Storage and elimination of urine in the infant bladder is entirely an autonomic function, without inhibitory or volitional control connections to the CNS. The bladder itself is composed of smooth muscle, while the length of the urethra contains an increasing presence of striated muscle as it projects distally from the bladder. As the bladder wall accommodates expansion in the storage process, a trigger threshold of fluid capacity is reached. An afferent neural message is sent through the pudendal nerve to sites at S2, S3, and S4, where a synapse is activated with nerves that innervate efferent muscles. Additional neural pathways connect this reflex with regions in the pons and detrusor motor nucleus. The bladder normally contracts in synchrony with the relaxation of sphincter muscle, expelling urine in one continuous stream. When bladder control persists in this automatic fashion in the absence of physical causes, such as a primary disease affecting the nervous system, the child is said to have a pediatric unstable bladder or bladder displaying uninhibited contractions. This can result in a chronic day or night wetting problem.

A child who does not show complete daytime urinary continence often experiences repeated and unexpected contractions of the bladder (primary diurnal enuresis [PDE]). These contractions result in intermittent wetting episodes, with accidents occurring at small capacities. Such a youngster has never been dry for a continuous 3-month period. In the presence of an intact nervous system, the child does not respond to a sensation of a gradient of bladder filling but rather will perceive a sensation of the bladder muscle in contraction. In the young child, the most readily available compensatory response to an uninhibited bladder reflex is a volitional contraction of the external sphincter muscles. The child eventually learns to apply pressure on the perineal area by crossing the legs and squeezing the thighs together or performing a “squatting” maneuver by sitting on the heel of one foot. At best, the child is able to inhibit some but not all of the urine flow, because the compensatory maneuver is initiated only after the bladder has begun an uninhibited contraction.

Bedwetting is a relatively common problem that frustrates children and parents long after daytime continence has been achieved. Although the condition most often appears as a monosymptomatic, nonorganically based problem, the psychological impact and persistence of the problem over many years must and should be addressed with active treatment interventions.

Many myths have been constructed about the causes and cures of primary nocturnal enuresis (PNE) that are based on coincidence and faulty logic. These myths have evolved because of the pervasive epidemiology of the problem combined with unpredictable spontaneous remission rates. Speculation has therefore included small functional bladder capacity, dietary influences, allergies, and excessive water intake as examples of mechanisms underlying the incontinence. To date, there is no support that any of these factors is explanatory of a single underlying cause. Although early studies have been confirmatory of small functional bladder capacity, the occurrence of bladder retention in some patients can also occur, especially in the presence of a mild daytime unstable bladder component (Shima et al., 1998; Medel, Ruarte, Castera, & Podesta, 1998). These children may have learned an overcorrective maneuver by chronic tightening of perineal muscles to overcome any symptoms of diurnal urine loss.

Explanatory mechanisms involving bladder storage have explored the notion of small functional bladder capacity interacting with high urine production at night (Rasmussen, Kirk, Borup, Norgaard, & Djurhuus, 1996; Djurhuus & Rittig, 1998). Conclusive evidence on this point has proven to be equivocal. Exceptions to the small functional capacity model are frequent, especially as children get older and often decrease their frequency of voluntary daytime voids because of previously acquired annoyance associated with trips to the bathroom. Norgaard, Djurhuus, Watanabe, Stenberg, and Lettgen (1997) implicated hormonal influences by studying bladder capacity with attention to rate of urine production and urine osmolality. Their findings built on work of a decade earlier, when they documented the presence of an insufficient nocturnal antidiuretic control in some patients with PNE, who were also usually treatment resistant (Norgaard, Pedersen, & Djurhuus, 1985).

Wide-scale distribution of DDAVP, a synthetic form of vasopressin, has shown the drug’s dramatic immediate effects on abating PNE. Recurrence of symptoms after the drug is withdrawn is high, however, suggesting that a pharmacogenic solution is not likely to “jump-start” the youngster who may have a vasopressin deficiency.

Depth of sleep is another competing controversy in the pursuit of an etiologic model for PNE. Many parents and primary care providers have assumed that the bedwetter sleeps too deeply and therefore cannot respond to full bladder cues to awaken and toilet at night. A contradictory view is apparent when one considers that very few normal children awaken at night to void, and if they do, such awakening might be considered a pathologic symptom of nocturia. In addition, children sleep more deeply than adults. This fact might result in a false conclusion that the child is an abnormally deep sleeper when a parent tries to awaken the child to void and keep the bed dry. For many years, studies monitoring electroencephalograms (EEG) and enuresis showed no relationship between depth of sleep and enuretic events in the absence of a known paroxysmal or primary seizure disturbance (Wolfish, Pivik, & Busby, 1997).

