The word enuresis is derived from a Greek word (enourein) that means “to void urine.” It can occur either during the day or at night (though some restrict the term to bedwetting that occurs at night). Enuresis can be divided into primary and secondary forms.
Signs and symptoms
The history is essential in making the proper diagnosis and should address the following:
Daytime voiding pattern
Toilet training history
Number and timing of episodes of bedwetting
Family history of nocturnal enuresis
Behavior, personality, and emotional status
Alertness should be maintained for symptoms of common underlying problems such as the following:
Overactive bladder or dysfunctional voiding
Cystitis and urinary tract infections (UTIs)
Major motor seizure
Diabetes mellitus or diabetes insipidus
A comprehensive physical examination should include the following:
Measurement of blood pressure
Inspection of external genitalia
Palpation in the renal and suprapubic areas
Palpation of the abdomen
Thorough neurologic examination of the lower extremities, including gait, muscle power, tone, sensation, reflexes, and plantar responses
Assessment of the anal “wink”
Inspection and palpation of the lumbosacral spine
Abnormal physical findings are not usually present in children when enuresis is the sole symptom and are not necessarily present in children with overactive bladder or dysfunctional voiding. Abnormal findings might be present in patients with cystitis, constipation, neurogenic bladder, urethral obstruction, ectopic ureter, or obstructive sleep apnea (OSA).
See Presentation for more detail.
If an underlying problem is identified and successfully treated and the enuresis persists, the enuresis should be considered a separate problem. Adverse effects of medications should be considered as possible causes.
Laboratory studies that may be helpful include the following:
Urinalysis (the most important screening test in a child with enuresis)
Ensure the urinalysis is performed on a concentrated urine specimen. Dilute specimens with a specific gravity under 1.010 might not reveal infection.
If the urinalysis findings suggest cystitis, urine culture and sensitivity testing
Blood tests usually are not needed
Other studies that may be considered are as follows:
Uroflowmetry with bladder scanning (helpful in screening patients suspected of having voiding dysfunction, neurogenic bladder and urthrakl obstruction)
Ultrasonography of the bladder and kidneys, both before and after voiding
Voiding cystourethrography (only if either the bladder wall is thickened or trabeculated on ultrasonography or a significant postvoid residual volume of urine [>50 mL) is noted or if neurogenic bladder is suspected or there is a history of febrile UTI)
Magnetic resonance imaging (MRI) of the spine (if the patient has an abnormal neurologic examination finding of the lower extremities, a visible lumbosacral spine defect, the triad of encopresis plus gait abnormality plus and daytime symptoms, or dysfunctional voiding that does not improve after 3 months of therapy)
Urodynamic studies and cystoscopy (if the patient has urethral obstruction or neurogenic bladder or has dysfunctional voiding that does not improve after 3 months of therapy
See Workup for more detail.
Preliminary management focusing on behavioral modification and positive reinforcement is often helpful. Bladder training exercises are not recommended. The only therapies proved to be effective are alarm therapy and treatment with desmopressin acetate or imipramine. Enuresis per se is not a surgically treated condition. Treatment is usually not recommended for children younger than 6 or 7 years.
Initial management includes the following:
Caring and patient parental attitude, acknowledging that the child has no control over the wetting
Behavioral modification with positive reinforcement
Explanation of the probable cause of the enuresis
Keen attention to establishing and maintaining a normal daytime voiding pattern, normal bowel pattern, and normal hydration
If following this approach for up to 3 months does not result in dryness, either alarm therapy or pharmacologic therapy should be considered.
Alarm therapy should be considered for every patient. However, if the child is still wet after a minimum of 3 months of consecutive use, alarm therapy can be discontinued and considered unsuccessful. Failure does not preclude future successful treatment once the child is older and more motivated.
Pharmacologic therapies include the following agents:
Desmopressin acetate (the preferred medication for treating children with enuresis); combination of alarm therapy with desmopressin therapy may yield dryness not achievable with either therapy alone
Anticholinergic agents such as oxybutynin chloride and tolterodine (especially in patients with overactive bladder, dysfunctional voiding, or neurogenic bladder); the combination of desmopressin acetate and oxybutynin chloride may be efficacious in children with overactive bladder or dysfunctional voiding who show daytime response to anticholinergic therapy but continue to wet at night; long-acting preparations of oxybutin may be more efficacious for combination therapy with desmopressin
Imipramine (because of the unfavorable adverse effect profile and the significant risk of death with overdose, not recommended by the World Health Organization for treatment of enuresis)
See Treatment and Medication for more detail.
