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DISORDERS OF MICTURITION
Dr. Sreemayee Kundu
MD PAEDIATRICS
CONTENTS
• Introduction
• Physiology of micturition
• Maturation of micturition & sequence
• Voiding disorder-types,evaluation & treatment
• Nocturnal enuresis
• Neurogenic bladder
INTRODUCTION
• Urinary bladder functions as a storage organ that
can empty to completion at appropriate time and
place.
• Problems related to bladder are often obvious
like nocturnal enuresis, incontinence, dribbling or
may not be apparent like recurrent UTIs, day time
urgency frequency syndrome.
• Early intervention may prevent renal damage
from retrograde effects of high bladder pressures.
PHYSIOLOGY OF MICTURITION
FILLING
• Regular peristaltic contractions move the
urine from the renal pelvis to the bladder.
• Sympathetic systems T11-L2 spinal segments
responsible for effective bladder filling
• Sympathetic & pudendal nerve mediated
inhibition of detrusor contractility with
closure of bladder neck & proximal urethra.
PHYSIOLOGY OF MICTURITION
EMPTYING
• Contraction of detrusor muscle, mainly responsible
for emptying bladder during micturition.
• Bladder Neck along with elastic fibers form internal
urethral sphincter
• Urogenital diphragm with its skeletal muscle form
external urethral sphincter.
• Co-ordination among these three structures
responsible for emptying.
• Parasympathetic system S2-S4 for micturition.
MATURATION OF BLADDER
FETUS/
AT
BIRTH
Spinal cord reflex Spontaneous micturition
1-2
YEARS
bladder capacity +
Neural maturation of
frontal and parietal lobe
Sensation of bladder filling
present but voiding is reflex
3-4
YEARS
Voluntary control of EUS
when awake(day time)
Can delay micturition
5 YEARS Cortical inhibitory control
achieved
Dry by night
>6 yrs Ability to initiate voiding
even when bladder has
not given a “full” signal
Voiding under socially
acceptable circumstances
MATURATION SEQUENCE
• Night time fecal continence
• Daytime fecal continence
• Daytime urine continence
• Night time urine continence
DEFINITIONS (ICCS)
1. DECREASED DAYTIME
VOIDING FREQUENCY
</= 3 voidings/day
2. INCREASED DAYTIME
VOIDING FREQUENCY
>/= 8 voidings/day
3. POLYURIA >2 lit/m2 BSA - 24hrs
> 5ml/kg/hr
4. EXPECTED BLADDER
CAPACITY
[30+ (age in yrs x 30)] ml
5. RESIDUAL URINE Excess of 5-20ml indicates
incomplete bladder
emptying
DEFINITIONS (ICCS)
URINARY
INCONTINENCE
uncontrollable leakage
of urine
• CONTINUOUS continuous leakage of
urine , not in discrete
portions
malformation or
iatrogenic damage
• INTERMITTENT leakage in discrete
portions during
day/night
night = nocturnal
enuresis
• URGE
INCONTINENCE
associated with
urgency
Ex - overactive
bladder
• VOIDING
POSTPONEMENT
In the presence of
habitual holding
maneuvers
VOIDING DISORDER
• Definition: These consist of essentially functional,
abnormal patterns of micturition in the presence
of an intact neuronal pathway and without any
congenital/anatomical abnormality of the urinary
tract. Also called as Functional incontinence.
• Functional UI may be caused by disturbances in
the filling (storage) phase, the voiding phase, or a
combination of both.
Classification
Voiding Disorders
(based on clinical symptoms & urodynamics study)
Overactive bladder Dysfunctional voiding
(filling phase disorder) (evacuation phase disorder)
-staccato
-fractional
dysynergia
hypotonic/underactive bladder
VOIDING DISORDER
OVERACTIVE BLADDER
• It is a filling phase defect.
• Characterized by frequent episodes of urgency.
• Countered by contractions of pelvic floor
muscles and holding maneuvers.
• Due to underlying detrusor overactivity.
