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162 Urinary Incontinence
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stimulation (TENS) is thought to improve bladder control by modifying interneuronal interaction at spinal cord level. Success rates of up to 60%
have been reported but the duration of improvement is variable.
Posterior Tibial Nerve
Neurostimulation
In this technique a ne needle is inserted into
the vicinity of the tibial nerve in the lower leg
and an electrode pad is placed over the heel.
Electrical impulses are transmitted via the tibial nerve to the spinal cord and sacral plexus.
Treatment typically consists of weekly sessions
of 30 minutes duration over 12 weeks. Posterior
tibial nerve neurostimulation has been approved
by the UK National Institute for Clinical
Excellence (NICE) for the treatment of refractory detrusor overactivity. Although mainly
used in adults it has also been used in children
and young people.
Sacral Nerve Stimulation
is is an invasive intervention which entails surgical implantation of a stimulator in the region
of the sacral nerves. It has been used more extensively in adults but experience in children is very
limited.
Intravesical Botulinum
A Toxin Injection
is approach is being increasingly used in children with severe bladder overactivit y which has not
responded to other forms of treatment. Cystoscopy
is performed under general anaesthesia and small
doses of Botulinum A toxin are injected into the
bladder wall muscle at multiple sites.
Up to 15% of children experience impaired
bladder emptying or urinary retention following intravesical Botox injection and for this
reason the possible requirement for clean intermittent catheterisation (CIC) must be explained
(or even taught) prior to the procedure. e
duration of response to intravesical Botox is
variable but may be of the order of 6–9 months.
One or more further injections may be required.
Nevertheless, intravesical Botox injections may
be valuable in conferring a period of symptomatic relief while other measures are being
introduced.
OTHER FORMS OF
FUNCTIONAL URINARY
INCONTINENCE
Urge Syndrome/Motor Urgency
Daytime wetting is accompanied by symptoms of
urgency in more than 80% of children. e child
only becomes aware of the sensation of needing
to void shortly before the act of voiding supervenes. Indeed, many children claim that they do
not realise that they are voiding at all.
Urgency tends to occur when the bladder is full
rather than during lling. e cause is unknown
but it is likely to be a manifestation of delayed
maturation of normal bladder control. Children
may attempt to prevent impending leakage of
urine by contracting their urethral sphincter
and pelvic oor muscles. In some children this
may be reinforced by additional manoeuvres –
notably crouching with the heel pressed into the
perineum (Vincent’s curtsy sign).
Dysfunctional Voiding
is is characterised by a urinary ow which is
of varying intensity or interrupted (“staccato”)
voiding. Urodynamic studies demonstrate
detrusor-sphincter dyssynergia with either
incomplete relaxation of the sphincter or alternating phases of contraction and relaxation.
Voiding is oen incomplete. e most likely
explanation is that children who have learned
to use voluntary contraction of the urethral
sphincter to suppress leakage due to detrusor instability then go on to adopt a pattern of
behaviour which prevents them from relaxing
the sphincter during deliberate voiding. e
condition is virtually conned to girls and is
accompanied by recurrent urinary infections in
more than 90% of cases. Vesicoureteric reux
(with or without renal scarring) is present in
Other forms of functional urinary incontinence / Diurnal Urinary Frequency 163
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around 30% of cases. is is mostly secondary
reux caused by sustained exposure to elevated
intravesical pressures generated by a combination of detrusor overactivity and detrusor-sphincter dyssynergia. e treatment of
dysfunctional voiding centres on “re-educating
the voiding mechanism” – initially with a regular voiding regimen and other simple measures.
For those suering from more severe forms of
dysfunctional voiding a range of techniques is
now available which can be grouped under the
heading “Urotherapy” or “Cognitive Bladder
Training.” e key elements involve biofeedback
(using uroowmetry and dedicated computer
programmes) to train the child to relax their
sphincter mechanism and pelvic oor during
voiding in response to visual and sensory signals. High success rates have been reported but
these techniques are time consuming, demanding and require the input of a fully trained urotherapist and appropriate equipment.
Non-Neuropathic Neuropathic
Bladder/Hinman’s Syndrome
is is a rare disorder in which the bladder
behaves like a “neuropathic” bladder despite the
absence of identiable neurological cause. e
radiological features resemble those of genuine neuropathic bladder – including trabeculation, sacculation and elongation of the bladder
(“r-tree” bladder). Upper tract dilatation and
other secondary changes in the upper renal tracts
are also present in the majority of cases.
