Enuresis is defined as the involuntary passage of urine, usually during sleep, occurring more than once a month. Although often considered a childhood problem, enuresis is also found in adolescents, causing major emotional problems and family stress. Current urology literature uses the following terminology regarding enuresis:
- Primary nocturnal enuresis: Nighttime wetting without prior periods of dryness.
- Secondary nocturnal enuresis: Nighttime wetting that occurs in patients who have a history of 6 months of dryness.
- Monosymptomatic nocturnal enuresis (MNE): Isolated nocturnal enuresis. No daytime symptoms and no other symptoms suggestive of problems or abnormalities of the urogenital tract.
- Diurnal enuresis: Involuntary or intentional urination into clothing while awake.
- Polysymptomatic nocturnal enuresis (PNE): Nighttime wetting associated with other bladder symptoms such as urgency, frequency, instability, or voiding dysfunction.
- Dysfunctional voiding: Nocturnal enuresis with daytime symptoms, which can range from urgency and frequency, to daytime incontinence. This is also known as complexorcomplicated enuresis. Diurnal enuresis is linked with dysfunctional voiding.
- Dysfunctional elimination syndrome: Nocturnal enuresis with urinary and bowel symptoms.
Etiology of Monosymptomatic Nocturnal Enuresis
Most cases of MNE are related to nonorganic causes. The causes may be multifactorial, with maturational delay as an important etiology.
Only 2% to 3% of patients have a true organic cause. Five percent to 10% of the enuresis cases are associated with urgency (polysymptomatic enuresis).
- Neurological lesions
- Myelomeningocele, the most common neurological cause of enuresis
- Mental retardation
- Spinal cord injury
- Urological abnormalities: Controversy exists over the role and prevalence of urological lesions in enuresis. The prevalence of urological abnormalities in enuretic patients ranges from 2% to 97% in different studies. Described problems include the following:
- Recurrent urinary tract infections (UTIs)
- Obstructive lesions: Urethral obstruction or posterior urethral valves
- Detrusor instability: Khan et al. (1993) found that the mean threshold volume at which detrusor instability was demonstrated was 200 mL in enuretic patients. The mean bladder capacity of age-matched nonenuretic patients was 325 mL.
- Incomplete bladder emptying: The common symptom of incomplete bladder emptying is urinary frequency. Common causes of incomplete bladder emptying are lower urinary tract obstruction, neurogenic bladder, and dysfunctional voiding. Adolescents who voluntarily withhold urination during the day and only impartially void at bedtime suffer from dysfunctional voiding. These patients are prone to develop reflux and renal damage.
- Renal concentrating defects (e.g., sickle cell anemia)
- Diabetes mellitus and diabetes insipidus: Chronic polyuria is associated with diabetes insipidus and diabetes mellitus. Alcohol, caffeine, and some medications can cause a transient polyuria.
The evidence for genetic transmission explains the common occurrence of a positive family history in enuretic patients. The prevalence of enuresis in families is as follows:
Twin studies not only provide evidence that there is a genetic etiology to enuresis but they also show that the genetics of enuresis is modulated by environmental factors.
The prevalence in an identical twin of an enuretic twin ranges from 43% to 68%. Prevalence in a fraternal twin of an enuretic twin ranges from 19% to 36%. Genetic studies have shown that the most common mode of inheritance is autosomal dominant with high penetrance. Autosomal dominant inheritance with low penetrance is the next common mode of inheritance, followed by autosomal recessive inheritance. One third of cases appear to be due to sporadic occurrence. Arnell et al. (1997) revealed evidence of sex-linked or sexinfluenced factors, which would account for the ratio of affected males to females of 3:1. Possible gene loci that have been identified include 13q, 8q, 12q, and 22q.11.