• Also called detrusor instability.
• Can be associated with incontinence (urge
incontinence).
VOIDING DISORDER
OVERACTIVE BLADDER
• Functional bladder capacity is small.
• Voiding pattern is normal with appropriate
relaxation of pelvic floor muscles.
• Associated with constipation.
( triggers detrusor contraction by stimulation
of stretch receptors in bladder wall by extrinsic
fecal mass or by colonic contractions via shared
neural pathways.)
VOIDING DISORDER
DYSFUNCTIONAL VOIDING
• It is a voiding phase defect
• Characterized by infrequent voiding and
straining to void.
• Associated with bladder-sphincter
incoordination.
• Referred as bladder-sphincter dysynergia.
• It may be staccato or fractional voiding.
VOIDING DISORDER
DYSFUNCTIONAL VOIDING
Staccato voiding:
• Bursts of pelvic floor muscle activity during
voiding
• Causes interruption in the urine flow.
• Prolonged flow duration and incomplete
voiding.
VOIDING DISORDER
DYSFUNCTIONAL VOIDING
Fractionated voiding:
• Micturition occurs in several small fractions.
• Emptying is incomplete due to hypo-activity of
detrusor muscles.
• Abdominal muscles are used to increase
pressure on the bladder (valsalva voiding).
• Irregular but continuous flow rate.
VOIDING DISORDER
DYSFUNCTIONAL VOIDING
Underactive bladder:
• Due to under active detrusor muscle.
• Long term result of bladder-sphincter
dysynergia with detrusor decompensation.
• Large post residual volume
• Recurrent UTIs.
• May lead to overflow incontinence.
VOIDING DISORDER
Hinman Syndrome
• Severe form of detrusor-sphincter dysynergia.
• Failure of external sphincter to relax during
voiding.
• Trabeculated bladder develops a high
pressure state with B/L VUR and large PVR
akin to a neurogenic bladder without any
obvious neurological abnormality.
• Non –neurogenic neurogenic bladder.
OTHER VOIDING DISORDER
GIGGLE INCONTINENCE
• Involuntary voiding during sudden laughter
• Seen in school girls and adolescents.
• Results from instability of bladder
• Due to inappropriate detrusor contraction and
sudden relaxation of urinary sphincter.
OTHER VOIDING DISORDER
VOIDING POSTPONEMENT
• Postpones imminent micturition until
overwhelmed by urgency.
• Uses holding maneuvers.
• Associated with low frequency.
• Over-activity of urethral sphincter is a behavioral
maladjustment.
• It is associated with other behavioral problems in
these children.
OTHER VOIDING DISORDER
VAGINAL VOIDING
• Seen in obese girls using western toilet.
• May not part their thighs adequately.
• This result in incontinence on standing due to
vaginal pooling.
• Volume of urine – 5-10 ml.
• Most common cause – Labial adhesion
OTHER VOIDING DISORDER
POLLAKIURIA
• Child voids extremely frequently at 30-60 min
interval.
• No dysuria, pain or incontinence.
• Nocturia is unusual.
• No organic cause.
• Stress related.
EVALUATION- VOIDING DISORDER
History – should assess the following :
• Pattern of incontinence
• Frequency of micturition
• Volume of urine
• Association with urgency or gigling
• Sensation of incomplete voiding
EVALUATION- VOIDING DISORDER
History – should assess the following :
• Urine stream
• Recurrent UTI
• Constipation
• Neurologic disorder
• Sexual abuse
• Family history of duplication disorder
DYSFUNCTIONAL VOIDING SYMPTOM SCORE QUESTIONAIRE
EVALUATION-VOIDING DISORDER
Physical examination
• Abnormal maneuvers – Vincent’s curtsy sign
EVALUATION-VOIDING DISORDER
• Abdominal examination:
- Abdominal masses
- Palpable bladder / kidney
- Stool-filled colon
- Abdominal muscle tone
EVALUATION-VOIDING DISORDER
• Back and spine examination:
- Significant scoliosis / kyphosis
- Asymmetry of the buttocks, legs, or feet
- Spinal or sacral anomaly
- Naevus
- Small dimple
- Tuft of hair
- Dermal vascular malformation
- Subcutaneous lipoma
EVALUATION-VOIDING DISORDER
• Neurological examination:
- look for any neurological deficit
• Genitalia:
- Location and size of the urethral meatus
- Labial adhesions
- Vaginal pooling
VOIDING DIARY
EVALUATION-VOIDING DISORDER
Investigations
Urine analysis:
Glycosuria
Bacteriuria
Proteinuria
hyposthenuria
Pyuria
EVALUATION - VOIDING DISORDER
USG abdomen:
 Rule out structural anomalies of kidneys and urinary
tract.