The word enuresis is derived from a Greek word (enourein) that means “to void urine.” The International Children’s Continence Society [ICCS] restricts the term to wetting that occurs at night. Enuresis can be divided into primary enuresis (PE) and secondary enuresis (SE). A child who has been continent for at least 6 months before the onset of the bedwetting is considered to have SE. The pathogenesis of PE is similar to that of SE. [1, 2]
In PE, psychological problems are almost always the result of the condition and only rarely the cause. In SE, however, psychological problems are a possible cause, albeit not a common one. The comorbidity of behavioral problems is two to four times higher in children with enuresis.
The emotional impact of enuresis on a child and family can be considerable. Children with enuresis are commonly punished and are at risk for emotional and physical abuse. Numerous studies of children with enuresis report feelings of embarrassment and anxiety, loss of self-esteem, and effects on self-perception, interpersonal relationships, quality of life, and school performance.  A substantial negative impact on self-esteem is reported even in children whose enuretic episodes occur as infrequently as once per month.
Diagnostic criteria (DSM-5)
The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), classifies both enuresis and encopresis under the heading of elimination disorders.  DSM-5 criteria for enuresis are as follows:
Repeated voiding of urine into bed or clothes, whether involuntary or intentional
The behavior either (a) occurs at least twice a week for at least 3 consecutive months or (b) results in clinically significant distress or social, functional, or academic impairment
The behavior occurs in a child who is at least 5 years old (or has reached the equivalent developmental level)
The behavior cannot be attributed to the physiologic effects of a substance or other medical condition
Enuresis can be further divided into the following three subtypes on the basis of the time of occurrence  :
Nocturnal (ie, during sleep)
Diurnal (ie, during waking hours)
Nocturnal and diurnal (also known as nonmonosymptomatic enuresis)
Normal achievement of continence
Dryness at night usually follows achievement of continence by day (see Table 1 below). During the second year of life, children start to develop the ability to relax the external urethral sphincter voluntarily and to initiate voiding, even in the absence of the desire to void. By approximately age 4 years, all children with normal bladder function should have acquired this ability.
Table 1. Percent of Children Dry by Day and Night at Various Preschool Ages (Open Table in a new window)
|Age, y||Dry by Day, %||Dry by Night, %|
Numerous studies report varying but high prevalence of the condition in other family members of patients with enuresis. According to the highest reported familial prevalence rates, 56% of fathers, 36% of mothers, and 40% of siblings experience a problem with enuresis. Enuresis is reported in 43% of children of enuretic fathers, 44% of children of enuretic mothers, and 77% of children when both the mother and father had enuresis. A family history of bedwetting is found in approximately 50% of children with SE.
Enuresis is usually transmitted in an autosomal dominant fashion. Chromosome 22 was identified as the site of enuresis locus in a Danish family in 1995.  Subsequent reports link enuresis in other families to loci chromosomes 8, 12, and 16.  Identified genes cannot control for enuresis per se. Rather, an identified gene would have to control a pathophysiologic factor such as arousal, nocturnal polyuria, or bladder capacity.
A family history of enuresis does not seem to influence the outcomes of any of the various treatments.
Possible causes of PE and SE are summarized in Table 2 below.
Table 2. Possible Causes of Primary and Secondary Enuresis (Open Table in a new window)
|Causes of Primary Enuresis||Causes of Secondary Enuresis|
Disorder of sleep arousal
Small nocturnal bladder capacity
Disorder of sleep arousal
Small nocturnal bladder capacity
|Overactive bladder or dysfunctional voiding||Overactive bladder or dysfunctional voiding|
|Urethral obstruction||Acquired neurogenic bladder|
|Ectopic ureter||Obstructive sleep apnea|
|Diabetes insipidus||Diabetes mellitus|
|Acquired diabetes insipidus|
|Acquired urethral obstruction|
If no cause can be identified, the important pathophysiologic factors include a disorder of sleep arousal, nocturnal polyuria, and a low nocturnal bladder capacity.
Disorder of sleep arousal
Sleep studies reveal that children with enuresis do not wake up normally in response to an auditory signal; this finding confirms a problem in arousal.
Arousal to the sensation of a full or contracting bladder involves interconnected anatomic areas, including the cerebral cortex, the reticular activating system (RAS), the locus ceruleus (LC), the hypothalamus, the pontine micturition center (PMC), the spinal cord, and the bladder. The RAS controls depth of sleep, the LC controls arousal, and the PMC initiates the command for a detrusor contraction. Various neurotransmitters are involved, including norepinephrine, serotonin, and antidiuretic hormone (ADH).
