Download Voiding Dysfunction

Voiding Dysfunction
Synonyms and related keywords: detrusor instability, functional voiding
disorder, infantile bladder, nonneurogenic neurogenic bladder, non-neurogenic
neurogenic bladder, occult neuropathic bladder, unstable urinary bladder, urge
incontinence, urge syndrome, Hinman syndrome, patter-of-little-feet syndrome,
Author: Stanley Hellerstein, MD, Pediatric Nephrologist, Children's Mercy
Hospital of Kansas City; Ernest L Glasscock, MD, Chair in Pediatric Research,
Professor of Pediatrics, University of Missouri School of Medicine at Kansas
City
RESUMEN:
Antecedentes: El síndrome miccional, con urgencia, frecuencia, vacilación, goteo de orina
y sobre todo incontinencia, reflejan alteraciones en la función de la vejiga urinaria. La
patogénesis de los trastornos miccionales se entiende mejor cuando se ve como
desviacion del ciclo miccional normal.
La capacidad de la vejiga aumenta con el crecimiento. La mayoría de los niños de 1-2
años comienzan a percibir la vejiga llena y desarrollar la capacidad de anular o inhibir la
micción, mientras están despiertos. Los niños de 3-5 años han aumentado la sensación
de vejiga llena y desarrollan la capacidad de anular o inhibir la micción hasta que el niño
decide en que momento y el lugar para orinar. Durante este período, se produce la
adquisición de control cortical de la micción. Disfunción miccional no se diagnostica
habitualmente en el niño normal antes de la conseguir el control urinario durante el día.
Este artículo se centra en trastornos miccionales en niños que no tienen anomalías
neurológicas ni obstrucción anatómica del tracto urinario. La enuresis nocturna aislada,
que puede ser considerado como un tipo de trastorno de la micción, no se considera
aquí.
Pathophysiology: The micturition cycle involves 2 discrete processes: bladder filling and storage
of urine and bladder emptying. These functions are opposing and normally alternating. Muscular
activities of the bladder that result in storage and expulsion of urine are under control of the
somatic and autonomic nervous systems.
During the filling phase of micturition, regulatory influence of the sympathetic nervous system
allows the bladder to expand at low pressure with increasing outlet resistance. Urine storage is a
coordinated response of the sympathetic system–mediated inhibition of detrusor contractile activity
accompanied by increased muscular tension of the bladder neck and proximal urethra. The primary
neurohumoral transmitter for sympathetic activity is norepinephrine; therefore, drugs with
adrenergic activity (eg, ephedrine) facilitate the storage of urine.
Expulsion of urine normally occurs as a result of simultaneous contraction of the detrusor and
relaxation of the bladder outlet. This is mediated by the parasympathetic nervous system, in which
the primary neurohumoral transmitter is acetylcholine. Cholinergic agents, such as bethanechol,
stimulate bladder emptying. During bladder filling, afferent impulses are transmitted to sensory
neurons in the dorsal root ganglia of sacral spinal segments 2-4 and convey information to the
brainstem. Nerve impulses from the brainstem inhibit parasympathetic outflow from the sacral
spinal micturition center. During the voiding phase, inhibition of the sacral parasympathetic
outflow is removed, and detrusor contraction occurs.
Inhibition of sympathetic outflow to the bladder results in relaxation of the trigonal and proximal
urethral muscles. Impulses traveling along the pudendal nerve act to relax the smooth and skeletal
muscle of the external sphincter. The result is expulsion of urine with minimal outlet resistance.
CNS control over the lower urinary tract coordinates the micturition cycle. Normal development is
characterized by increasing awareness of bladder distension and acquisition of the ability to inhibit
voiding at any level of bladder fullness. Voiding symptoms in the neurologically and anatomically
intact child, who has neither a urinary tract infection (UTI) nor local urethral irritation, is a result of
functional disturbance of the normal micturition cycle.
Frequency:
 In the US: A study of children aged 5-9 years (n = 583) showed that urinary urgency and
pelvic-tightening maneuvers to postpone voiding and prevent leakage were the most
common voiding problems. Urge incontinence was reported in 7% of girls and 3% of boys.
Another study demonstrated that daytime wetting varies by age and sex. The prevalence of
daytime wetting with a frequency of at least once every 2 weeks was 10% in children aged
5-6 years, 5% in children aged 6-12 years, and 4% in children aged 12-18 years.
 Internationally: Studies from the United States and Sweden have addressed the frequency
of voiding disorders in school-aged children. A Swedish study of 7-year-old students (n =
3556) showed that 21% of girls and 18% of boys had moderate-to-severe urinary urgency.