In the classic form (Hinman’s syndrome),
there is almost invariably a background of
domestic turmoil or a history of severe physical
or psychological upset occurring at, or shortly
aer, the time of toilet training. It is thought that
some children, who are unusually fearful of wetting themselves, grossly overuse their external
urethral sphincter to counteract unstable detrusor contractions in a desperate attempt to stay
dry. is leads to elevated intravesical pressure
and reduced compliance, with secondary upper
tract complications.
e condition typically presents at around
5–8 years of age with unusually severe urinary
incontinence which is compounded in most
cases by UTIs and marked disturbance of bowel
habit. However, this condition may also develop
at a later age and, as in younger children, may
be accompanied by symptoms of renal insufciency in severe or longstanding cases. e
natural history is variable but, if untreated, the
condition carries a very real threat of severe
upper tract damage and renal insuciency.
Expectant management is not a safe option. e
treatment options are the same as those for the
management of true neuropathic bladder (see
Chapter 13). Very rarely a child will present with
the features of a non-neuropathic neuropathic
bladder despite the lack of any history of psychological disturbance. Bowel function is usually
normal. e management is the same as for true
neuropathic bladder
Sensory Urgency
is poorly understood condition is largely
conned to girls. Despite clinical features
which are strongly suggestive of detrusor overactivity, urodynamic evaluation reveals a stable
bladder. e symptoms of urgency are purely
sensory in origin. Sensory urgency in adults
is a feature of interstitial cystitis but it is very
doubtful whether this condition occurs in children. e use of intravesical oxybutynin has
been described.
Diurnal Urinary Frequency
is condition aects mainly boys aged 4–7 years
in whom it is characterised by the sudden onset of
severe daytime urinary frequency. In some cases
this may be as oen as every 10–15 minutes. Even
when the sensory frequency is severe it is only
rarely accompanied by wetting. e symptoms
are conned to the day time and there is no corresponding nocturia. Urine culture is negative and
ultrasound ndings are normal. e aetiology is
unknown but is likely to involve a strong behavioural component. e symptoms do not respond
to anticholinergics. e condition is always selflimiting – typically over a period of 3–12 weeks.
However, a few children experience recurrent
episodes over the next 1–2 years.
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Deferred Voiding
is is common in both sexes and occurs most
oen at around 4–6 years of age. e child suddenly becomes aware of an urgent need to void
(due to presumed unstable detrusor contraction)
and experiences some degree of involuntary wetting if voiding is delayed. is usually occurs
because the child is engrossed in other activities,
for example playing outdoors, which take precedence over the social demands of continence. No
treatment is required in this age group because
the condition is self-limiting. Deferred voiding is
less common in older children – in whom it may
be a manifestation of broader behavioural disturbance. Psychological input may be required in
such cases.
Lazy Bladder
Aecting mainly girls in age range 8–10 years,
this condition usually presents with daytime
incontinence and/or UTI. However, because the
bladder remains visibly and palpably distended
aer voiding the condition may sometimes present with the incidental nding of a lower abdominal swelling.
e upper renal tracts are always non dilated
and the urodynamic picture is one of lowpressure retention with detrusor-sphincter
dyssynergia and non-sustained detrusor contractions. e condition is almost certainly behavioural in origin. It is usually self-limiting and
oen resolves quite suddenly during the course
of puberty. For children who are troubled by
symptoms, cognitive bladder retraining has
the best outcome. In severe cases CIC may be
indicated – although this may not be tolerated.
Anticholinergics should be avoided or used with
caution.
Giggle Incontinence
normal. Giggle incontinence is a source of considerable embarrassment and distress in older
children and teenagers – both at school and during social activities. Urodynamic examination
may reveal some mild detrusor instability but
the ndings are usually normal. Giggle incontinence is generally believed to be a neurological
(rather than urological) phenomenon which is
analogous to a form of cataplexy disorder mediated via higher neurological centres in which a
sudden loss of muscle tone is triggered by emotion. ere is oen a family history. Whether it
is a genuinely self-limiting condition is unclear
because apparent improvement in puberty and
early adult life may, in reality, represent no
more than adaptation to avoid the precipitating
circumstances.