Enuresis may be associated with incomplete sudden arousal from a deep sleep. In these cases, there is difficulty in arousing the patient. Parents of affected teens often report that their child sleeps too soundly or deeply. Often, the adolescent fails to awaken due to the sensation of a full bladder or even when the bedding becomes wet. However, some studies have demonstrated that enuretic patients are normal sleepers. Sleep studies have shown that sleep patterns are similar between patients with enuresis and those without. Enuretic episodes can occur at random throughout the night and can occur in all stages of sleep, but enuresis primarily occurs during nonrapid eye movement (non-REM) sleep (which occurs in the early part of the sleep cycle).
It has been postulated that a developmental delay in adequate neuromuscular maturation of the bladder, as well as an immaturity of the central nervous system inhibition of the micturition reflex, is responsible for enuresis. Further evidence for maturational delay is the fact that enuretic patients become dry with time, whether or not there is a therapeutic intervention.
Small Functional Bladder Capacity
The current thinking among enuresis experts is that affected teens either produce large nighttime volumes of urine with a normal bladder capacity or produce a large nighttime volume with a small bladder capacity. Symptoms of a small bladder capacity include daytime frequency, wetness every night, occasional wetness several times per night, and the presence of the problem since birth.
Most enuretic patients are psychologically normal and psychological stressors do not cause enuresis. It is important to remember that the teen is not deliberately wetting the bed. An increased prevalence of emotional difficulties, including poor self-esteem, family stress, and family isolation, has been described in affected adolescents. However, this may often be a result of suffering from enuresis, rather than a causative factor.
Normally, vasopressin levels rise during the night, resulting in a smaller volume of more concentrated urine at night. Although first postulated in 1985 that MNE is due to nocturnal polyuria with relative nocturnal deficiency of antidiuretic hormone (ADH), more recent studies have questioned this theory with 25% to 100% of adolescents having a lack of nocturnal rise in ADH. This wide variability suggests the presence of other etiological factors.
Another theory postulates that as children approach adolescence, a faulty circadian rhythm of arginine vasopressin (AVP) secretion may be the paramount pathogenetic factor.
When adolescents with MNE were compared to normal children, a 3% to 5% incidence of uninhibited bladder activity was found in both populations. However, if a patient has refractory primary MNE, bladder dysfunction should be considered.
Etiology of Diurnal Enuresis
Primary Diurnal Enuresis
- Neurogenic bladder: Myelomeningocele is the most common neurological cause of enuresis. Other causes of a neurogenic bladder include cerebral palsy, sacral agenesis, transverse myelitis, spina bifida, and spinal cord trauma.
- Congenital urethral obstruction: Characterized by a weak or interrupted urinary stream and the patient may need to push to initiate urination.
- Ectopic ureter: Patients complain of constant wetness or dampness.
- Congenital diabetes insipidus
Secondary Diurnal Enuresis
- Constipation: It has been postulated that the pressure effect of stool in the descending or sigmoid colon triggers uninhibited contraction of the detrusor muscle, resulting in enuresis.
- UTIs: Enuresis due to UTIs is most commonly seen in preschool children, but can affect girls of any age.
- Giggle incontinence: Giggling or laughter results in complete involuntary emptying of the bladder. It can develop in up to 8% of girls. It is seen most commonly in school-aged girls and can be familia Although it tends to improve with age, it can persist into adulthood.
- Stress incontinence: This occurs in situations associated with increased intraabdominal pressure. If the bladder outlet and proximal urethra fail to compensate for the increased pressure, then wetting occurs. It can occur with jumping, running, and high-impact landing, which is why it is seen more frequently in athletic adolescents. It can be managed by bladder emptying before exercising.
- Emotional stress: An isolated episode of stress can result in wetting, as can prolonged stress, such as with child abuse.
- Hinman syndrome: The bladder behaves like a neuropathic bladder, although there are no neurological deficits. Boys are affected more commonly and it is an acquired behavior, usually during toilet training. There is inappropriate voluntary contraction of the striated urinary sphincter during the process of micturition. This results in a functional urinary obstruction that eventually causes UTIs, myogenic bladder failure, hydronephrosis, and renal insufficiency.