Daytime urinary incontinence occurred at least once weekly in 3.1% of girls and 2.1% of
boys.
Mortality/Morbidity:
 Functional voiding disorders do not cause death.
 A child with a voiding disorder may have few symptoms or almost continuous urinary tract
problems. The child who voids infrequently but who does not have UTIs or urinary
incontinence may not be recognized as having a voiding disorder. In contrast, some children
with functional voiding disorders have ongoing urge incontinence, urinary dribbling, or
recurrent UTIs. These children may experience severe social and emotional problems
because of the voiding disorder.
 A few children with a functional voiding disorder, ie, nonneurogenic neurogenic bladder
(Hinman syndrome), have marked voiding dysfunction and may incur significant renal
damage.
Race: No known studies have shown the incidence of voiding disorders related to race. Clinical
experience indicates no racial predilection.
Sex:
 Studies on the prevalence of voiding disorders in school children indicate that daytime
urinary incontinence occurs more frequently in girls (6-7%) than in boys (3%).
 In the authors' voiding dysfunction clinic, girls accounted for 72.6% of children with a
functional voiding disorder over a 2-year period.
Age: A functional voiding disorder in a neurologically and anatomically healthy child is not usually
recognized before the acquisition of daytime urinary control.
Many children have a transient period of urinary urgency, occasionally with wetting, when daytime
continence is first being achieved.
 Most of these children develop normal urinary control in a relatively short period; however,
some children may have persistence of urinary urgency and wetting, and they subsequently
develop additional symptoms of a functional voiding disorder.
 Other children may have a normal voiding pattern until a UTI or an emotionally traumatic
event triggers the onset of a voiding disorder.
 Approximately 50% of children have symptoms of voiding dysfunction when daytime
urinary control is first accomplished.
History:
 Voiding symptoms, such as urgency, frequency, and incontinence may be transient,
intermittent, or persistent.
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Transient voiding symptoms are commonly encountered as a result of nonspecific urethritis
or periurethral irritation due to vaginitis or a UTI, or they may occur without a recognized
explanation.
Symptoms caused by local factors usually clear after the irritant is removed and the local
inflammation subsides. Local factors include the following:
 Detergents in bubble bath or shampoo, which may remove protective secretions
from the urethral mucosa
 Mechanical and chemical irritation from urine-soaked underclothes
 Local trauma due to tight undergarments
 Pinworm infestation
Hypercalciuria usually causes hematuria, along with dysuria and urinary urgency, but it may
also cause voiding symptoms with scant hematuria.
Extraordinary daytime urinary frequency (patter-of-little-feet syndrome) has the following
characteristics:
 This disorder occurs in a toilet-trained child of preschool or elementary school age.
 It is characterized by the sudden onset of painless urinary frequency.
 Urinary urgency may occur as often as every 5 minutes, though, in most children, it
occurs 3-4 times per hour. In some, urinary frequency is most marked in the
morning or afternoon. Urinary frequency does not occur at night.
 In most instances, incontinence is not present. Nocturnal enuresis, if present, is
unchanged or mildly increased.
 Children with this condition do not have a UTI, hypercalciuria, or other known local
or systemic disorder that accounts for the urinary frequency.
 A key diagnostic feature is that urinary frequency occurs during the day, with not
significant change in the nighttime voiding pattern.
 The etiology is unknown.
Asymptomatic daytime urinary incontinence in a child with daytime urinary control
 Many children aged 3-5 years tend to delay urination because of intense
concentration on playing or watching television. As a result, they occasionally have
damp or soaked clothing. If the voiding pattern is otherwise normal, this pattern of
voiding dysfunction usually subsides without intervention.
 Occasionally, an older child who has had a normal daytime voiding pattern for
months or years may inexplicably develop asymptomatic daytime incontinence.
 Rule out UTI.
 Daytime urinary incontinence usually clears within a few days to 2 weeks without
intervention.
Other factors may result in daytime dampness or wetting.
 Vaginal reflux of urine may cause dampness when the child assumes an upright
posture after voiding. This is particularly likely in an obese girl in whom the labia do
not open widely during urination because of the thickness of her thighs. The
diagnosis may be confirmed by having the child void in a reverse sitting position
while embracing the toilet tank or its equivalent or by have the child widely extend
his or her thighs while voiding in the usual position.
 Interlabial adhesions of the labia minora may cause daytime wetting due to the
pooling of urine in the vagina. Treatment of the labial adhesions eliminates this
cause of urinary incontinence.
 Persistent but otherwise asymptomatic daytime urinary incontinence with dribbling
or overt wetting may have an underlying neurologic, anatomic, or functional basis.
Daytime wetting is considered a problem in the developmentally normal child aged
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4 years or older who is wet several days each week and in the previously continent
child who develops daytime wetting.