Methylphenidate (Ritalin) is the most consis-
tently eective agent. However, it is a regulated
drug and should be reserved for severely aected
patients. Oxybutynin is helpful in some cases and
Imipramine can also be considered.
Night Time Urinary Incontinence
(Nocturnal Enuresis)
Nocturnal enuresis (bedwetting) is one of the
commonest conditions of childhood. Around
10% of 7-year-old children wet the bed three or
more times a week and a small minority experience intractable nocturnal enuresis which persists into late adolescence and adulthood.
Urinary incontinence which only occurs at
night is termed “monosymptomatic” whereas
noctur nal enuresis which is al so accompanied daytime wetting is termed “non-monosymptomatic”
or “polysymptomatic”.
Nocturnal enuresis is classied as “primary”
if the child has always wet the bed and “second-
ary” if the child has previously been dry at night.
Butler and Holland postulated a “3 Systems
Model” to account for the main causes of nocturnal enuresis (Figure 12.6) i.e.
is distinctive form of incontinence occurs
mainly in girls – in whom it typically presents at
around 9–12 years. Urinary leakage only occurs
with giggling or laughing but at no other time.
Other aspects of voiding function are entirely
●
Low release of Arginine Vasopressin (AVP)
with overproduction of urine at night
●
Lack of arousal from sleep
●
Bladder overactivity and associated daytime
symptoms
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Figure 12.6 The 3 systems model of nocturnal enuresis.
e aim of management is to identify which of
these factors is most likely to be responsible in the
aected child and plan t heir treatment accordingly.
Primary Monosymptomatic
Nocturnal Enuresis
is is twice as common in boys as girls. e clinical features are variable and whilst some children
wet the bed every night others are less severely
aected, with less severe leakage, fewer wet beds
or alternating spells of wet and dry nights.
e aetiology is multifactorial and in any
individual one or more of the following factors
may apply:
A positive family history (in upwards of 75%
of cases).
Absence of a circadian rhythm of vasopressin
release. Levels of vasopressin normally
increase at night. However, vasopressin
release is absent or reduced in up to 75%
of children who wet the bed (and in an
even higher proportion of those with a
positive family history). is leads to a
nocturnal urinary output which exceeds
the functional bladder capacity.
Sleep arousal diculty. Nocturnal enuresis
does not, as is commonly supposed, result
from abnormally deep sleep, as bed wetting occurs at all stages of the sleep cycle.
However, many aected children lack the
arousal from sleep which would normally
occur when the bladder lls to the point
where it approaches its functional bladder
capacity. e child usually sleeps through
the episode of incontinence, being
unaware that they have wet the bed.
Although nocturnal enuresis is sometimes a manifestation of emotional problems or behavioural
disorders, the great majority of children with
primary monosymptomatic nocturnal enuresis
are normally adjusted. Apart from a urine dipstick test (to exclude glycosuria and diabetes)
investigations are rarely indicated. e prognosis
is excellent, with spontaneous resolution by the
time of physical maturity occurring in 97–99% of
aected individuals. e probability of cessation
in any 1 year is approximately 1 in 6.
Secondary Monosymptomatic
Nocturnal Enuresis
In the majority of cases the onset can usually be
linked to some physical or emotional upset.
However, it is important to exclude the possibil-
ity of an underly ing organic condition – par ticularly
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one associated with polyuria such as diabetes
mellitus or diabetes insipidus. However, such causes
are rare.
Treatment of Monosymptomatic
Nocturnal Enuresis
is should not usually be considered until the
age of 5 years. e choice of treatment is partly
determined by the clinical features. But regardless what treatment is chosen its success will be
heavily dependent on the motivation of the child
and the family. Although treatment provides a
way of managing rather than curing the condition, eective symptomatic relief may help to
expedite the resolution of the underlying nocturnal enuresis sooner than might otherwise have
been the case.
Parents should be encouraged to adopt a positive attitude to treating the bedwetting. Scolding
and punishment are to be avoided at all costs.
e management of monosymtomatic nocturnal
enuresis is generally undertaken in a community
setting by primary care doctors, paediatricians
and specialist continence nurses.
Simple Measures to Reduce
Overnight Urine Production
e child should not drink aer a set time in the
evening (e.g. 6 pm) and should try to maintain a
steady intake of uid throughout the day rather
than drinking more in the aernoon or early evening. It is also important that the child empties
their bladder before going to bed.
e use of star charts, combined with rewards,
can be particularly helpful in younger children.