- Traumatic or infectious urethral obstruction: Traumatic strictures of the urethra can occur after traumatic urethral catheterization, presence of a foreign body in the urethra, or pelvic trauma. Infectious strictures can result from purulent urethritis due to bacteria such as Neisseria gonorrhoeae.
- Diabetes mellitus
- Acquired diabetes insipidus
- Myogenic detrusor failure: Seen commonly in neurogenic bladders and in patients with posterior urethral valves. It develops over time, so it is usually not recognized until early adolescence. Affected teens suffer from residual urine in the bladder, which makes them prone to UTIs. As there is a hyperreflexic state of the detrusor, hydronephrosis develops before decompensation.
- Prevalence: Decreasing prevalence occurs with increasing age.
- Age 4: 30%
- Age 5: 14% to 20%
- Age 6: 10%
- Age 10: 5% to 10%
- Age 12: 3%
- Age 15: 2%
- Age 18: 1% to 2%
- Army recruits: 0.1% to 2.5% (according to studies of this group)
- Sex: Male to female ratio is 3:2.
- Race: More African-American teens are affected than white teens.
- Timing: Eighty percent to 85% of teens have nocturnal enuresis only, whereas 15% to 20% of teens have nocturnal and daytime enuresis. Eighty percent of adolescents have primary MNE and 20% have secondary MNE.
A thorough history, a focused physical examination, and simple laboratory tests are all that are usually needed to evaluate enuresis, because significant organic lesions are infrequent. The prevalence of organic lesions is higher in adolescents than children. The prevalence of a psychological or organic cause is higher in secondary and daytime enuresis.
The history should include the following:
- Severity of enuresis: How many dry nights per month, most consecutive dry nights, frequency of urination, urgency of urination, evening fluid intake, and whether the bladder is emptied at bedtime.
- Type of enuresis: Primary or secondary, polysymptomatic or monosymptomatic.
- Symptoms of organic disease: Dysuria, intermittent daytime wetness, polydipsia, central nervous system trauma, constipation, or encopresis can indicate an organic disease. Patients with ectopic ureter will complain of constant wetness or dampness. Spinal tumors cause a change in gait, constipation, or encopresis.
- History of UTIs
- Toilet-training history
- Family history of enuresis or small bladders
- Awakening to use toilet at night: Self-awakens to full bladder, self-awakens to wetness, never awakens spontaneously, awakened by parent, evidence of deep sleep, sleepwalking.
- Prior therapeutic modalities and results
- Functional bladder capacity measurement
- Adolescent's and family's adjustment to the problem
- Family member responsible for changing sheets and laundry
- History of any sleep disorders, such as night terrors or unusually deep sleep
- General psychosocial review of family, peers, and school
- Timing of wetting: Adolescents who suffer from vaginal reflux of urine, labial fusion, or postvoid dribble syndrome wet after voiding. Other etiologies of enuresis cause wetting before voiding.
- Voiding history: Teens with urethral obstruction need to push to initiate or sustain voiding. The urinary stream is often weak, interrupted, or of narrow caliber. A history of dribbling or hesitancy suggests posterior urethral valves.
- Urgency of urination: The common causes of urgency of urination are UTIs, bacteria without dysuria (which can irritate bladder mucosa and cause urinary urgency), or constipation. Rare causes include a bladder calculus, a bladder foreign body, and hypercalciuria.
- Check blood pressure.
- Abdomen: Check for masses.
- Genitourinary tract: Check the urethral meatus for evidence of stenosis. Observe the urinary stream to see whether it is full and forceful or narrow and dribbling.
- Look for midline defects in the lumbosacral area, abnormalities of the gluteal fold, or abnormal tufts of hair.