 If dribbling and ongoing wetting have been present lifelong, an ectopic ureter should
be ruled out by using imaging studies such as a CT or an intravenous pyelography
(IVP).
 The diagnoses of detrusor instability or a neurogenic bladder are usually evident
from the patient's history, but results of voiding cystourethrography (VCUG) may
suggest the condition. In some instances, urodynamic study may be needed to define
the cause of relatively asymptomatic daytime incontinence.
 Asymptomatic daytime wetting, as well as symptomatic daytime urinary
incontinence, in a previously continent child suggests the possibility of sexual abuse
or other trauma.
Giggle incontinence
 This is the occurrence of involuntary complete bladder evacuation induced by
laughter.
 This typically appears in children aged 5-7 years. It persists throughout the school
years and usually improves or disappears with age. The voiding pattern is otherwise
normal.
 Episodes of incontinence may occur with giggling in some children; in others, they
are induced by only vigorous laughter.
 The etiology is unknown. Giggle incontinence is not a form of stress incontinence,
nor is it due to weakness of the sphincter.
 The authors of 1 study found a high incidence of daytime voiding symptoms in
patients in whom they diagnosed giggle incontinence. The authors concluded that
laughter induced unstable detrusor contractions in children susceptible to detrusor
instability.
Detrusor instability
 This is the cause of urge syndrome and urge incontinence in children who do not
have a UTI. It is the result of overactive detrusor contractions during the filling
phase of micturition.
 Voiding symptoms result from detrusor contractions during bladder filling. During
voiding, outlet relaxation and normal bladder emptying occur.
 This voiding disorder often occurs in children with recurrent UTIs and is a risk
factor for UTI for which effective intervention is possible. The children are
commonly seen because of 1 or more UTI or daytime urinary incontinence.
 A careful history usually reveals that the child has had ongoing urinary urgency with
various posturing maneuvers in an attempt to prevent incontinence.
 Urinary urgency and risk of urge incontinence occur during bladder filling because
of uninhibited detrusor contractions. This appears to result from a lack of inhibitory
cerebral control over reflex detrusor contractions during bladder filling. The
problem may have been present since daytime urinary control began developing, or
it may appear in a child who previously had a normal voiding pattern.
 The appearance of detrusor instability in a child who previously had daytime urinary
control may occur after a UTI or it may appear with no apparent triggering event.
 Children with urge syndrome and urge incontinence who do not attempt to prevent
wetting by posturing maneuvers that compress the urethra are probably not at
increased risk for UTIs. Those who use posturing maneuvers are at risk for UTI
because of “milking back” of bacteria-laden urine from the distal urethra into the
urinary bladder (urethrovesical reflux).
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Obstruction of the urethra during a detrusor contraction causes high intravesical
pressure. Increased intravesical pressure has been shown to contribute to persistence
of vesicoureteric reflux (VUR) and to the recurrence of VUR after ureteral
reimplantation.
 Stool retention is common in children with urinary urgency who use pelvic
withholding maneuvers to prevent incontinence. When chronic constipation has
been present in a child with a voiding disorder, it may be the primary cause of
bladder dysfunction. More commonly, constipation is secondary to the use of
anticholinergic medication and/or contraction of the pelvic floor and urogenital
diaphragm to prevent incontinence.
 The urogenital diaphragmatic component of the external sphincter is primarily a
skeletal muscle, over which one has voluntary control. Contraction of this muscle
normally inhibits detrusor contractility, but it is also associated with contraction of
the anal sphincter.
Dysfunctional voiding
 This is caused by overactivity of the pelvic floor muscles during the voiding phase
of the micturition cycle. The syndromes due to dysfunctional voiding vary from
mild daytime frequency and post void dribbling to daytime and nighttime wetting,
urgency, urge incontinence, pelvic holding maneuvers, and UTIs. In the most severe
form, children with dysfunctional voiding resemble those with anatomic or
neurologic bladder outlet obstruction.
 Although the etiology is not known, it is thought to reflect a deviation in the normal
development of urinary control. Normal micturition consists of a sustained detrusor
contraction with concomitant relaxation of the bladder outlet and complete bladder
emptying at normal voiding pressures. As daytime urinary control is being
accomplished, many children have a transitional phase in which pelvic withholding
maneuvers are used to prevent incontinence. This is not necessarily abnormal;
contraction of the external urethral sphincter, which occurs with pelvic floor
musculature contraction, causes physiologic inhibition of a detrusor contraction.