Studies reveal nocturnal polyuria in some but not all children with enuresis. Although nocturnal polyuria is important in the pathophysiology of enuresis, overproduction of urine per se cannot be the sole causal factor. Nocturnal polyuria does not explain why children with enuresis do not wake up to the sensation of a full or contracting bladder or enuresis that occurs during daytime naps.
Nocturnal polyuria in children with enuresis likely has multiple causes, including the following:
Increased fluid ingestion from the time a child arrives home from school through the afternoon and evening to bedtime
Reduced fluid ingestion from the time a child wakes through the school day
Food consumption from the time a child arrives home from school through the afternoon and evening to bedtime
Low nocturnal secretion of ADH
Increased nocturnal solute excretion
Ingestion of fluids from the time a child arrives home from school through to bedtime is a common cause. Solid food ingestion is also a cause because excretion of solute by the kidney is accompanied by an obligate amount of water.
Many children with bedwetting drink very modest amounts of fluids at breakfast and throughout the school day. Accordingly, they arrive home from school hungry and thirsty, and most of their fluid intake often occurs in the few hours between arriving home and bedtime. This pattern favors nocturnal polyuria.
Production of urine is controlled by several factors, including ADH, which directly controls water absorption, and atrial natriuretic peptide (ANP) and aldosterone, which control solute and thus indirectly affect water excretion.
Norgaard et al first reported the absence of the expected nocturnal increase in ADH secretion in adults with enuresis.  Subsequent reports suggested that low nocturnal secretions of ADH are present in some but not all children with enuresis.  Urine sodium and potassium excretion are increased in some children with enuresis, but the reasons for these increases are not clear. Rittig et al report that secretion of ANP in children with enuresis shows a normal circadian rhythm and that the renin-angiotensin-aldosterone system is intact. 
Bladder distention may influence nocturnal secretion of ADH. Some studies report that ADH secretion is increased in response to bladder distention and reduced with bladder emptying. If ADH secretion falls with bladder emptying, the observed low nocturnal blood levels of ADH may be a consequence of enuresis rather than a cause.
Small nocturnal bladder capacity
Small functional bladder capacity (FBC) is now known to play a role in the pathogenesis of enuresis. For some time, it was considered a less likely explanation for enuresis in children without daytime symptoms, but studies confirmed that children without daytime symptoms may have a low nocturnal bladder capacity and that this is a very common factor in enuresis.
In a study by Mattsson and Lindstrom, FBC was positively correlated with nighttime urine output.  It has been theorized that children with enuresis may maintain a smaller nocturnal bladder volume and that this situation may condition the detrusor muscle to contract at a lower volume. According to this theory, the low nocturnal bladder capacity is a consequence of enuresis rather than a cause.
Bloom et al suggested a problem with the external urethral sphincter as a possible cause of low nocturnal bladder capacity,  noting that the control of voiding rests at the external urethral sphincter, where constant activity is present as a guarding reflex to preserve continence. They speculated that the activity of the external urethral sphincter might fall below a critical level during sleep and thereby trigger a detrusor contraction.
Overactive bladder or dysfunctional voiding
Overactive bladder or dysfunctional voiding is more common among girls in preschool or elementary school, usually presenting with urinary frequency, urgency, squatting behavior, daytime wetting, and enuresis.
Squatting behavior, a common and distinct symptom of overactive bladder or dysfunctional voiding, is a learned response and an attempt to suppress an unexpected and unwelcome detrusor contraction. The squatting posture elicits a bulbar detrusor inhibitory reflex. In some children, a period of normal voiding occurs, and the onset of the bedwetting is compatible with SE. If enuresis is present, the cause is presumed to be a low nocturnal bladder capacity, but a disorder of arousal must also be present. Squatting is commonly associated with a history of cystitis.
Symptoms tend to improve or resolve with time and are less common after puberty. Vesicoureteral reflux is more common in these children, and cystitis and constipation are frequent complicating problems. Urodynamic studies reveal unstable detrusor contractions early in the filling phase.
Cystitis is a common cause of enuresis and an aggravating factor associated with other causes; cystitis associated with enuresis may present at any age. Cystitis causes uninhibited detrusor contractions that can lead to episodes of day and nighttime wetting.