- Perform a neurological examination including:
- Lower extremity: Motor and sensory
- Deep tendon reflexes
- Perineal sensation
- Rectal sphincter tone
- Bulbocavernosus reflex
- Urinalysis: Every patient should have a urinalysis. This simple, noninvasive test can screen for UTIs, diabetes mellitus, and diabetes insipidus (a specific gravity of
>1.015 g or a specific gravity >1.025 g after a 14-hour fluid restriction rules out diabetes insipidus). Look for the presence of glucose, protein, or white blood cells, and assess the specific gravity. Urethral obstruction can be associated with hematuria.
- Urine culture: Obtain a urine culture if the urinalysis suggests a UTI.
- Uroflowmetry: A noninvasive measure of urine flow rate. It can assist in screening for patients with neurogenic bladder and urethral obstruction. Patients void into a special toilet with a pressure-sensitive rotating disk at the base. A normal uroflow study shows a single bell-shaped curve with a normal peak and average flow velocity for age and size. Patients with urethral obstruction or neurogenic bladder have a prolonged curve or an interrupted series of curves and a low peak and average urine flow velocity.
- Bladder capacity: The teen and his or her family can measure their bladder capacity at home or in the office. The patient drinks 12 oz of water and then the volume of urine is measured when the patient needs to void. Although the formula, age in years plus 2, for calculating the bladder capacity applies to measuring children's bladder capacity, it does not apply to adolescents. Normal adult bladder capacity is 10 to 15 oz.
- Imaging studies: Radiological studies are not needed routinely. If a urethral obstruction or a neurogenic bladder is suspected, then a voiding cystourethrogram is indicated (the neurogenic bladder will appear as a trabeculated “Christmas tree” or “pine cone” configuration). If a neurogenic bladder is suspected and there is no obvious cause, then obtain a spinal magnetic resonance image to look for spinal cord abnormalities. Ultrasonography is indicated for patients with persistent daytime wetness or for patients with failure to empty the bladder (whether due to urge syndrome, urethral obstruction, or neurogenic bladder). A prevoiding and postvoiding bladder ultrasonography can be obtained to rule out partial emptying (normal residual bladder volume is lt;10 mL).
If a urological lesion is discovered, then referral to an urologist for appropriate management is recommended. If an occult spinal dysraphism is detected, then neurosurgical referral is warranted. As stated, most affected adolescents are without organic lesions. In most teens, the cause of enuresis is generally multifactorial and includes genetic predisposition, small bladder capacity, a sleep disorder, maturational delay, detrusor instability, nocturnal polyuria, or abnormal secretion of ADH. Because of the multifactorial causes of enuresis, treatment requires several months before improvement or resolution is achieved. The parents must be willing to participate and the family environment should be supportive. Both the parents and the teen need to understand that relapses can be expected and that short-term failure is possible. A goal-oriented therapeutic approach is more successful and the patient needs to be motivated to participate in treatment.
Therapy includes the following:
- Motivational counseling: Regardless of any other modalities chosen, motivational counseling is helpful. Studies indicate that counseling alone leads to a 25% to 70% remission rate. The relapse rate is 5%. If there is a lack of improvement after 3 to 6 months, other methods should be tried. Through motivational counseling, the teen learns to assume responsibility and become an active participant in the management program. In such a program, the practitioner does the following:
- Reassures the adolescent and family members that this problem is common to many teens. The parents and the teen should not feel guilty about “causing” the problem.
- Gives the adolescent an active role by putting him or her in charge of changing the sheets and placing them in the laundry machines. The parents should be encouraged to take a backseat position in dealing with the problem.
- Reduces secondary friction caused by enuresis.
- Gives positive reinforcement for dryness.
- Provides close initial follow-up with the practitioner.
- Self-awakening or parent-awakening programs: These programs work by training adolescents to recognize when their bladder is full, awakening, and walking to the bathroom. It is useful to inform the teens that they do not need to “hold” their urine all night.