 Most children eventually develop a pattern of coordinated voiding, with central
control over detrusor and bladder outlet contractions that make it unnecessary to
contract the external sphincter to prevent incontinence. A few children who have a
delay in establishing cerebral control over detrusor contractions continue to use
pelvic-tightening maneuvers. Over time, these maneuvers appear to become
involuntary.
 Some have suggested that this pattern of dysfunction of the muscles of the pelvic
floor is a consequence of overtraining of the urinary bladder.
 Children with this condition have ongoing symptoms of voiding dysfunction with
increased intravesical pressure on voiding, incomplete bladder emptying, UTIs,
persistent VUR, dilatation of the upper tract, and (sometimes) renal damage.
 Evaluation should include VCUG, urinary tract ultrasonography, urodynamic
studies, and (in some instances) MRI of the lumbosacral spine to rule out a
neurologic etiology. The appearance of the urinary bladder may be similar to that of
a patient with posterior urethral valves or a neurogenic bladder.
Lazy bladder syndrome
 This term describes the voiding disorder in children who void infrequently.
Infrequent voiding is diagnosed if a child voids 3 or fewer times in 24 hours or if a
child does not void for 12 hours.
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This voiding pattern may be a variant of normal. It is not clinically significant if
urgency with voiding, UTIs, and incontinence are absent.
 However, if identified, the voiding pattern should be treated with behavioral
modification of the child's voiding regimen.
 If symptoms are present, the pattern of infrequent voiding is clinically important.
The detrusor muscle may be hypocontractile; voiding may be accomplished by
increased intra-abdominal pressure as the driving force to expel urine. The diagnosis
may be confirmed by means of urodynamic study.
 Dysfunctional elimination syndrome
 Constipation and detrusor instability are so frequently associated that the term
dysfunctional elimination syndrome has been introduced in the literature.
 In many instances, constipation is the primary or contributing cause of a voiding
disorder; therefore, this should always be considered in the evaluation of a child
with symptoms of detrusor instability.
 Many people are reluctant to discuss their stooling history. In most instances, bowel
movements are considered a private matter. Often, neither the child nor the parent
appears to have accurate information about stooling frequency or character.
 The effects of constipation on bladder function are related to the retained fecal
material distending the rectosigmoid colon.
 Indicators of constipation include the following:
 Infrequent passage of stools
 Small hard stools or elongated wide-bore stools
 Palpable stool on abdominal examination
 Dilated rectal vault on digital examination
 Skid marks in the underwear (often interpreted as due to improper or careless
wiping)
 Encopresis
 Large quantities of stool in the colon, and especially the rectosigmoid area
on abdominal radiography
Physical:
 No notable positive findings are noted on physical examination of the child with a
functional voiding disorder.
 Perform careful physical examination to rule out a suprapubic mass or abnormality of the
lumbosacral area that suggests occult spinal dysraphism. The latter includes a sacral dimple
or tuft of hair, dermal vascular malformations, a small lipomeningocele, or absence of the
gluteal cleft with flattened buttocks (sacral agenesis).
 Carefully examine the genitalia to be certain they are normal. Look for labial adhesions in
girls and meatal stenosis in boys. In the young girl, the genitalia should be examined to rule
out sexual abuse.
 In most instances, the anus should be inspected, perianal sensation should be checked, and a
digital examination of the rectum should be performed. Normal anal sphincter tone suggests
normal neurologic input to the bladder.
Causes:
 Voiding dysfunction may be caused by uninhibited detrusor contractions (detrusor
instability), dysfunction of the pelvic floor musculature (dysfunctional voiding), or a
combination of these.
 Detrusor instability is evident during the filling phase of the micturition cycle.
 This reflects a detrusor contraction when an individual who has (or should have)
urinary control should be able to inhibit micturition.
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Detrusor instability is due to lack of central inhibition of cholinergic stimulating
nerve impulses from the sacral micturition center. (This pattern of voiding
dysfunction in a child with neurogenic bladder, such as occurs with myelodysplasia,
is called detrusor hyperreflexia.)
 Dysfunctional voiding occurs because of incomplete or total absence of relaxation of the
pelvic floor musculature during a detrusor contraction.
 Voluntary contraction of the pelvic floor musculature to prevent urinary
incontinence is not uncommon, nor necessarily abnormal, when a child is first
learning urinary control.
 When voluntary contraction of the pelvic floor musculature is regularly used to
prevent incontinence, this response may become involuntary and cause
dysfunctional voiding.
 Some have suggested that dysfunction of the pelvic floor musculature is a
consequence of overtraining of the urinary bladder. It may have its onset during the
acquisition of urinary control in early childhood, or it may develop later, often after
a UTI in which local irritation has caused dysuria and urgency. (This pattern of
voiding incoordination in a child with a neurogenic bladder is called detrusor
sphincter dyssynergia.)