 Dilatation of upper urinary tract
 Bladder size
 Wall thickness - >5mm on empty bladder is abnormal
 Evidence of cystitis.
 PVR (Post void residue) determination: >5ml is
significant in a child within 5 min of voiding.
EVALUATION - VOIDING DISORDER
Micturating Cystourethrogram(MCU):
–Presence/absence of reflux
–Bladder instability
• Spinning top bladder
• Bladder wall irregularity (trabeculations)
• elongated bladder shape
• filling of posterior urethra
EVALUATION - VOIDING DISORDER
• MRI LS spine:
- If neurogenic bladder suspected.
• Urodynamic Study :
- Invasive study reproducing the patient’s
voiding complaints and offer a
pathophysiologic explanation to the problem.
Plan for correct therapeutic intervention
TREATMENT - VOIDING DISORDER
–Treatment of intercurrent infections
–Institution of structured voiding patterns with
good hydration, hygiene and timed voiding.
–Treatment of coexisting bowel disorders
• Constipation: Increased fluid intake, high
fibre diet, laxative(polyethylene glycol)
• Encopresis: Child-parent psychological
counseling.
TREATMENT - VOIDING DISORDER
Pharmacotherapy:
• Oxybutinin - start with 5mg/day BD to a
max of 15-20mg/day
• Tolterodine - 1mg BD for children aged 5-10
yrs. Minimum side-effects.
• Side effects: Dry mouth, Constipation,
Somnolence, Nausea
TREATMENT - VOIDING DISORDER
Biofeedback therapy:
 Retraining children to develop relaxed voiding
 Pelvic floor muscle exercise developed by keigel
 Uroflowmetry based – bell shaped urine flow curve
(6 hrs)
 EMG based – sphincter tone traces (45-60 min)
 Limitations: Requires equipment and expertise
TREATMENT - VOIDING DISORDER
Behavioral intervention:
• Useful alternative, also called as bladder
re-education initiative. It has 5 components
– Patient education
– Scheduled voiding regimen with gradual increasing
levels
– Urgency control strategies
– Self monitoring
– Positive reinforcement to learn pelvic floor muscle
relaxation
TREATMENT - VOIDING DISORDER
Combination Therapy:
–Biofeedback + alpha blockers
–Terazocin or Doxazocin- (0.5-1mg/day)
–Used in refractory cases of dyfunctional
voiding
TREATMENT - VOIDING DISORDER
Clean intermittent catheteration(CIC)
- useful in children with large PVR to lower
intravesical pressures
- instituted usually at night
- very useful in children with valve bladders
considered for renal transplantation
NOCTURNAL ENURESIS
NOCTURNAL ENURESIS
• Definition: Normal, nearly complete, evacuation of
bladder at a wrong place & time at least twice a month
after 5th year of life.
• 85% of children attain bladder control by 5 years age.
• Remaining 15% will gain continence at a rate of 15%
per year.
• By adolescence 0.5-1% continue to have enuresis.