Use of a Vasopressin Analogue Such
as Desmopressin
is mimics the circadian rhythm by decreasing the obligatory production of urine by the
kidneys overnight. e success rate is up to 70%
but the relapse rates aer cessation of treatment
are relatively high (30–50%). is treatment is
more likely to be eective in children with a
family history of nocturnal enuresis and those
who wet the bed shortly aer going to sleep. e
success rate is lower in children who also suffer from day time wetting. Desmopressin nasal
spray products are no longer available because
of the small risk of serious adverse reactions
which included hyponatraemia, seizures and
water intoxication.
Oral formulations have a more favourable
risk-benet prole. Currently, these are available as Desmotabs (200–400 mg at night) or
Desmomelt (120–240 mg at night) and are usually taken 1hour prior to bedtime.
Enuresis Alarm
Children with a deep sleeping pattern are the best
candidates for treatment with an enuretic alarm.
ese alarms are intended to sensitise the child
to the feeling of a full bladder and raising their
level of awareness whilst asleep. Aer a while the
child acquires the ability to respond appropriately by waking before leakage of urine occurs.
e equipment typically consists of an auditory
or vibratory alarm connected to a pad placed
on the mattress (Figure 12.7). e alarm is activated when the rst drop of urine leaks onto
the pad. Enuresis alarms are more eective in
children aged 7 years and upwards – in whom
success rates are typically in the range 60–75%.
Subsequent relapse rate are much lower than
those aer treatment with medication. Alarms
are less successful in children who are not motivated to become dry and those who also suer
from daytime wetting.
Nocturnal hypoxia has been identied as a
possible cause of nocturnal enuresis in some children with history of snoring and/or poor attention during the day at school. e ndings of
sleep studies have also been cited by proponents
of this possible explanation. Although, tonsillectomy has been reported to cure nocturnal enuresis in selected cases this has not been conrmed
by a recent prospective controlled trial.
Non-Monosymptomatic or
Polysymptomatic Nocturnal Enuresis
When nocturnal enuresis is accompanied by
day symptoms such as urgency, frequency, stress
incontinence and constipation, the rst priority
Other forms of functional urinary incontinence / Non-Monosymptomatic 167
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KEY POINTS
●
e initial priority is to exclude organic
causes of urinary incontinence –
although these are rare.
●
Most organic (anatomical or neurological) causes of daytime wetting can be
excluded on the basis of history, examination and ultrasonography.
●
Day time wetting in children is most
commonly due to detrusor instability.
In the majority of children the natural
history is one of spontaneous resolution but this can usually be expedited
by simple measures.
●
Primary monosymptomatic nocturnal
enuresis seldom, if ever, has an underlying organic basis.
Figure 12.7 (a) Enuresis alarm. The pad is
placed under the bed sheet, with bedside
battery powered buzzer. (b) Compact enuresis
alarm suitable for the treatment of nocturnal
enuresis or ambulatory treatment of diurnal
enuresis. The buzzer device is pinned to the
pyjamas (or clothes when used in the day time)
and the sensor worn between two pairs of
underclothes.
should be to investigate the possible cause(s) of
the daytime symptoms. In practice the nocturnal
enuresis is unlikely to respond to measures such
as an enuresis alarm until the day time wetting
has been eectively treated. When used selectively
(principally in children who are also troubled by
daytime urgency and frequency) anticholinergic
agents such as Oxybutynin are eective in up to
two-thirds of cases. A combination of treatments
may be required in some children – for example,
the use of Desmopressin and an enuresis alarm.
Imipramine, a tricyclic antidepressant, is no
longer recommended as rst-line treatment and
should never be prescribed in conjunction with
Desmopressin.
FURTHER READING
1. Tryggve Nevéus, von Gontard Alexander,
Hoebeke Piet, Hjälmås Kelm, Bauer
Stuart, Bower Wendy, Jørgensen Troels
Munch, Rittig Søren, Walle Johan Vande,
Yeung Chung-Kwong, Djurhuus Jens
Christian. The standardization of terminology of lower urinary tract function in children and adolescents: report
from the Standardisation Committee of
the International Children’s Continence
Society. J Urol. 2006;176:314–324.
2. Butler R, Holland P. The Three Systems: a
conceptual way of understanding nocturnal enuresis. Scan J Urol Nephrol.
2000;34:270–277.