Lab Studies:
 Urinalysis and quantitative urinary cultures may be performed to detect or rule out a UTI.
Imaging Studies:
 VCUG, radiography of the lumbosacral spine, contrast-enhanced CT, or MRI of the
lumbosacral spine is needed in select cases.
 If dribbling and ongoing wetting have been present lifelong, a neurogenic bladder or
anatomic anomaly (eg, ectopic ureter) must be ruled out. The best study for this evaluation
is contrast-enhanced CT, though IVP was commonly used in the past.
Procedures:
 If neither the patient's history nor VCUG provides an explanation for the voiding disorder,
urodynamic studies should be conducted to detect uninhibited detrusor contractions,
dysfunction of the pelvic floor muscles, or a hypotonic bladder.
Medical Care:
 Extraordinary daytime urinary frequency
 Reassure the parents and the child that no significant underlying pathology is present
and that the condition will spontaneously resolve.
 Resolution usually occurs after a few weeks, though some cases of urinary
frequency can persisted for many months.
 In a report of 46 children with the syndrome, symptoms lasted 2 weeks to 42
months. The average time of resolution after onset was 7.4 months for boys and 13.5
months for girls.
 Interventions are empiric and include avoidance of caffeine-containing foods and
beverages and carbonated drinks.
 In addition, encourage children to attempt to lengthen the periods between voids as
long as they can to do so without undue discomfort or risk of incontinence.
 Asymptomatic daytime urinary incontinence
 Wetting secondary to vaginal reflux may be resolved by having the girl pay close
attention to complete emptying of the vaginal vault on voiding. This is accomplished
by spreading the labia majora when she urinates. If this is unsuccessful, the child
may assume an upright position over the commode immediately after voiding to
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empty the vagina. Alternatively, the child may void in a reverse sitting position on
the commode, which causes the thighs to be abducted and the labia majora to
separate.
 Labial adhesions have been attributed to local inflammation caused by less-thanoptimal genital hygiene in association with the hypoestrogenic state of a
preadolescent child. In many instances, lack of good genital hygiene does not appear
to play a role; however, local irritation caused by aggressive cleansing may. Use of a
warm-water sitz bath for 10-15 minutes 2-3 times a day may be the best way to
cleanse the vaginal area in an infant or young girl. Fecal contamination should be
wiped from the perineal area before the bath. Recommended treatment consists of
genital hygiene and application of a topical estrogen cream to only the fused area.
Elimination of the adhesions may take 2-8 weeks. After the adhesions have
separated, a bland petroleum jelly should be applied to the medial surfaces of the
labia minora once daily for 1-2 months.
 If no specific diagnostic etiology is found, management of persistent otherwise
asymptomatic daytime urinary incontinence is primarily supportive. All caffeinecontaining foods and beverages should be eliminated, and an anticholinergic agent
should be introduced. A trial with diazepam may be helpful because of the
psychological side effects of persistent daytime urinary incontinence. Ongoing
support from the physician and family is essential, and professional psychiatric help
may be warranted.
 Treatments for giggle incontinence are proposed and based on various hypotheses
concerning the etiology. Results are difficult to assess because of the high rate of
resolution with maturity. Those who hypothesize that giggle incontinence is a
special form of detrusor instability have used timed voiding, anticholinergic agents,
and imipramine (see the Medication section below). Patients may need to
accommodate the problem by trying to avoid situations that cause laughter when in
public places. If incontinence occurs frequently, a trial of an anticholinergic agent
with a timed voiding schedule may be warranted.
Detrusor instability
 The goal is to foster development of cerebral inhibition of detrusor contractions
during bladder filling so that urgency and urge incontinence do not occur. No known
medication or procedure is has been shown to accomplish this; however, certain
interventions appear to help.
 Anticholinergic medications (see the Medication section below) are frequently
helpful. However, these medications are meant to help the child develop a normal
voiding pattern and not long-term solutions. Ultimately, the child must develop the
ability to use cerebral mechanisms to inhibit detrusor contractions.
 A voiding retraining program is an essential component of the management of the
child. In most instances, the voiding retraining program should be tried for 2-3
weeks before an anticholinergic medication is introduced.
 Guidelines for a voiding retraining program include the following:
 Small girls should have a footstool or other solid surface placed in front of
the commode so that their feet are on a solid surface. Girls should remove
their underpants or lower them to the ankles to permit relaxed separation of
the thighs. During voiding, the child should be comfortable and relaxed.
Neither boys nor girls should rush to void (eg, during a television
commercial).
 Boys should be instructed to free their penis before voiding. The zipper or
buttons should be completely opened. If the underwear constricts the penis,
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this should be corrected. The boys should be relaxed and take sufficient time
to completely empty the bladder.
