondary enuresis 32,33 and for enuresis persisting into adolescence (34). One study that specifically evaluated risk factors for development of secondary enuresis found that delayed attainment of initial nocturnal continence and exposure to four or more stressful life events in a year were significantly related to the development of secondary enuresis (35). Similar results with regard to the relationship between psychosocial stress and secondary enuresis have been reported by von Gontard et al. (36) However, at least one large study in the Netherlands found no difference in psychopathology between children with primary and secondary enuresis (37). Of interest is an investigation by Van Hoecke et al. (38), that compared the results of the Child Behavior Checklist and the Disruptive Behavior Disorder Rating Scale in 154 children with enuresis and 153 controls. The results indicated that although the children with enuresis scored significantly higher on both scales, when the socioeconomic status of the children was controlled for the relationship was no longer present.

The occurrence of the enuretic episodes during sleep naturally led to a series of studies investigating the relationship between sleep states and the occurrence of enuretic events. The earliest of these studies suggested that the enuretic events occurred in “deep” sleep and led to a theory that enuretic events were dream equivalents (39). This theory was subsequently supplanted by Broughton’s (40); (41) view that enuresis was a disorder of arousal. This research suggested that enuretic episodes were preceded by arousal signals and originated in delta sleep. A further elaboration of this theory held that psychiatrically disturbed children with enuresis received normal arousal signals but did not respond to them, whereas those without psychiatric disturbance did not generate arousal signals (42). The largest and most convincing sleep studies indicate that enuretic episodes occur in each sleep stage in proportion to the time spent in that stage, when time of night also is considered 27,43,44. There have been three studies that suggested that children with primary enuresis may be more difficult to arouse from sleep than control subjects, although the methodology is somewhat subjective with regard to defining arousability 6,45,46. Other research in this area has focused on combining sleep studies with cystometry (47), and may eventually lead to the identification of subtypes of children with enuresis 48,49.

The development of desmopressin acetate (DDAVP) as a treatment for enuresis (described later) has led to the observation that some children with enuresis do not have the ability to concentrate the urine they produce during the night and reduce urine volume (50). In a further investigation of this hypothesis, Rittig et al. (51) compared the circadian variation of plasma atrial natriuretic peptide (ANP) with the clearance of creatinine and the excretion of sodium and potassium. Subjects in the study consisted of 15 children with nocturnal enuresis and 11 control subjects matched for age, sex, and weight. The children with enuresis did not differ from control subjects with regard to ANP, but during the first hours of sleep, they did manifest significantly more polyuria, natriuresis, and kaliuresis despite normal levels of ANP. The authors concluded that children with enuresis display abnormal diurnal rhythmicity in the urinary excretion of potassium and sodium that is not correlated with plasma levels of ANP. They speculated that the abnormalities in sodium and potassium may be related to abnormal tubular handling. This hypothesis has been further supported by subsequent research 52,53,54 that used radioimmunoassay to evaluate the circadian rhythmicity of plasma arginine vasopressin (AVP) in 55 children with enuresis and 15 control subjects. The AVP levels were measured under conditions of controlled water intake three times per day for 72 hours. Only 14 of the 55 children with enuresis had a significant decrease in AVP compared with control subjects. Nine of these 14 AVP-deficient children subsequently were found to be totally dry with DDAVP treatment.