ENURESIS INCONTINENCE
Complete evacuation of bladder Incomplete evacuation of bladder
Bed soaking wet not
Always functional Organic causes
NOCTURNAL ENURESIS
ENURESIS intermittent nocturnal incontinence
a. MONO
SYMPTOMATIC
Without any lower urinary tract symptoms
b. NON-MONO
SYMPTOMATIC
With lower urinary tract symptoms –
daytime incontinence, urgency, holding
maneuvers
c. PRIMARY Previously dry for < 6 mnths/ Never been dry
d. SECONDARY Previously dry for =/> 6 months(minimum)
NOCTURNAL ENURESIS
ETIOLOGY
Maturational delay:
• Most common cause
• Spontaneous cure rates increase with age.
• Developmental delay, Anxiety, stress.
• Boys > girls.
NOCTURNAL ENURESIS
ETIOLOGY
ADH: (circadian rhythm, more secretion at night
and peak from 4am-8am)
• Loss of circadian rhythm
• Impaired response of kidneys to ADH.
NOCTURNAL ENURESIS
ETIOLOGY
Bladder capacity:
• Imbalance between the bladder capacity and
nocturnal urine production.
• If bladder capacity is less, may lead to enuresis.
NOCTURNAL ENURESIS
ETIOLOGY
Genetics:
• 1 parent – 40% ,Both– 70% chance
• Linked with chromosomes 8,12,13 & 22
• ENUR 1 gene on long arm of chr-13
• Autosomal dominant
• modulated by environmental factors and
other genes.
NOCTURNAL ENURESIS
ETIOLOGY
 Sleep factor: Inadequate arousal– impair
vasopressin secretion– polyuria.
Co-morbid conditions:
- Constipation
-ADHD
NOCTURNAL ENURESIS
INVESTIGATIONS
Less than 5% - organic causes
Uncomplicated enuresis - no further evaluation
 Clinical & Neurological Examination
Urine R/E: Rule out infection, proteinuria and
glycosuria in all children
Voiding dairy: Urine output (frequency,volume),
fluid intake – 2 days, day time accidental voiding ,
bladder symptoms, bowel habits- 7 days
NOCTURNAL ENURESIS
USG abdomen and MCU: For suspected
neurological and urological dysfunction.
Screening test: Uroflowmetry + pelvic floor
and abdominal muscle EMG
Cystometry: Invasive and only in suspected
functional voiding disorder
NOCTURNAL ENURESIS
TREATMENT
Supportive measures Pharmacotherapy
NOCTURNAL ENURESIS
TREATMENT
Supportive measures
• Timely treatment - prevent psychological damage
to the child and provide relief to the family
• Assess the level of motivation of the child and
parents
• General advice to all enuretic children
• Active treatment after the age of 6 years.
NOCTURNAL ENURESIS
TREATMENT
Supportive measures
• Caffeinated drinks like coffee, tea and soda
should be avoided in evening.
• Adequate fluid intake :
- 40% morning
- 40% afternoon
- 20% evening.
NOCTURNAL ENURESIS
TREATMENT
Supportive measures
• Dry bed training :
a) emptying bladder before retiring to bed
b) encourage bed time resolution
c) keeping wet and dry night charts
d) rewarded for active co-operations
NOCTURNAL ENURESIS
TREATMENT
Supportive measures
• Bladder training exercises:
- for those with smaller functional bladder
capacity
- Recent trials show these are not effective.
NOCTURNAL ENURESIS
TREATMENT
Supportive measures
• Motivational therapy :
- reassurance
- emotional support
- positive reinforcement
- Gift technique
NOCTURNAL ENURESIS
TREATMENT
Supportive measures
• Behavioral modification
- Good bladder and bowel habits
• Stool softener
• Supportive parent, motivated child and
Paediatrician with time n patience.
NOCTURNAL ENURESIS
TREATMENT
Supportive measures
• Alarms:
- To elicit a conditioned response
- Awakening to the sensation of full bladder.
- Best for children >7yrs of age.
- Use at least for 6 months (min 2 -3 moths
trial)
- Continue till 14 consecutive dry nights are
achieved.