NICE Clinical guidelines https://www.nice.org.
uk/guidance/cg111 (Bedwetting)
https://www.nice.org.uk/guidance/ipg362/
chapter/1-Guidance (PTNS)
Websites:
www.i-c-c-s.org
www.eric.org.uk
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Neurogenic Bladder
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KYLE O ROVE and CHRISTOPHER S COOPER
Topics covered
13
Etiology
Pathophysiology
Prenatal intervention
Newborn evaluation and management
Investigations
Treatment and outcomes
Catheterization
INTRODUCTION
AND DEFINITION
Neurogenic bladder is a non-specic term that
implies an abnormality of innervation causing
bladder dysfunction. Injury to the nervous system
may be congenital or acquired, peripheral or central, isolated or syndromic. As the primary functions of the bladder are to store and empty urine
through coordinated activity of the detrusor muscle and urinary sphincter, dysfunction may result
in urinary incontinence, elevated storage or voiding pressures, or incomplete emptying. Children
and young people with neurogenic bladder are
at risk of progressive deterioration in bladder
function leading to kidney damage. Appropriate
surveillance and management are crucial to maintaining renal function, achieving continence, and
improving quality of life for these patients.
Increasing bladder capacity and reducing
pressure
Bladder outlet procedures
Transition to adulthood
Sexual function
Neurogenic bowel
ETIOLOGY
Spina bida is the most common cause of congenital neurogenic bladder. In the United States,
approximately 1,500 children with spina bida
are born each year and the worldwide reported
incidence is 3.1 per 10,000 births. e incidence
has been decreasing over the last two decades
but varies considerably by country and ethnicity. Myelomeningocele is the most severe form of
spina bida, accounting for 90% of cases, while
the remaining 10% are comprised of lipomyelomeningocele or meningocele. Other congenital causes of neurogenic bladder include closed
and occult forms of neural tube defects such
as tethered spinal cord, intradural lipoma, and
intraspinal cysts. See Table 13.1. e term “spina
bida occulta” may also be applied to an isolated vertebral anomaly consisting of incomplete
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Table 13.1 Etiology of childhood neurogenic
bladder
Congenital Acquired
Myelomeningocele Spina cord injury
Sacral agenesis Spinal cord infarction
Tethered cord Spinal cord tumor
Closed and occult
forms of neural tube
defects
Anorectal malformations Neuroblastoma
Sacrococcygeal
teratoma
Transverse myelitis
Cerebral palsy
Idiopathic causes
formation of the posterior spinous process. is
anomaly, which is oen an incidental nding, is
found in up to 15% of the population. It is conned to the bony elements the vertebrae and is
rarely accompanied by any underlying neurological lesion.
e critical period of neurulation (closure of
the neural tube from cephalad to caudad) occurs
in the rst few weeks of pregnancy. Adequate
levels of folic acid are important for normal
closure of the neural tube and low maternal
dietary intake of folate or dysregulated folate
metabolic pathways have been implicated as a
major risk factor for the development of neural
tube defects. In the United States, it is recommended that women should commence folate
supplements 2 months prior to conception and
women of childbearing age should consume 400
mcg folic acid daily. Other risk factors implicated in the etiology of neural tube defects
include maternal obesity, diabetes mellitus, and
advanced maternal age.
Survival rates of children born with myelomeningocele have improved dramatically since
the 1950s when less than 20% survived beyond
24 months of age. e development of the ventriculoperitoneal (VP) shunt for the control of
hydrocephalus led to signicantly improved survival and by the mid-1970s the survival rate had
increased to over 50%. It is predicted that more
than 90% of the infants currently being born with
spina bida will survive, with the majority living
into adulthood. e introduction of clean intermittent catheterization (CIC) by Lapides in 1972
was an important advance in the management of
neurogenic bladder. Subsequently, the widespread
introduction of urodynamic investigations led to
recognition of the need for proactive management if the leak point pressure exceeded 40 cm of
water or other adverse parameters of neurogenic
dysfunction were demonstrated on urodynamics.
Other causes of congenital neurogenic bladder include partial and complete sacral agenesis
(caudal regression syndrome) which may occur
in isolation or conjunction with anorectal and
cloacal malformations. Acquired neurogenic
bladder may be due to spinal cord trauma,
tumors, extensive pelvic surgery, spinal cord
infarction, transverse myelitis, developmental
syndromes and cerebral palsy. Finally, certain
adverse features of neurogenic bladder may
be present in the acquired condition of nonneurogenic neurogenic bladder (or Hinman’s
sy ndrome).