- Self-awakening programs: This method can be taught in several ways. One technique is to have the teen lie in bed with eyes closed and pretend it is the middle of the night and his or her full bladder is trying to wake him. The teen then goes to the bathroom and empties her bladder. Another technique has the teen go to bed when he or she has the urge to urinate. The teen then pretends to sleep, “awakens,” and walks to the bathroom to urinate. A third technique has the teen use self-hypnosis at bedtime with the posthypnotic suggestion that the teen will wake up and use the bathroom during the night.
- Parent-awakening programs: If self-awakening is not effective, then parent awakening can be used. The parent awakens the patient, but the teen must locate the bathroom alone. It is recommended that the parent use the minimal prompt necessary to awaken the teen. Parents need to awaken their child at the parent's bedtime each night until the teen awakens quickly to sound for seven consecutive nights. At that point, the patient is either cured or ready for an enuresis alarm.
- Dry bed training: This is a more labor-intensive parent-awakening program. The teen needs to be awakened once an hour until 1 a.m. on the first night. When the teen is awake enough to speak coherently, the parent asks him or her if she needs to use the bathroom. The teen is praised if she is dry. If wet, the teen is encouraged to change the clothes and bedding. At 1 a.m., the teen is instructed to try voiding, even if dry. For the next five nights, the teen is awakened only once. The teen is awakened 3 hours after falling asleep the first night. The second night, the teen is awakened 2.5 hours after falling asleep. By the fifth night, the teen should be awakened 1 hour after falling asleep. On the sixth night, the teen is instructed to self-awaken from then on. If the teen relapses (defined as three consecutive wet nights), then repeat the six nights of awakening. One study found that the cure rate was 92% using this technique and that the relapse rate was 20% (with all patients who relapsed responding to a second trial of training).
- Alarm systems: Enuresis alarms have the highest cure rate of any available treatment for enuresis. Several
studies have shown comparable cure rates between medications and alarms in the short term. However, these same studies showed persistent effectiveness only with the alarm. The teen has the choice of either wearing an audio alarm or a tactile alarm. The alarms are comfortable, convenient, and inexpensive. The disadvantages to the alarm are that they are time intensive (they need to be used for 2 to 3 months and continued until 3 weeks after dryness has been achieved) and the teen and parent must be motivated to use them properly. By learning to awaken as quickly as possible to the alarm, the teen eventually learns to awaken to the internal stimulus of a full bladder.
- Types: Older alarms required elaborate pad-and-bell systems. Newer alarms are lightweight, easy to use, and relatively inexpensive ($40–$90). The alarms consist of two clips attached to the teen's underwear and connected to a wrist alarm or pajama collar alarm. The alarm buzzes if a small amount of wetness occurs on the underwear. Alarms are available from:
- If the teen's family cannot afford to buy an enuresis alarm, then a clock radio, alarm clock, or wristwatch alarm set for 3 hours after going to sleep can be used.
- Basis for using alarm: The alarm awakens the teen and usually leads to a contraction of the external bladder sphincter. In order for enuresis alarms to be effective, the teen needs to be able to awaken to touch or sound. Therefore, it is worthwhile to see whether the patient can respond to parent awakening or alarm clock awakening. Further, the teen must want to use the alarm. This technique is ineffective for teens indifferent to using the alarm. The alarm should be continued until 3 weeks after dryness has been achieved.
- Results: Long-term cure rates average 70%. Alarm failure rates range from 20% to 30%. Common reasons for alarm failure include the following:
- The parents discontinue the alarm too soon.
- The teen fails to hear the alarm because he or she is such a deep sleeper.
- The teen refuses to use the alarm.
- The teen refuses to try any technique.
- The teen suffers from polysymptomatic enuresis (may need oxybutynin in addition to an alarm).
- The teen wets during deep sleep when it is difficult to awaken the teen (combined treatment with drugs may be necessary; once the teen is dry on drugs, the alarm can be restarted and the drug tapered).