The circadian rhythmicity of AVP has continued to be a focus of investigation because it theoretically could explain both the pathophysiology of enuresis and its response to DDAVP. Accordingly, researchers have been particularly interested in any differences that could be detected between DDAVP responders and nonresponders. One study has reported significant differences in morning values of AVP between normal control subjects (n = 7) and children whose enuresis responded to DDAVP (n = 6), as well as between the responders (n = 6) and nonresponders to DDAVP (n = 5). Thus, the morning AVP levels were able to differentiate the children with enuresis from the control subjects, and the responders from the nonresponders (Medel et al., 1998) (55). However, further complicating this line of research has been
the finding that AVP is secreted in a “pulsatile pattern,” which dictates frequent sampling of plasma levels to be meaningful (56). Studies using frequent measurements of AVP have produced mixed results. Two studies that used more frequent AVP measurements 56,57 found no differences between responders and nonresponders to DDAVP. Aikawa et al. 58,59 addressed this question in a series of studies that measured AVP secretion on an hourly basis for 24 hours. The first set of these studies looked at AVP secretion profiles in children with enuresis (n = 9) and control subjects (n = 8). The results did establish that the plasma AVP level was significantly lower in the children with enuresis in the 11 PM to 4 AM time period. They then looked at the secretion dynamics in two phenomenologic subgroups of children with enuresis: those with low urinary osmotic pressure and large nocturnal urine output, as opposed to a group with normal urinary osmotic pressure and small nocturnal urine output. The results showed that the mean nocturnal AVP levels were significantly lower in the first (large nocturnal output) group and that treatment with DDAVP did produce a significant increase in AVP for this group as a whole, but not for every child.

Another area of research has been the role of urine osmolality in the production of nocturnal enuresis. Three separate studies that looked at first morning urinary specific gravity in preschool children have suggested that children who wet the bed tend to have lower mean urinary specific gravity than those who do not, but the findings do not reach statistical significance 60,61,62. An investigation into nocturnal and daytime urine volume, osmolality, and ion excretion in children with primary enuresis and controls reported a significant decrease in the ratio of nocturnal/daytime urine osmolality, as well as urine chloride and potassium excretion, and urine osmolality in children with enuresis as compared to controls (63). However, these values were not found to be predictive of response to either treatment with DDAVP or behavioral conditioning therapies. Hypercalciuria has also been discussed as a potential pathogenetic factor. However, a study involving DDAVP-responsive children, therapy-responsive children and controls found no difference in urinary excretion between children with enuresis and controls (64). An investigation by Valenti et al. (65) suggested that there may be a subgroup of enuretic children who present with hypercalciuria. Their investigation involved 46 children with enuresis, of whom 26 had hypercalciuria. All of the children received DDAVP, and those with hypercalciuria were also treated with a low calcium diet. In those children who had low AVP levels prior to treatment, the levels were normalized after treatment and the low calcium diet effectively resolved the hypercalciuria.

The effect of fluid restriction on AVP levels and urine osmolality also has been investigated. These studies indicate that AVP levels are increased in both control subjects and in children with enuresis in response to fluid restriction, and that the degree of AVP secretion is related to plasma osmolality (66). When DDAVP responders and nonresponders are compared with control subjects, all three groups manifest an increase in AVP, but the DDAVP responders showed a smaller increase than the other groups (67). Studies involving adolescents and adults with refractory enuresis also have suggested that the primary pathophysiologic mechanism may be an abnormal tubular processing of sodium related to a relative insensitivity to AVP [Hunsballe et al. 68,69] that is corrected to some degree by DDAVP. Similar research in children led Eggert and Kuhn (70) to hypothesize that the primary difference between children with enuresis and control subjects may be at the distal tubular AVP receptor level.

Although this line of research has primarily involved DDAVP, it also has led to a reexamination of the therapeutic effect exerted by imipramine. Hunsballe et al. (71) reported a decrease in urine output and reduced osmolar clearance induced by imipramine that was, in part, contributed to by a lower excretion of sodium and potassium.

One of the newest areas of research has been the exploration of genetic linkages. It has long been known that enuresis tends to run in families, and that a positive family history can be related to positive treatment outcome (72). In general, genetic studies involve large numbers of families with multigenerational transmission of primary nocturnal enuresis. The chromosomes that have been identified to date include 13q, 12q, 8, and 22 73,74,75. In some families, an autosomal dominant mode of transmission with penetrance above 90% has been identified (76).

Loeys et al. (77) studied 32 families with extensive histories of nocturnal enuresis, which ranged from two to four generations. Linkage to an area on chromosome 22q11 was noted in nine families, to 13q13-14 in six, and to 12q in four. Evidence of linkage to chromosome 8q could not be established. Thus, the findings were heterogeneous with regard to the chromosome sites involved. A genetic investigation of a large, four-generation family with a history of both nocturnal and diurnal enuresis indicated an autosomal dominant pattern with high penetrance. The author concluded that, “The most likely genetical model in this kindred seems to be a gene located on chromosome 4p16.1 causing primary nocturnal enuresis.” However, involvement of chromosome 12q24.3 could not be excluded (78).