NOCTURNAL ENURESIS
Pharmacotherapy:
Treatment initiated
Continue for 2 weeks
Assess efficacy and adjust dose
If child dry
Maintain for 3 to 6 months
Gradually wean over 3 to 4 weeks
Medications for Enuresis
DRUG DOSE DURATION AGE FOR
USE
DDAVP nasal
spray
10 – 40 mcg/
day
Until 4 weeks
dry
Any if
supervised
Oxybutynin 5 – 20 mg/day 3 -6 months > 6 years
Imipramine 0.9 – 1.5
mg/kg/day
(25 – 50 mg)
3 -6 months > 7 years
Tolterodine 1 mg twice
daily
Until
uninhibited
blader
improves
5 – 10 years
NEUROGENIC BLADDER
NEUROGENIC BLADDER
• Neurogenic bladder dysfunction is usually
congenital
• Results from neural tube defects and other
spinal anomalies
• Acquired and traumatic lesions of spinal cord
are less common
NEUROGENIC BLADDER
Causes:
– Spinal dysraphism
• Meningocoele
• Meningomyelocoele
• Spina bifida occulta
• Sacral agenesis
NEUROGENIC BLADDER
Causes:
– Spinal trauma
• Sacrococcygeal teratoma
– Spinal tumours
– Degenerative disorders
• Autonomic neuropathy
• Transverse myelitis
NEUROGENIC BLADDER
Effects:
-Socially unacceptable incontinence
-Renal failure
Types:
1. Bladder sphincter dysynergia
2. Synergic low pressure incontinent bladder
3. Completely denervated bladder
NEUROGENIC BLADDER
Evaluation:
-Physical examination
-MRI LS spine
-USG
-MCU
-DMSA
NEUROGENIC BLADDER
Treatment:
– Constipation- laxatives
– Crede’s maneuver- suprapubic massage causes
reflex bladder contraction and should be avoided.
– CIC: Improves the outcome significantly by
maintaining low intravesical pressures
– Oxybutinin: decreases detrusor overactivity
– Antibiotics: before CIC in dilated upper tract.
NEUROGENIC BLADDER
Treatment:
– Surgery:
• Bladder augmentation in low capacity bladder
• Urinary diversion for upper tract deterioration
despite conservative measures
Sphincterotomy in bladder outlet obstruction
Reimplantation of ureters in vesicoreteral reflux.
Case 1:
A twelve year old male child presented
with complaints of intermittent pain in the
shaft of the penis of 3 years duration.
associated with urgency and frequency.
Case 1:
Ultrasound had shown- evidence of cystitis,
IVP had been interpreted as showing a trabeculated
bladder.
Cystoscopy reported normal.
Uroflow EMG was advised to confirm / exclude
dysfunctional voiding.
Uroflow showed a bell shaped curve with a peak flow of
20mls/sec.
What was striking was the complete silence of the
external sphincter during voiding indicating good synergy
between the detrusor and the external sphincter
Case 1:
Voiding dysfunction was therefore totally eliminated.
Once dysfunctional voiding is identified on the Uroflow EMG
remedial measures can be instituted.
The simplest is double voiding – asking the child to go back, sit on
the toilet and void again.
This is efficacious for the preoccupied child who is busy with a
computer game or a TV programme and tries to postpone voiding.
For the older adolescent who has made a habit of not voiding in
school and has thereby enlarged her bladder to an unusual capacity,
timed voiding is the answer.
these children should be encouraged to drink more fluids and to void
at regular intervals.
Case 2:
A ten year old obese girl was brought with
severe wetting and constipation refractory to
anticholinergics and alpha blockers.
Case 2:
Micturiting Cystourethrogram showed vaginal
pooling after voiding and a dribble on standing
up.
Uroflow EMG showed an interrupted pattern
of voiding (staccato voiding) with low peak flow
and pronounced detrusor activity.