 Successful management requires ongoing support, instruction, and education.
Children should be helped to understand that normal urination is the result of
relaxing the sphincters and permitting the bladder muscle to expel the urine,
not a matter of forced voiding using the abdominal muscles.
 A timed voiding schedule should be used when the child is awake, even in
those with urinary frequency. Children should develop a regular voiding
pattern, with bladder evacuation every 1.5-2 hours. This is a basic
component of bladder retraining. Writing letters to a school nurse, teacher, or
principal to carry out this program is almost always necessary and of value.
 Introduce calendars to keep record of the voiding pattern and bowel
movements. The latter is important, even in the child with no history of
constipation, particularly if an anticholinergic medication is introduced.
Ongoing management may be accomplished via telephone, if the family
keeps good records.
 Suppressive antibacterial therapy should be used for children with recurrent
UTIs and those with VUR.
Dysfunctional voiding (pelvic floor muscular dysfunction with or without uninhibited
detrusor instability)
 Treatment of this voiding disorder, which has been described as a disharmony
between the detrusor and sphincters, consists of a voiding retraining program with
emphasis on good voiding technique, suppressive antibacterial agents for those
prone to UTIs, anticholinergic medication, and (in some instances) an alpha1adrenergic receptor blocker (see the Medication section below).
 Prevent constipation.
 Dysfunctional voiding is the most worrisome functional voiding disorder in children
because it may progress in a pattern similar to a neurogenic bladder or outlet
obstruction. In the infrequent instances of severe functional bladder outlet
obstruction the condition has been termed occult neuropathic bladder,
nonneurogenic neurogenic bladder, psychological nonneuropathic bladder, and
Hinman syndrome.
 When the upper urinary tract is normal, management should focus on the
development of effective relaxed voiding using the interventions described for
detrusor instability. Biofeedback training for carrying-out Kegel exercises (pelvic
floor relaxation and contraction) has been successful in many centers.
 Persistent symptoms, including dribbling of urine, incomplete emptying, and bladder
spasms may be alleviated using an alpha1-adrenergic receptor blocker in addition to
an anticholinergic drug. Diazepam, psychological counseling, hypnosis, and
biofeedback have been used with varying degrees of success. If these approaches are
unsuccessful, particularly in children with upper tract damage, a trial of clean
intermittent catheterization should be introduced. Residual urine should be checked
to monitor progress.
 In rare instances, those with compromised upper urinary tracts who do not improve
with the preceding measures may benefit from temporary urinary diversion.
Lazy bladder syndrome
 Children who void as infrequently as 2-3 times every 24 hours but who do not have
UTIs, urinary urgency, or incontinence do not have a discrete clinical indication for
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intervention. However, encouraging more frequent voiding may be wise to avoid
potential problems at a later age.
 Children who void infrequently and who are prone to UTIs or have urgency or
incontinence should be encouraged to empty their urinary bladders every 2-3 hours.
They are at risk for UTIs because prolonged bladder incubation of urine
compromises the protective effect of regular bladder washout, which clears bacteria
that gain access to the bladder during voiding due to eddy currents.
 Urinary incontinence is usually due to overflow from a large hypotonic bladder.
Those with persistent voiding symptoms or UTIs should undergo urodynamic
evaluation. Children with large capacity hypotonic urinary bladders who are
unwilling or unable to comply with an improved voiding schedule should have a
trial on bethanechol (see the Medication section below). If bethanechol is not
helpful, clean intermittent catheterization may be needed for a period.
Constipation and detrusor instability
 When constipation is diagnosed in a child with detrusor instability, treating the
constipation is important to determine if it is the cause of bladder instability and to
improve bowel evacuation.
 Anticholinergic medications, which are frequently administered to control
uninhibited detrusor contractions, also act on the musculature of the rectosigmoid
colon and foster fecal retention.
 Treatment of chronic constipation requires initial complete evacuation of the colon
followed by ongoing high-fiber diet and medication. Although daily enemas may be
used, one option is relatively aggressive treatment with a solution of polyethylene
glycol and electrolyte (see the Medication section below), which is prepared by
diluting the powder and administering it once a day or more frequently. This therapy
has gained widespread use for evacuation of the colon.
Pharmacologic therapy of voiding dysfunction in children usually centers on inhibiting unexpected
detrusor contractions and, at times, decreasing bladder outflow resistance. Most of the
neurohumoral stimulus for bladder contraction is the stimulation of muscarinic-cholinergic receptor
sites on bladder smooth muscle. Atropine and atropinelike agents can depress normal and
uninhibited bladder contractions. In some instances, bladder outlet resistance is increased because
of stimulation of alpha1-adrenergic receptors in the bladder neck. This effect may be decreased by
the use of alpha1-adrenoreceptor blockers.