PATHOPHYSIOLOGY
Vertebral anomalies in the lumbosacral region
account for about 50% of cases with lumbar and
thoracic lesions accounting for 28% and 20%
of cases respectively. It should be noted, however, that the level of the vertebral abnormality
does not correlate closely with the level of the
neurological decit or the outcome for bladder
function.
e functions of the normal bladder are to
store urine and to empty under voluntary control. ese functions are organized at the level
of the brainstem and spinal cord. e sympathetic innervation of the detrusor muscle and
urethral smooth muscle is mediated through
the hypogastric nerve bers emanating from the
lumbar region. e parasympathetic innervation of the detrusor muscle is mediated by pelvic
nerve pathways transmitted via the sacral roots
S2 - 4 and the striated sphincter is innervated by
the pudendal nerves also originating from the
sacrum. Upper motor neuron lesions lead to an
overactive bladder with no voluntary sphincter
Newborn evaluation and management / Initial Management 171
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control. Contractions of an overactive bladder against the resistance created by a nonrelaxing sphincter (termed detrusor/sphincter
dyssynergia) typically lead to detrusor hypertrophy and a thick-walled bladder. Lower motor
neuron lesions are characterized by an acontractile, accid detrusor, small, smooth walled
bladder, and denervation of the external sphincter. However, most spina bida patients have a
mixed neurologic picture with features of both
upper and lower motor neuron lesions.
PRENATAL INTERVENTION
As a consequence of widespread prenatal detection of myelomeningocele by ultrasonography,
fetal surgical intervention for the repair of these
lesions has become a clinical reality. One prospective, randomized trial found that fetal intervention reduced the requirement for VP shunts
and was associated with improved lower limb
function at 12 and 30 months age. However, it
did not result in any improvement in urodynamic parameters or any signicant reduction in
the requirement for CIC. More recent data have
suggested, however, that prenatal repair may
reduce the need for CIC between 6 and 10 years
of age and may perhaps increase the potential
for spontaneous voiding. e complications of
fetal repair include preterm delivery and uterine
dehiscence.
neurogenic bladder in newborn infants with spina
bida. e timing of commencement of CIC is
considered below. A baseline renal and bladder
ultrasound scan is performed aer 24–48 hours
and renal function is assessed with serum creatinine or cystatin c. Following discharge from
hospital a voiding cystourethrogram (VCUG)
or video urodynamic study is performed aer
3 months of age. Baseline urodynamic parameters assessed by this study should include; lling
pressures, compliance, presence of detrusor overactivity, sphincteric function, leak point pressures, presence of vesicoureteral reux (VUR),
and conguration of the bladder neck (open or
closed). e ultrasound appearances of the kidneys and bladder are abnormal in up to 20% of
infants with myelomeningocele.
Spina Bida Occulta (Occult
Spinal Dysraphism)
ese abnormalities include lipomeningomyelocele, tethered cord, and sacral agenesis. External
signs of the underlying abnormality (prominent
sacral dimple, fatty subcutaneous mass, tu of
hair, hemangioma, or skin tag) are present in
more than 80% of cases. External evidence of
sacral agenesis is less obvious but may be apparent as an asymmetric gluteal cle. e spine can
be evaluated with ultrasound in the rst 2 to
3 months of life but thereaer spinal magnetic
resonance imaging (MRI) scan is the “gold standard” imaging modality.
NEWBORN EVALUATION
AND MANAGEMENT
Cesarean section is recommended to minimize
trauma to the exposed neurologic tissue. At the
time of delivery, an open myelomeningocele is
immediately apparent as an exposed plaque of
neural tissue. Closure of the lesion within the rst
24 hours is recommended to minimize the risk of
ascending infection (meningitis).
ere are currently no standard evidence-
based guidelines for urologic management of
Initial Management
CIC is commenced if the bladder is not emptying
to completion. However, when adequate bladder
emptying is conrmed by clinical observation and
ultrasound two options can then be considered;
1. Immediate commencement of clean inter-
mittent catheterization and anticholinergic
medication.
Proponents of the early commencement
of CIC argue that this is a logical form of
management because at least 80% to 90% of
patients with myelomeningocele will have
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