- Fluid restriction: Have the teen take 40% of their daily fluid intake in the morning hours (7 a.m.–12 noon), 40% in the afternoon (12 p.m.–5 p.m.), and only 20% in the evening (after 5 p.m.). Beverages consumed in the evening should be caffeine free.
- Other behavioral methods: Biofeedback and pelvic floor muscle retraining have been tried, with varying degrees of success. Bladder exercises have been used to increase bladder tone and size for patients (primarily children) with small bladder capacity. Hypnosis has been shown to be effective in curing enuresis in noncontrolled studies (Olness, 1979;Johnson, 1981). Hypnosis may be successful in treating enuretic patients who are highly motivated. The technique involves suggestions that the adolescent wake up when the urge to urinate occurs and go to the bathroom.
- Medications: No drug exists that is adequately safe and effective for curing enuresis. However, most pediatricians agree that intermittent use of drugs is appropriate for teens when needed for camping trips, school trips, vacations, or overnights. The major drugs available include the following:
- Desmopressin (DDAVP)
- Action: DDAVP is a synthetic analog of vasopressin. The mechanism of action of the drug is the reduction of urine production by increasing water retention and urine concentration in the distal tubules. Treatment of enuresis using DDAVP is based on the hypothesis that ADH secretion at night is insufficient.
- Dose: DDAVP is tasteless and odorless and can be administered either intranasally or orally. It is given in the late evening to reduce urine production during sleep. The medication comes as a nasal spray that delivers 10 µg per spray or as a graduated intranasal tube (Rhinal Tube) that delivers doses of 5, 10, 15, and 20 µg per spray. The usual initial dose is 20 µg, or one spray in each nostril, at bedtime. The dose can be increased by 10 µg weekly to a maximum dose of 40 µg. Some individuals may respond to a dose as low as 5 µg/day. The Rhinal Tube must be used if 5-µg doses are required. If the patient remains completely dry on a particular dose, then a dose of 10 µg less should be tried. The duration of action is 10 to 12 hours.
- Results: DDAVP was approved for the treatment of nocturnal enuresis at the end of 1989. The response to DDAVP improves with increasing age in patients with nocturnal enuresis. Therefore, the best results are seen in patients older than 10 years. A family history of nocturnal enuresis at ages older than 10 years and a normal bladder capacity are also predictors of a positive response to DDAVP. Seventy percent of patients with nocturnal enuresis who receive DDAVP stop their bed-wetting completely or reduce it significantly. A positive effect of the medication is seen within a few days and is maintained as long as the drug is administered. Most patients have a relapse after drug withdrawal, particularly if the drug is stopped abruptly (relapse rates can be as high as 50%–95%). Therefore, the drug should be tapered off slowly. Long-term treatment lasting at least 1 year is becoming more routine. Several long-term studies have found that 50% to 85% of patients on long-term treatment halved the number of wet nights and 40% to 70% became almost completely dry during treatment. The efficacy of DDAVP continued or improved throughout the treatment period, suggesting that patients did not develop tolerance to DDAVP. During long-term therapy, treatmentfree windows of approximately 3-month intervals are essential to avoid treating a child who has become dry.
- Side effects: Side effects are infrequent but can include symptomatic hyponatremia (limit fluid intake to 8 oz in the evening hours to avoid this adverse effect), headache, abdominal discomfort, nausea, nasal congestion, rhinitis, nosebleeds, abdominal cramps, and sore throats. These symptoms usually disappear with a reduction in the dose.
- Oral DDAVP: Stenberg and Lackgren (1993) found that oral DDAVP is as effective as intranasal DDAVP and as safe, with similar adverse effects (e.g., headache and abdominal pain). However, at least a tenfold increase in the DDAVP dose is required, compared with the intranasal dose. The initial dose is 0.2 mg (one tablet), given 1 hour before bedtime. If there is no response within a week, increase the dose by 0.2 mg up to a maximum of 0.6 mg nightly.