Conversely, increasing numbers of recent scientific reports suggest that a possible deficit in CNS arousal underlies PNE (Kawauchi et al., 1998a; Watanabe, Imada, Kawauchi, Koyama, & Shirakawa, 1997). Clinical observations confirming that arousal factors may be implicated include the tendency for the child with PNE to sleep dry on occasion when going to bed very late or sleeping in a different bed when away from home (eg, at sleepovers or at relatives’ houses). Jenkins et al. (1996) and Neveus, Lackgren, Tuvemo, and Stenberg (1998) found that children with PNE were indeed harder to bring to full awakening than a nonenuretic population. PNE has also been classified along the lines of arousability by sleep researchers who propose three distinct clinical groups (Watanabe, 1998; Imada et al., 1998):

Kawauchi et al. (1998b) propose that type I may involve an immaturity in the function of the thalamus, while type IIa may implicate the pons or the lower urinary tract. Type IIb most closely resembles a neurogenic bladder profile. Refer to Chapter 62 for more information about the use of medications in managing PNE.

Chronic encopresis is mostly an outcome of functional or behavioral causes for stool retention or inappropriate bowel elimination habits. Physical causes or syndromes are consequently an unlikely reason for a child’s encopresis. An exception is Hirshsprung’s disease, which is an anatomic basis of stool incontinence. Hirshsprung’s disease is often apparent at birth or is identified long before the child is seen for encopresis. Other problems involving the integrity of the rectal sphincter and spinal cord innervation also must be considered before accepting a functional cause for incontinent stool loss. Children with functional encopresis (FEN) do not have identifiable anatomic malformations or neurogenic lesions. Abnormal pudendal nerve function, which often
contributes to fecal incontinence in adults, does not appear to be implicated in FEN (Sentovich et al., 1998).

The most common presentation of encopresis is a minor stool loss or staining of the underpants (“skid marks”) accompanied by retentive toileting habits. Stool retention results in the compaction of large amounts of hard feces in the lower bowel. The passage of loose stool from farther up the intestine is then allowed to “leak” between the hardened stool and the wall of the lower bowel. Many parents mistake the cause of soiled underpants as being related to poor hygiene or wiping technique.

About 1% to 5% of children are believed to experience daytime wetting in the absence of physical findings, including bacterial infection of the lower urinary tracts (Bower, Moore, Shepherd, & Adams, 1996). However, Swithinbank, Brookes, Shepherd, and Abrams (1998) reported that a recent survey of 1176 healthy English school children revealed prevalence estimates as high as 12% for day wetting in children aged 11 to 12 years. Nevertheless, the prevalence is much greater in girls than boys. This sex difference is probably related to higher incidence of chronic urinary tract infections (UTIs) seen in girls with PDE, secondary to the shorter urethral distance in girls, which may carry bacteria to the bladder.

Primary nocturnal enuresis occurs in about 10% of all 5-year-old children who are otherwise normal in all other developmental functions. This estimate would include from 5 to 10 million children in North America. The National Kidney Foundation estimates that 5 to 7 million children age 6 years or older have PNE (1999). The prevalence rates vary among cultures, although the condition is documented among all cultures and racial groups (Kalo & Bella, 1996; Trombetta, Savoca, Siracusano, & Liguori, 1997; Chiozza et al., 1998; Chao et al., 1997; Yeung, 1997; Serel et al., 1997; Popper & Steingard, 1996; Byrd, Weitzman, Lanphear, & Auinger, 1996).

It is estimated that up to 70% of children with PNE have a primary relative who shares that history. There is also a 67% concordance rate for identical twins. Recent discoveries of genetic markers for PNE have clearly established a genetic basis of PNE (Hublin, Kaprio, Partinen, & Koskenvuo, 1998; von Gontard, Eiberg, Hollmann, Rittig, & Lehmkuhl, 1997; von Gontard et al., 1997; Arnell et al., 1997; Eiberg, 1998; von Gontard, Eiberg, Hollmann, Rittig, & Lehmkuhl, 1998).

The most conventional criterion for diagnosing PNE is wetting the bed on average at least two times per month. The number of children remitting without treatment is about 15% per year, which reduces the prevalence to 1% by puberty (Petrican & Sawan, 1998). When considering whether PNE will persist into adulthood, Hjalmas (1997) asserts that, if not treated, 10% of these youngsters will persist with PNE for life.

Special needs children have higher rates of PNE. This is especially true for youngsters diagnosed with attention deficit disorder with hyperactivity (ADHD). PNE in such children may in part be related to a “hyperactive” bladder or to behavioral problems encountered in toilet training. These problems may have emerged because of attentional impediments to efficient learning. Pervasive and chronic hyperactivity of the parasympathetic nervous system may also pay a role in uninhibited bladder contractions (Yakinci, Mungen, Durmaz, Balbay, & Karabiber, 1997). Refer to Chapter 21 for more information on diagnosing and managing ADHD.

Prevalence rates of FEN are frequently underestimates of actual occurrence. This may be a result of mild forms of stool loss going unnoticed or being tolerated by family members. Reasons for this tolerance may be multidetermined and can involve individual family and culture-bound attitudes toward hygiene or the belief that stool loss is not a treatable, medical symptom.