If cystitis is the only cause of enuresis, other symptoms of infection are usually present, and the wetting resolves with an appropriate antibiotic. Cystitis is more common in children with overactive bladder or dysfunctional voiding, neurogenic bladder, urethral obstruction, ectopic ureter, or diabetes mellitus. In these conditions, daytime symptoms do not resolve completely with antibiotic treatment.
Various common situations predispose to a psychological cause of enuresis, including birth of a new sibling, parental divorce or separation, death in the family, child abuse, or any other cause of social dysfunction at home or school.
A study by von Gontard et al found that children with SE have a significantly higher rate of behavioral disorders, life events, and continuous psychosocial stress than those with PE.  Stressful life events and psychiatric diagnoses are reported to precede the diagnosis of SE. The later the onset of SE, the greater the likelihood of preceding psychological stress.
Constipation can cause both PE and SE and is a common aggravating factor that should be considered when other causes are present.
Although the mechanism is not clear, the pressure effect of stool in the descending or sigmoid colon likely restricts bladder capacity, and colonic movements at night might trigger an uninhibited detrusor contraction. Constipation is usually present in children with neurogenic bladder and is more common in those with overactive bladder or dysfunctional voiding.
Sleep-disordered breathing (SDB) is a disorder associated with both an abnormality in arousal and enuresis. The most common cause of SDB in childhood is adenotonsillar hypertrophy, which has a peak incidence in children aged 2-5 years. Nocturnal polyuria is reported in individuals with obstructive sleep apnea (OSA). A decrease in nocturnal secretion of ADH and an increase in ANP secretion are possible explanations for nocturnal polyuria.
A neurogenic bladder can result from a lesion at any level in the nervous system, including the cerebral cortex, the spinal cord, and the peripheral nerves. As many as 37% of children with cerebral palsy have enuresis. Patients with myelomeningocele almost always have enuresis. Other spinal cord abnormalities, such as caudal regression syndrome, tethered cord, tumors, anterior spinal artery syndrome, and spinal cord trauma, can cause enuresis.
Specific dysfunction in the external urethral sphincter can develop after pelvic extirpative surgery, radiation therapy for pelvic malignancy, pelvic fracture, or incontinence surgery. Sacral agenesis can be associated with a neurogenic bladder. As many as 5% of patients with an imperforate anus have a neurogenic bladder, and most patients also have a lumbosacral anomaly.
Urethral obstruction can be congenital (as with posterior urethral valves, congenital stricture, or urethral diverticula) or acquired (as with a traumatic or infectious stricture or with meatal stenosis after circumcision). Traumatic strictures may develop after a traumatic urethral catheterization, a foreign body in the urethra, or pelvic trauma. Infectious strictures are a complication of purulent urethritis due to bacteria such as Neisseria gonorrhoeae.
Meatal stenosis is a common cause of distal urethral obstruction in circumcised males, but it is not considered a cause of enuresis.
SE may be a symptom of an unobserved overnight major motor convulsion in a child with a known seizure disorder. New-onset seizures rarely occur only at night; consequently, bedwetting is a rare manifestation.
Ectopic ureter is due to the insertion of the ureter in a location other than the lateral angle of the bladder trigone. The most common site of the ectopic orifice is adjacent to the external urethral meatus and is below the external sphincter in females. Children with ectopic ureter tend to wet constantly. Enuresis results when the insertion is distal to the external urethral sphincter. Ectopic ureter is three to four times more common in girls than in boys and causes incontinence only in females.
Enuresis usually is not the presenting complaint in a child with new-onset diabetes mellitus. Conventional symptoms of insulin deficiency usually overshadow the presence of bedwetting.
SE in a child with established diabetes mellitus may be a symptom of suboptimal control, with nocturnal polyuria due to hyperglycemia. Although nocturnal polyuria is presumed to be the cause of the bedwetting, a disorder of arousal is also likely to be present because most school-aged patients develop nocturia but maintain a dry bed. Diabetes mellitus is also associated with abnormalities in the afferent sensory pathways to the bladder, which may contribute to enuresis.
Diabetes insipidus is a very rare cause of enuresis. Although nocturnal polyuria is often presumed to be the cause of bedwetting, a disorder of arousal may also be present. Diabetes insipidus may be either central or nephrogenic. Central diabetes insipidus may result from an intracranial tumor, head trauma, encephalitis, or meningitis; nephrogenic diabetes insipidus may result from any cause of renal failure, diffuse renal cortical or medullary damage, hypokalemia, hypercalcemia, or nephrotoxic drugs.