- Imipramine (Tofranil)
- Action: This drug combines an anticholinergic effect that increases bladder capacity with a noradrenergic effect that decreases bladder detrusor excitability. Imipramine is also thought to increase excretion of ADH from the posterior portion of the pituitary gland.
- Dose: Imipramine is taken 1 hour before bedtime. The duration of action is 8 to 12 hours. Start the patient at 50 mg/day and increase the dose weekly, as needed, to a maximum dose of 75 mg/day. A sustained-release form of imipramine, Tofranil-PM, is also available.
- Results: Response rate is 25% to 40%; relapse rate can be as high as 75%. The relapse rate is higher when the drug is stopped abruptly or prematurely. The maximal effect of imipramine usually occurs in the first week of therapy. However, one should continue therapy for 1 to 2 weeks before deciding on efficacy and whether to adjust the dose. The current recommendation is to treat for 3 to 9 months and then taper the drug by decreasing the dose by 25 mg decrements over 3 to 4 weeks. If the patient has a relapse, one can repeat a course of therapy. The drug is most beneficial for occasional use when dryness is necessary (e.g., trips, vacations, sleepover parties). Imipramine and DDAVP have been found to be equivalent in effectiveness (Glazener and Evans, 2000). An advantage of imipramine is that it is inexpensive ($5/month for generic formulations versus $150–250/month for DDAVP).
- Side effects: Nervousness, gastrointestinal distress, syncope, and anxiety can occur. Because of imipramine lethality when taken in overdose, both parents and teens need to be aware of its toxicity.
- Oxybutynin (Ditropan)
- Action: Oxybutynin provides an anticholinergic, antispasmodic effect that reduces uninhibited detrusor muscle contractions and increases bladder capacity. Therefore, it may be most beneficial for patients with small capacity bladders who also have daytime frequency or enuresis associated with uninhibited bladder contractions.
- Dosage: A sustained-release formulation of oxybutynin is available (10 mg/day), as well as a conventional formulation (5 mg twice daily). Birns et al. (2000) found that the effectiveness and side effect profile are comparable with either formulation.
- Results: A success rate of 90% was reported in one study of individuals with daytime enuresis, bladder instability, or both. The drug is rarely helpful in treating patients with MNE. It is to be used in teens with PNE, urge syndrome, or neurogenic bladder.
- Side effects: Dry mouth, flushing, drowsiness, and constipation.
- Combined drug therapy with enuresis alarms: Combining drugs with an alarm is very effective in the treatment of enuresis. Glazener and Evans (2000) found that combining drugs with alarms is more effective than using alarms alone. Teens who have frequent enuresis are candidates for this therapy. The drug can both prevent the necessity of awakening to use the bathroom and delay the filling of the bladder until early morning. The enuresis alarm is the backup system. After the adolescent is dry for 3 weeks, the drug is tapered gradually (if using DDAVP, decrease by one spray every 2 weeks; if using imipramine, decrease by 25 mg every 2 weeks).
Treatment Relapses and Failures
Treatment relapse is defined as the recurrence of enuresis after having been dry for at least 1 month. The remedy is to reinstitute the treatment that was effective previously. Treatment failure occurs when the patient cannot remain dry despite using the alarm or combined therapy. For adolescents, the best approach is to put the teen in charge of solving the problem and emphasize that he or she will become dry once she learns to self-awaken.