Management of constipation is also an important component of treatment of voiding dysfunction in
children.
Drug Category: Anticholinergic agents -- These drugs inhibit the binding of acetylcholine to
the cholinergic receptor, thereby suppressing involuntary bladder contraction of any etiology. In
addition, they increase the volume of the first involuntary bladder contraction, decrease the
amplitude of the involuntary bladder contraction, and possibly increase bladder capacity.
Drug Name
Hyoscyamine (Levsin) -- L-isomer of hyoscyamine, which is almost entirely
responsible for antimuscarinic activity of atropine. Atropine is racemic mixture
D/L-hyoscyamine.
Adult Dose
0.125-0.3 mg PO qid
Pediatric Dose
0.003 mg/kg/d PO divided bid; not to exceed 0.1 mg/kg/d divided qid
Contraindications
Documented hypersensitivity; obstructive uropathy; narrow-angle glaucoma;
myasthenia gravis; obstructive GI tract disease
Interactions
Effects decrease with concurrent antacids; toxicity increases with concurrent
phenothiazines, amantadine, haloperidol, MAOIs, and tricyclic antidepressants
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Impairment of sweating may limit use in children during vigorous exercise on hot
days; observe for development or aggravation of constipation and impairment of
sweating; must titrate dose for effectiveness without unacceptable adverse
effects
Drug Name
Propantheline bromide (Pro-Banthine) -- Quaternary ammonium antimuscarinic with
peripheral effects similar to those of atropine.
Adult Dose
15 mg PO bid/qid
Pediatric Dose
0.5 mg/kg/d PO/SL divided bid; not to exceed 0.5 mg/kg/d divided qid
Contraindications
Documented hypersensitivity; ulcerative colitis; narrow-angle glaucoma;
obstructive disease of the GI or urinary tract
Interactions
Effects decrease with concurrent antacids; toxicity increases with concurrent
disopyramide, tricyclic antidepressants, phenothiazines, corticosteroids, and
bretylium
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Impairment of sweating may limit use in children during vigorous exercise on hot
days; observe for development or aggravation of constipation and impairment of
sweating; must titrate dose for effectiveness without unacceptable adverse
effects
Drug Name
Oxybutynin (Ditropan, Ditropan XL) -- Synthetic tertiary amine; like atropine,
antagonizes muscarinic actions of acetylcholine. Direct spasmolytic effect on
detrusor muscle and small intestine and local anesthetic action. Reduces
incidence of uninhibited detrusor contractions.
Adult Dose
5 mg PO bid/qid or extended release 5-10 mg qd; increase in 5-mg increments; not
to exceed 30 mg/d
Pediatric Dose
Immediate release:
1-5 years: 0.2 mg/kg/dose 2-3 times/d
>5 years: 5 mg bid; up to 5 mg 3 times/d
Extended release:
¡Ý6 years: 5 mg qd; increase in 5-mg increments as tolerated; maximum 20 mg/d
Contraindications
Documented hypersensitivity; ulcerative colitis; narrow-angle glaucoma;
obstructive disease of the GI or urinary tract
Interactions
CNS effects increase when administered concurrently with other CNS depressants
Pregnancy
B - Usually safe but benefits must outweigh the risks.
Precautions
Do not chew or crush extended-release tablets; impairment of sweating may limit
use in children during vigorous exercise on hot days; observe for development or
aggravation of constipation and impairment of sweating; behavioral changes
necessitate discontinuation to determine if drug is the cause; must titrate dose
for effectiveness without unacceptable adverse effects
Drug Name
Imipramine (Tofranil) -- Tricyclic antidepressant. Facilitates urine storage by
decreasing bladder contractility and increasing outlet resistance.
Adult Dose
10-25 mg PO qd/tid initially and increase gradually prn; not to exceed 200 mg/d
Pediatric Dose
<6 years: Not recommended
6-12 years: 0.7-1.2 mg/kg/d PO divided bid
>12 years: 1.2 mg/kg/d PO divided tid; not to exceed 200 mg/d
Contraindications
Documented hypersensitivity; narrow-angle glaucoma; in acute recovery phase
following myocardial infarction; concurrent administration of MAOIs or
fluoxetine or administration in the previous 2 wk (avoid)
Interactions
Increases toxicity of sympathomimetic agents (eg, as isoproterenol, epinephrine)
by potentiating effects and inhibiting antihypertensive effects of clonidine
Pregnancy
D - Unsafe in pregnancy
Precautions
Consider baseline ECG in all patients; before use, perform cardiac evaluation in
those with family history of sudden death, baseline PR interval >90th percentile
for age, or any alteration in intraventricular conduction; long-term high-dose
therapy should not be abruptly discontinued; caution in seizure disorders,
hyperthyroidism, or thyroid replacement therapy
Drug Category: Alpha1-adrenergic antagonists -- These agents are used to
decrease smooth muscle tone in the bladder outlet.