United States and international statistics
In the United States, the prevalence of PE varies by age. At age 4 years, 25% of children frequently wet the bed, but by age 7 years, only 5-10% still wet the bed, and by age 10 years, fewer than 5% of children do so.
The resolution rate of PE is approximately 15% per year; by the late teenaged years, very few patients have the condition. This high resolution rate is often used as a justification for waiting and not treating PE. However, it probably is not applicable to children who wet every night and likely applies only to those children who have already started to have dry nights.
Worldwide, the prevalence of PE seems to be approximately the same, though no standardized evaluation of the prevalence of bedwetting has been made on a global basis.
Age-, sex-, and race-related demographics
The prevalence of enuresis gradually declines during childhood. Of children aged 5 years, 23% have enuresis. During elementary school years, 10% of 7-year-old children and 4% of 10-year-old children still experience enuresis. In adults, however, the reported prevalence of enuresis is 0.5-2%. A Korean epidemiologic study found that the overall prevalence of nocturnal enuresis in subjects aged 16-40 years was 2.6%. 
When PE and SE are reported, a secondary onset accounts for about 25% of cases. The prevalence of SE as a percentage of all cases increases with age. In a cohort of New Zealand children, 7.9% developed SE by the age of 10 years. 
Enuresis is more common in males. The reported prevalences of enuresis at the ages of 7 and 10 years are 9% and 7%, respectively, in boys and 6% and 3%, respectively, in girls. No racial predisposition has been documented.
Mortality attributable directly to enuresis has not been reported, but children with enuresis have been fatally abused by parents and other caregivers, and bedwetting was considered a “trigger” for the abuse in some situations. The morbidity, in terms of psychosocial stress, has been recognized in the psychology literature.  Enuresis can also be associated with significant family stress. Punishment should be considered a potential morbid consequence of enuresis.
Severe perineal, genital, and lower abdominal rash may also occur in patients with enuresis, potentially leading to skin breakdown and, rarely, cutaneous infections.
Relapse of the enuresis is the most common complication and requires restarting the treatment that resulted in an improvement or cure of the condition.
The most important reason to treat enuresis is to improve the loss of self-esteem and other secondary psychological or behavioral problems resulting from this behavior. Improvement in self-esteem is noted with all therapies, reaching levels comparable to those in children without enuresis after only 6 months of treatment.
Even without treatment, the reported spontaneous cure rate is reportedly about 15% per year. However, children who wet every night are unlikely to become dry in the short term and many of these children continue to wet until adolescence.
When enuresis is the sole symptom, behavioral therapy or a bedwetting alarm can be curative. The only therapies that have been shown to be effective in randomized trials include alarm therapy and treatment with desmopressin and imipramine.
A Cochrane review of alarm therapy concluded that alarm therapy is beneficial; about two thirds of children on alarm therapy were dry.  A Cochrane review of desmopressin therapy concluded that it reduces bedwetting; treated children had an average of 1.3 fewer wet nights per week than those receiving a placebo.  A Cochrane review of imipramine therapy concluded that imipramine reduces bedwetting; treated children had an average of 1 fewer wet nights per week those receiving a placebo. 
When daytime symptoms are also present, the prognosis depends on the underlying cause. The prognosis is excellent when enuresis is due to cystitis, ectopic ureter, OSA, diabetes mellitus, diabetes insipidus, or seizure disorder. Enuresis due to cystitis should resolve with appropriate antibiotic therapy; ectopic ureter and OSA respond to specific surgical interventions; and diabetes mellitus and diabetes insipidus respond to specific medical interventions.
Enuresis due to overactive bladder or dysfunctional voiding usually resolves, but daytime symptoms continue after puberty and into adulthood in as many as 20% of patients. The prognosis for enuresis due to neurogenic bladder depends on the neurologic cause and on whether a surgical solution is available.
Punishment has no role in the treatment of enuresis. The impact of enuresis on the child’s self-esteem and emotional health of the child is already sizable enough without the added insult of punishment for a problem beyond the child’s control.
Punishment is not always overt and intentional; it can be subtle and unrecognized by an otherwise well-meaning parent. A child easily interprets fluid restriction and requests to wear diaper training pants or to launder sheets and clothes as punishment. Accordingly, parents benefit from education regarding how to present such requests sensitively so as to minimize any sense of being punished on the part of the child.
For patient education resources, see the Children’s Health Center and the Kidneys and Urinary System Center, as well as Bedwetting, Bladder Control Problems, and Understanding Bladder Control Medications.
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