Reported spontaneous cure rates (Forsythe and Redmond, 1974) are as follows:
- Ages 5 to 9: 14%/yr
- Ages 10 to 14: 16%/yr
- Ages 15 to 19: 16%/yr
- After age 20: 3%/yr
For Teenagers and Parents
http://www.kidney.org/patients/bw/. The National Kidney Foundation's Web site. This link connects to the patient section of the Web site, where information is provided on enuresis in children, teens, and young adults.
http://www.childrensmemorial.org/depts/urology/enuresis.asp. Children's Memorial Hospital of Chicago's enuresis Web site. It provides good information for parents and teens on enuresis, medications, recommended readings, and related web links.
http://www.eric.org.uk/. A Web site based in the United Kingdom. It provides good information on the etiology, epidemiology, and treatment of enuresis.
http://www.parenthood.com/articles.html?article_id=5351. A Web site aimed at parents. It provides links to pertinent Web sites about enuresis with a helpful rating system of the Web sites.
http://www.parenthood.com/articles.html?article_id=5351. The Web site of the International Children's Continence Society. It offers a free membership area with relevant research articles pertinent to the field of enuresis, offers a message board, and offers links to support groups and recommended readings.
References and Additional Readings
Arnell H, Hjalmas K, Jagervall M, et al. The genetics of primary nocturnal enuresis: inheritance and suggestion of a second major gene on chromosome 12q. J Med Genet1997;34:360.
Austin PF, Ritchey ML. Dysfunctional voiding. Pedr Rev 2000;21(10):336.
Banerjee S, Srivastav A, Palan BM. Hypnosis and self-hypnosis in the management of nocturnal enuresis: a comparative study with imipramine therapy. Am J Clin Hypn1993;36:113.
Birns J, Lukkari E, Malone-Lee JG. Oxybutynin CR Clinical Trial Group. A randomized controlled trial comparing the efficacy of controlled-release oxybutynin tablets (10 mg once daily) with conventional oxybutynin tablets (5 mg twice daily) in patients whose symptoms were stabilized on 5 mg twice daily of oxybutynin. BJU Int 2000;85:793.
Bloom D. The American experience with desmopressin. Clin Pediatr 1993;July (Spec No):28.
Derman O, Kanbur NO, Kinik E. The evaluation of desmopressin in treatment of adolescent nocturnal enuresis. Int J Adolesc Med Health 2004;16:377.
Devitt H, Holland P, Butler R, et al. Plasma vasopressin and response to treatment in primary nocturnal enuresis. Arch Dis Child 1999;80:448.
Eggert P, Kuhn B. Antidiuretic hormone regulation in patients with primary nocturnal enuresis. Arch Dis Child 1995;73:508.
Forsythe WI, Redmond A. Enuresis and spontaneous cure rate. Arch Dis Child 1974;49:259.
Fritz GK, Rockney RM, Yeung AS. Plasma levels and efficacy of imipramine treatment for enuresis. J Am Acad Child Adolesc Psychiatry 1994;33:60.
Glazener C, Evans J. Desmopressin for nocturnal enuresis in children. Cochrane Database Syst Rev 2000;2:CD002112.
Gonzales ET. Approach to the child with nocturnal enuresis and management of nocturnal enuresis in children. Up To Date 2005.
Hogg RJ, Husmann D. The role of family history in predicting response to desmopressin in nocturnal enuresis. J Urol 1993;150:444.
Janknegt R, Zweers H, Delaere K, et al. Oral desmopressin as a new treatment modality for primary nocturnal enuresis in adolescents and adults: a double-blind, randomized, multicenter study. J Urol 1997;157:513.
Johnson RL. Use of hypnosis with enuretic adolescents. J Curr Adolesc Med 1981;2:39.
Key DW, Bloom DA, Sanvordenker J. Low-dose DDAVP in nocturnal enuresis. Clin Pediatr 1992;31:299.
Khan Z, Starer P, Singh VK, et al. Role of detrusor instability in primary enuresis. Urology 1993;41:189.
Kodman-Jones C, Hawkins L, Schulman SL. Behavioral characteristics of children with daytime wetting. J Urol 2001;166:2392.
Lawless M, McElderry D. Nocturnal enuresis: current concepts. Pedr Rev 2001;22(12):399.
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