Drug Name
Doxazosin mesylate (Cardura) -- Selective inhibitor of alpha1-adrenergic
receptors. Blockade of these receptors in bladder neck decreases outflow
resistance. Available as tablet.
Adult Dose
1 mg PO qhs initially to avoid the first-dose effect; may be increased gradually
over 1-2 wk; not to exceed 8 mg/d for urodynamic effect
Pediatric Dose
0.5 mg PO qhs initially to avoid first-dose effect; may increase by 0.5 mg after
interval of several wk; not to exceed 2 mg/d; safety and effectiveness not
determined
Contraindications
Documented hypersensitivity
Interactions
Effects decrease with coadministration of NSAIDs; effects increase with
coadministration of diuretics and antihypertensive medications
Pregnancy
B - Usually safe but benefits must outweigh the risks.
Precautions
Caution in renal impairment; may cause marked hypotension following first dose
Drug Name
Terazosin hydrochloride (Hytrin) -- Selective inhibitor of alpha1-adrenergic
receptors. Blockade of these receptors in bladder neck decreases outflow
resistance. Available only as capsule.
Adult Dose
1 mg PO qhs; increase slowly to effect; not to exceed 20 mg/d
Pediatric Dose
1 mg PO qhs initially to avoid first-dose effect; dose should not be increased
for several wk; not to exceed 2 mg/d; safety and effectiveness not determined
Contraindications
Documented hypersensitivity
Interactions
Effects decrease with coadministration of NSAIDs; effects increase with
coadministration of diuretics and antihypertensives
Pregnancy
B - Usually safe but benefits must outweigh the risks.
Precautions
Caution in renal impairment; may cause marked hypotension following first dose
and coadministration with beta-blockers
Drug Name
Polyethylene Glycol 3350 NF Powder for solution (Miralax, GlycoLax) -Polyethylene glycol solution is osmotic agent that causes water to be retained
in stool. Despite lack of specific recommendations, widely given to children
with voiding dysfunction by primary care physicians, pediatric
gastroenterologists, and pediatric nephrologists caring for children.
Recommended for occasional constipation in adults.
Adult Dose
17 g/din 8 oz water, juice, soda, coffee, or tea
Pediatric Dose
Not established; no recommended dose in manufacturer's literature, Physicians'
Desk Reference (2005) or Pediatric Dosage Handbook (2005); 8.5-17 g in 8 oz.
fluid qd/qod being used; prolonged use may be common because of ongoing
constipation
Contraindications
GI obstruction, gastric retention, bowel perforation, megacolon
Interactions
None if used for occasional constipation; when used for bowel cleansing,
increased peristalsis may decrease absorption of oral medications
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Caution in ulcerative colitis, impaired gag reflex, or regurgitation or
aspiration during administration; treatment duration for occasional constipation
should not exceed 2 wk
Further Outpatient Care:
 Ongoing follow-up is essential.
 Most follow-up visits can be handled with regular telephone contact with the parents or the
child if they monitor voiding and stooling.
 Parents and children should pay attention to maintenance of the recommended voiding
interventions and to bowel function with regard to constipation.
 Medication changes can be made by means of ongoing telephone contact.
Complications:
 Persistence of daytime wetting may markedly disrupt the social lives of older children.
 Detrusor instability with pelvic withholding maneuvers may foster recurrent UTIs or
persistence of VUR.
 Dysfunctional voiding can cause persistence of VUR and frequent UTIs. In rare cases, this
results in dilatation of the upper urinary tract and kidney damage.
Prognosis:
 The prognosis for complete or partial resolution of a functional voiding disorder is excellent
for children with daytime urinary incontinence and detrusor instability.
 The prognosis is good for children with giggle incontinence, who tend to outgrow it during
adolescence and for those with lazy bladder syndrome, who respond to intervention.

The prognosis is guarded for children with dysfunctional elimination syndromes and
dysfunctional voiding whose condition does not respond to intervention.
Patient Education:
 Patients should be educated about voiding retraining.
 This is the foundation of the treatment of children with functional voiding disorders.
 Although how a child achieves cerebral control over reflex detrusor contractions is
unclear, learning good voiding patterns appears to be helpful.
 Effective biofeedback training is especially helpful for management of muscular
dysfunction of the pelvic floor.
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