Diagnosis and management of nocturnal enuresis - includes patient information sheet

Author: Marla R. Ullom-Minnich
Date: Nov 15, 1996

The etiology of primary nocturnal enuresis remains somewhat controversial but may include genetic factors, decreased functional bladder capacity, increased diuresis at night, and constipation. Deep sleep and emotional illness usually play only a minimal role. A detailed description of the enuretic episodes should be obtained, and a neurologic examination should be performed as part of the physical evaluation of a child with nocturnal enuresis. In uncomplicated cases, urinalysis and a urine culture are the only required laboratory tests. The specific cause of the nocturnal enuresis usually is not determined. Treatment options include the urine alarm system, pharmacotherapy and complex regimens such as dry-bed training. Treatments are often combined. Nocturnal enuresis eventually resolves in the majority of cases.

Most children achieve control of both daytime and nighttime urine voiding before the age of five years. Failure to gain control of urination by this age can be a source of great frustration to parents and children. In such cases, the family physician is often consulted.


Enuresis refers to the involuntary discharge of urine after the age by which bladder control should have been established, usually considered to be the age of five years. The most common form of enuresis is nocturnal bed-wetting (nighttime voiding). Daytime incontinence (diurnal enuresis) after the age of five years is less common and can be associated with different physiologic mechanisms and conditions.

Primary enuresis is the failure to achieve dryness consistently. It accounts for more than 90 percent of all cases of enuresis.[1] Secondary enuresis refers to the return of incontinence after an extended period of dryness. This form of enuresis is more commonly associated with psychologic stressors than with organic pathology.


Nocturnal enuresis of at least one episode per month is found in approximately 10 to 20 percent of five-year-old children, 5 to 7 percent of 10-year-old children and 2 to 4 percent of 12- to 14-year-old children.[2,3] Spontaneous remission of enuresis occurs at a rate of about 15 percent per year into adulthood, when the prevalence remains at about 1 percent.[3] Enuresis is twice as common in boys as in girls.


The etiology of primary nocturnal enuresis is not clear. Studies have examined many factors, ranging from genetic predisposition to psychosocial stressors, often with conflicting results.

It is important for physicians to be familiar with the various hypotheses concerning enuresis, because parents and patients are often very interested in understanding the reason for this problem and they may have obtained both inaccurate and misleading information from a range of sources. Physicians need to be able to discuss inaccurate perceptions, as well as the factors that actually may contribute to the problem. The etiology of enuresis is most likely multifactorial, and the problem may represent a variation in normal bladder control rather than a true disease state.[3]


Heredity is believed to play a major role in enuresis, since it tends to occur in several members of a family. In families in which both parents had enuresis, the incidence in children is approximately 70 percent. If one parent was affected, the incidence is about 40 percent. If neither parent was affected, the incidence decreases to approximately 15 percent.[3] One study[4] suggested that enuresis follows an autosomal dominant mode of inheritance with a penetrance above 90 percent.


Bladder dysfunction may play a small role in enuresis. Early studies showed that compared with control subjects, bed-wetters exhibited more frequent and more intense spontaneous evoked contractions of the primary detrusor muscle and also experienced greater bladder pressure.[1] However, recent investigations have refuted these findings.[5] According to one study,[4] an unstable bladder is found in only 3 to 5 percent of patients with pure primary nocturnal enuresis. The new findings have led to the current recommendation that invasive urologic studies not be done routinely in patients with pure primary nocturnal enuresis, because of the low incidence of verifiable organic causes of neurogenic bladder.[6]


Decreased functional bladder capacity has also been implicated in the etiology of primary nocturnal enuresis. Functional bladder capacity is the volume of urine voided after micturition has been postponed for as long as possible. Compared with control subjects, patients with enuresis appear to have the same bladder capacity, but they may feel the urgent need to urinate at a much smaller volume. Children with enuresis often report that their need to urinate during the day comes on suddenly and with great urgency.[1]

Normal bladder capacity can be estimated using the following formula: the bladder capacity in ounces is equal to the age in years plus 2.[3] Functional bladder capacity in children with enuresis may be less than 50 percent of the normal calculated bladder volume.[7]

It has been hypothesized that the small functional bladder capacity either results from inadequate cortical inhibition of the bladder or is related to developmental delay. It has also been suggested that small bladder capacity may be part of an allergic reaction in which the bladder is maintained in spasm, which prevents it from accommodating larger volumes of urine.[8,9]

An alternative hypothesis is that low functional bladder capacity may be a result of the child's micturition habits, rather than a cause.[6] Since children with enuresis are unable to hold urine for long periods of time at night, their bladders do not become accustomed to holding larger volumes of urine; thus, they develop a lower functional bladder capacity. This hypothesis places low functional bladder capacity as a correlate, rather than a cause, of bed-wetting.


For many years, enuresis was thought to be the result of a sleep disorder. It was hypothesized that children with enuresis either spent more time in deeper sleep than other children or were more difficult to arouse from sleep. Sleep studies have since refuted this hypothesis. Evidence now shows that enuretic events tend to occur in approximate proportion to the amount of time spent in each particular sleep stage.[1,10] For example, if 30 percent of the sleep time is spent in rapid-eye-movement (REM) sleep and 40 percent of the time in delta sleep, then 30 percent of the episodes would be expected to occur during REM sleep and 40 percent during delta sleep.

Early sleeping patterns may play a role in nocturnal enuresis. One study[11] showed that the age for the attainment of bladder control varied with the reported duration of sleep at one and two years of age. As a general rule, children who were described as sleeping long periods at these ages were slower to achieve bladder control.


Psychologic stressors have long been thought to play a role in enuresis. Although such stressors may be significant in secondary enuresis, they have not been shown to be important in primary enuresis. In children with primary enuresis, emotional problems may be a consequence of the parental response to the bed-wetting, but they are rarely, if ever, the cause of the enuretic condition.[1]


A more recent hypothesis is that children with enuresis tend to diurese at night. Diurnal analysis of antidiuretic hormone levels showed that the serum levels were constant in children with enuresis, while control subjects showed a diurnal antidiuretic hormone variation with a nighttime increase.[12] These findings suggest that children with enuresis have a normal bladder capacity that is exceeded by a high urine output at night. This high urine output results from the lack of an increase in antidiuretic hormone secretion at night.[12] This hypothesis is the basis for desmopressin (DDAVP) therapy.[13]


Hypotheses for the cause of enuresis have also included enlarged tonsils, urinary tract infections, constipation, lumbosacral disorders and developmental delay. Unrecognized underlying medical disorders, such as diabetes mellitus, diabetes insipidus, sickle cell disease and seizure disorders, may also play a role in individual patients.



MARLA R. ULLOM-MINNICH, M.D. is in private family practice at Partners in Family Care, Moundridge, Kan. Dr. Ullom-Minnich received her medical degree from the University of Kansas School of Medicine, Kansas City, Kan., and completed a residency in family practice at St. Joseph Medical Center, Wichita. Previously, she served as assistant professor in the Department of Family and Community Medicine at the University of Kansas School of Medicine-Wichita.

Address correspondence to Marla R. Ullom-Minnich, M.D., Partners in Family Care, 115 N. Christian, Moundridge, KS 67107.

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