Case 2:
She was advised
1) Anticholinergics to prevent unstable bladder
contractions,
2) Diazepam at night to enable to relax chronically
contracted external sphincter
3) Double voiding and relaxed voiding aiming to
completely empty bladder and to eliminate dribbling
4) Posture on the toilet was reversed to eliminate
vaginal voiding. Reverse posture is to spread the
thighs wide apart, so that vaginal pooling is avoided
5) Weight reduction.
6) Treatment of constipation
REFERENCES
• Nelson Textbook of Pediatrics
• Pediatric Nephrology – Srinastava & Bagga
• Practical approach to a nocturnal enuresis &
voiding dysfunction - IJPP 2012; 14(2)
• Demystifying voiding dysfunction - IJPP
2007IJPP 2012; 14(2)
THANK
YOU

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Disorders of micturation (sreemayee)

  • 1. DISORDERS OF MICTURITION Dr. Sreemayee Kundu MD PAEDIATRICS
  • 2. CONTENTS • Introduction • Physiology of micturition • Maturation of micturition & sequence • Voiding disorder-types,evaluation & treatment • Nocturnal enuresis • Neurogenic bladder
  • 3. INTRODUCTION • Urinary bladder functions as a storage organ that can empty to completion at appropriate time and place. • Problems related to bladder are often obvious like nocturnal enuresis, incontinence, dribbling or may not be apparent like recurrent UTIs, day time urgency frequency syndrome. • Early intervention may prevent renal damage from retrograde effects of high bladder pressures.
  • 4. PHYSIOLOGY OF MICTURITION FILLING • Regular peristaltic contractions move the urine from the renal pelvis to the bladder. • Sympathetic systems T11-L2 spinal segments responsible for effective bladder filling • Sympathetic & pudendal nerve mediated inhibition of detrusor contractility with closure of bladder neck & proximal urethra.
  • 5. PHYSIOLOGY OF MICTURITION EMPTYING • Contraction of detrusor muscle, mainly responsible for emptying bladder during micturition. • Bladder Neck along with elastic fibers form internal urethral sphincter • Urogenital diphragm with its skeletal muscle form external urethral sphincter. • Co-ordination among these three structures responsible for emptying. • Parasympathetic system S2-S4 for micturition.
  • 6. MATURATION OF BLADDER FETUS/ AT BIRTH Spinal cord reflex Spontaneous micturition 1-2 YEARS bladder capacity + Neural maturation of frontal and parietal lobe Sensation of bladder filling present but voiding is reflex 3-4 YEARS Voluntary control of EUS when awake(day time) Can delay micturition 5 YEARS Cortical inhibitory control achieved Dry by night >6 yrs Ability to initiate voiding even when bladder has not given a “full” signal Voiding under socially acceptable circumstances
  • 7. MATURATION SEQUENCE • Night time fecal continence • Daytime fecal continence • Daytime urine continence • Night time urine continence
  • 8. DEFINITIONS (ICCS) 1. DECREASED DAYTIME VOIDING FREQUENCY </= 3 voidings/day 2. INCREASED DAYTIME VOIDING FREQUENCY >/= 8 voidings/day 3. POLYURIA >2 lit/m2 BSA - 24hrs > 5ml/kg/hr 4. EXPECTED BLADDER CAPACITY [30+ (age in yrs x 30)] ml 5. RESIDUAL URINE Excess of 5-20ml indicates incomplete bladder emptying
  • 9. DEFINITIONS (ICCS) URINARY INCONTINENCE uncontrollable leakage of urine • CONTINUOUS continuous leakage of urine , not in discrete portions malformation or iatrogenic damage • INTERMITTENT leakage in discrete portions during day/night night = nocturnal enuresis • URGE INCONTINENCE associated with urgency Ex - overactive bladder • VOIDING POSTPONEMENT In the presence of habitual holding maneuvers
  • 10.
  • 11. VOIDING DISORDER • Definition: These consist of essentially functional, abnormal patterns of micturition in the presence of an intact neuronal pathway and without any congenital/anatomical abnormality of the urinary tract. Also called as Functional incontinence. • Functional UI may be caused by disturbances in the filling (storage) phase, the voiding phase, or a combination of both.