Deen et al. (79) specifically investigated the aquaporin-2 water channel locus (AQP-2) in six families with a dominant pattern of transmission, as AQP-2 is necessary for concentrating urine and DDAVP enhances AQP2 expression. The authors indicated that they could not locate a mutation in the AQP2 coding sequence and, “The AQP-2 gene is excluded as a candidate for autosomal dominant DNE in these families in which the disease co-segregates with chromosome 12q.” The results of this line of research to date would support the view of von Gontard et al. (76) that “Nocturnal enuresis is a common, genetic, and heterogeneous disorder. The association between genotype and phenotype are complex and are susceptible to environmental influences.”

The fact that urinary tract infections can precipitate enuretic events in children means that a urinalysis should be performed to rule out this readily treatable cause of enuresis.

The use of more invasive and painful studies remains controversial. Although it is certainly possible that altered bladder physiology may lead to primary enuresis, the yield from these studies does not appear to be of sufficient magnitude to warrant subjecting all children with enuresis to them. A thorough review of this subject by Cohen (80), found the incidence of obstructive lesions in children with enuresis to be 3.7% in a primary care pediatric setting. Accordingly, he suggested that, “contrast studies are indicated only when there is significant evidence of anatomical or functional pathology by history or exam.” Subsequent studies have supported this general position 23,24, while suggesting that those children with daytime wetting and overt symptoms of voiding disturbance are more apt to have urinary tract abnormalities than those who wet solely at night (81). As discussed above, ultrasound bladder measurements may prove useful in the future, but currently this is viewed as a technique utilized in research only (25).

The differential diagnosis includes the possibility of urinary tract infection and altered bladder physiology. There are
scattered case reports of enuresis being secondary to other primary medical problems, such as hyperthyroidism (82), constipation (83), and central hormonal abnormalities (84). Although such reports are infrequent, the clinician should do a thorough physical examination and consider the possibility of underlying organic illness— particularly readily treatable constipation. Brooks and Topol (85) have reported an association between obstructive sleep apnea in children and nocturnal enuresis. They hypothesize that this could be related to the effects of sleep apnea on arousal patterns, and bladder dynamics on urinary hormone production.

There are reports of nocturnal enuresis occurring as a side effect of treatment with selective serotonin reuptake inhibitor antidepressants (SSRIs). Given the frequency with which these agents are prescribed to children, this should be considered. The chronological correlation between the initiation of treatment with an SSRI and the onset of enuretic episodes would tend to substantiate the diagnosis 86,87,88. Psychological testing in conjunction with structured interviews may provide further insight into the coexistence of psychopathology. However, the studies reviewed previously suggest that any coexisting psychological disorder should be viewed as an accompanying finding rather than as a causal effect.

The distinction between primary and secondary enuresis can be made by history.

Although psychotherapy may be helpful for managing the behavioral disorders that accompany enuresis, it appears to have little effect on primary enuresis itself, with studies showing a success rate of 20%, which may largely be accounted for by spontaneous remission (80). Psychotherapy may be more useful for those children with secondary enuresis, especially those whose episodes begin after a traumatic event or parental divorce, or in those cases where a specific parent–child conflict appears to be contributing to the continuation of the enuresis (89) (Table 5.12.1).

It has been shown that having nocturnal enuresis has a negative impact on self-esteem, which can be normalized by effective treatment 90,91,92. The factors related to negative self-image were male gender, primary enuresis, and a greater frequency of wet nights.

The two primary means of treating children with enuresis fall into the categories of behavioral and psychopharmacologic methods.