  • 12. Classification Voiding Disorders (based on clinical symptoms & urodynamics study) Overactive bladder Dysfunctional voiding (filling phase disorder) (evacuation phase disorder) -staccato -fractional dysynergia hypotonic/underactive bladder
  • 13. VOIDING DISORDER OVERACTIVE BLADDER • It is a filling phase defect. • Characterized by frequent episodes of urgency. • Countered by contractions of pelvic floor muscles and holding maneuvers. • Due to underlying detrusor overactivity. • Also called detrusor instability. • Can be associated with incontinence (urge incontinence).
  • 14. VOIDING DISORDER OVERACTIVE BLADDER • Functional bladder capacity is small. • Voiding pattern is normal with appropriate relaxation of pelvic floor muscles. • Associated with constipation. ( triggers detrusor contraction by stimulation of stretch receptors in bladder wall by extrinsic fecal mass or by colonic contractions via shared neural pathways.)
  • 15. VOIDING DISORDER DYSFUNCTIONAL VOIDING • It is a voiding phase defect • Characterized by infrequent voiding and straining to void. • Associated with bladder-sphincter incoordination. • Referred as bladder-sphincter dysynergia. • It may be staccato or fractional voiding.
  • 16. VOIDING DISORDER DYSFUNCTIONAL VOIDING Staccato voiding: • Bursts of pelvic floor muscle activity during voiding • Causes interruption in the urine flow. • Prolonged flow duration and incomplete voiding.
  • 17. VOIDING DISORDER DYSFUNCTIONAL VOIDING Fractionated voiding: • Micturition occurs in several small fractions. • Emptying is incomplete due to hypo-activity of detrusor muscles. • Abdominal muscles are used to increase pressure on the bladder (valsalva voiding). • Irregular but continuous flow rate.
  • 18. VOIDING DISORDER DYSFUNCTIONAL VOIDING Underactive bladder: • Due to under active detrusor muscle. • Long term result of bladder-sphincter dysynergia with detrusor decompensation. • Large post residual volume • Recurrent UTIs. • May lead to overflow incontinence.
  • 19. VOIDING DISORDER Hinman Syndrome • Severe form of detrusor-sphincter dysynergia. • Failure of external sphincter to relax during voiding. • Trabeculated bladder develops a high pressure state with B/L VUR and large PVR akin to a neurogenic bladder without any obvious neurological abnormality. • Non –neurogenic neurogenic bladder.
  • 20.
  • 21. OTHER VOIDING DISORDER GIGGLE INCONTINENCE • Involuntary voiding during sudden laughter • Seen in school girls and adolescents. • Results from instability of bladder • Due to inappropriate detrusor contraction and sudden relaxation of urinary sphincter.
  • 22. OTHER VOIDING DISORDER VOIDING POSTPONEMENT • Postpones imminent micturition until overwhelmed by urgency. • Uses holding maneuvers. • Associated with low frequency. • Over-activity of urethral sphincter is a behavioral maladjustment. • It is associated with other behavioral problems in these children.
  • 23. OTHER VOIDING DISORDER VAGINAL VOIDING • Seen in obese girls using western toilet. • May not part their thighs adequately. • This result in incontinence on standing due to vaginal pooling. • Volume of urine – 5-10 ml. • Most common cause – Labial adhesion
  • 24. OTHER VOIDING DISORDER POLLAKIURIA • Child voids extremely frequently at 30-60 min interval. • No dysuria, pain or incontinence. • Nocturia is unusual. • No organic cause. • Stress related.
  • 25. EVALUATION- VOIDING DISORDER History – should assess the following : • Pattern of incontinence • Frequency of micturition • Volume of urine • Association with urgency or gigling • Sensation of incomplete voiding
  • 26. EVALUATION- VOIDING DISORDER History – should assess the following : • Urine stream • Recurrent UTI • Constipation • Neurologic disorder • Sexual abuse • Family history of duplication disorder
  • 27. DYSFUNCTIONAL VOIDING SYMPTOM SCORE QUESTIONAIRE
  • 28.