Behavioral treatment should be attempted first because it is usually more innocuous than pharmacologic intervention. The underlying assumption of the behavioral strategy is that it is helping children with enuresis and their families master an affliction rather than tacitly implying that the children are either consciously or unconsciously causing the wetting themselves. One unfortunate consequence of various reward–punishment strategies is that they can subtly imply to children and their families that the disorder is quasivolitional. The bell and pad method of conditioning is a reasonable first approach. A review of this treatment modality indicated that it was first reported in 1904 and has been in routine use since the 1930s (93). In reviewing the results of several studies involving over 1,000 children, Werry (94) found a success rate of 75%, and subsequent studies have been consistent with this (95). There have been two relatively recent systematic reviews of the literature with regard to the efficacy of the alarm method of treatment for nocturnal enuresis. Glazener et al. (96) noted that approximately two-thirds of children treated with the alarm achieved nocturnal continence during treatment and nearly half who complete this form of treatment remained dry after the termination of treatment. In a similar study, Butler and Gasson (97) reviewed 38 studies involving at least 10 children, and found that the success rate ranged from 30% to 87%. However, there were considerable methodological differences, including the definition of success. When they narrowed the review to 20 relatively homogeneous studies, they found an overall 65% success rate and a relapse rate of 42%. There appear to be two subgroups of responders: those who sleep through the night after treatment without wetting, and those who wake up spontaneously to go to the bathroom (98). A psychiatric disorder in the child, and family stress, appear to be negative prognostic factors when predicting outcome with this modality (95). As noted previously, whenever reward–punishment contingencies are considered, it is extremely important to ensure that one is not unwittingly communicating that the disorder is quasivolitional.

An attempt has been made to investigate the relationship between bladder capacity and response to behavioral treatment. A study involving 50 children who were wet at least two nights a week found that children with small pretreatment maximal functional bladder capacities did better with the bell and pad method in conjunction with retention–control training, whereas the children with larger bladder capacities responded to the bell and pad method alone. However, this was a qualitative difference in response, as 92.5% of the 40 children who completed the study met the outcome criteria of 14 consecutive dry nights, regardless of which group they were in (99). A similar study that examined the impact of bladder capacity on response to the bell and pad system found no association with outcome (100). Both of these investigations indicated that behavioral disturbance was related to failure to respond to conditioning techniques 99,100. Butler and Robinson (101) found low functional bladder capacity and inability to be aroused by the alarm to correlate with lack of success, and a higher pretreatment frequency of enuretic events has been found to correlate with increased success with this form of treatment (102).

Bladder capacity also has been investigated with regard to changes occurring during treatment. Oredsson and Jorgensen (103) measured bladder capacity in 18 children with severe nocturnal enuresis before beginning a 6-week period of treatment with the bell and pad and again after treatment. Ten of the 18 children ceased wetting, but overall there was a significant increase in bladder capacity for the entire group that did not correlate with outcome. Subsequent investigations have also reported an increase in bladder capacity following treatment with the alarm method 104,105. This may explain why one study found that children whose nocturnal enuresis responded to the alarm also had significant improvement in daytime wetting (106).

Behavioral treatment continues to evolve. In a study involving 125 children, an attempt was made to replace the bell and pad mechanism with a simple alarm clock that was either set to go off at a time when the bladder might be expected to be reaching maximal capacity (group I) or after 2 to 3 hours of sleep (group II). The results were comparable with previously published figures for the bell and pad, with success noted in 77.1% of group I and 61.8% of group II, and respective 6-month relapse rates of 24.1% and 14.7% (107).

Another innovation involves replacing the pad that signals the enuretic event with a small ultrasonic monitor mounted to an elastic abdominal belt that signals the alarm when bladder capacity is reaching a predetermined threshold (108). Results of a clinical trial of this methodology were comparable with those obtained with the traditional bell and pad technique, and increases in nighttime bladder capacity also were noted (109).

An approach using bladder biofeedback has been developed for children with enuresis who are refractory to other forms of treatment, have small bladder capacities, and have evidence of an unstable detrusor. Specifically, the authors noted that of the 24 children who fit these criteria, 17 experienced complete remission (two of these later relapsed), six experienced a decrease, and in one, there was no change (110). A subsequent report by the same group (111) also reported an increase in bladder capacity with biofeedback treatment. As noted earlier, the presence of behavioral or family functioning problems can have a negative impact on the outcome of behavioral treatment. A successful intervention in refractory children with severe wetting who have these issues is to combine traditional alarm therapy with treatment with DDAVP 112,113.