  • 29. EVALUATION-VOIDING DISORDER Physical examination • Abnormal maneuvers – Vincent’s curtsy sign
  • 30. EVALUATION-VOIDING DISORDER • Abdominal examination: - Abdominal masses - Palpable bladder / kidney - Stool-filled colon - Abdominal muscle tone
  • 31. EVALUATION-VOIDING DISORDER • Back and spine examination: - Significant scoliosis / kyphosis - Asymmetry of the buttocks, legs, or feet - Spinal or sacral anomaly - Naevus - Small dimple - Tuft of hair - Dermal vascular malformation - Subcutaneous lipoma
  • 32. EVALUATION-VOIDING DISORDER • Neurological examination: - look for any neurological deficit • Genitalia: - Location and size of the urethral meatus - Labial adhesions - Vaginal pooling
  • 33.
  • 36. EVALUATION - VOIDING DISORDER USG abdomen:  Rule out structural anomalies of kidneys and urinary tract.  Dilatation of upper urinary tract  Bladder size  Wall thickness - >5mm on empty bladder is abnormal  Evidence of cystitis.  PVR (Post void residue) determination: >5ml is significant in a child within 5 min of voiding.
  • 37. EVALUATION - VOIDING DISORDER Micturating Cystourethrogram(MCU): –Presence/absence of reflux –Bladder instability • Spinning top bladder • Bladder wall irregularity (trabeculations) • elongated bladder shape • filling of posterior urethra
  • 38.
  • 39.
  • 40. EVALUATION - VOIDING DISORDER • MRI LS spine: - If neurogenic bladder suspected. • Urodynamic Study : - Invasive study reproducing the patient’s voiding complaints and offer a pathophysiologic explanation to the problem. Plan for correct therapeutic intervention
  • 41.
  • 42. TREATMENT - VOIDING DISORDER –Treatment of intercurrent infections –Institution of structured voiding patterns with good hydration, hygiene and timed voiding. –Treatment of coexisting bowel disorders • Constipation: Increased fluid intake, high fibre diet, laxative(polyethylene glycol) • Encopresis: Child-parent psychological counseling.
  • 43. TREATMENT - VOIDING DISORDER Pharmacotherapy: • Oxybutinin - start with 5mg/day BD to a max of 15-20mg/day • Tolterodine - 1mg BD for children aged 5-10 yrs. Minimum side-effects. • Side effects: Dry mouth, Constipation, Somnolence, Nausea
  • 44. TREATMENT - VOIDING DISORDER Biofeedback therapy:  Retraining children to develop relaxed voiding  Pelvic floor muscle exercise developed by keigel  Uroflowmetry based – bell shaped urine flow curve (6 hrs)  EMG based – sphincter tone traces (45-60 min)  Limitations: Requires equipment and expertise
  • 45. TREATMENT - VOIDING DISORDER Behavioral intervention: • Useful alternative, also called as bladder re-education initiative. It has 5 components – Patient education – Scheduled voiding regimen with gradual increasing levels – Urgency control strategies – Self monitoring – Positive reinforcement to learn pelvic floor muscle relaxation
  • 46. TREATMENT - VOIDING DISORDER Combination Therapy: –Biofeedback + alpha blockers –Terazocin or Doxazocin- (0.5-1mg/day) –Used in refractory cases of dyfunctional voiding
  • 47. TREATMENT - VOIDING DISORDER Clean intermittent catheteration(CIC) - useful in children with large PVR to lower intravesical pressures - instituted usually at night - very useful in children with valve bladders considered for renal transplantation
  • 48.
  • 50. NOCTURNAL ENURESIS • Definition: Normal, nearly complete, evacuation of bladder at a wrong place & time at least twice a month after 5th year of life. • 85% of children attain bladder control by 5 years age. • Remaining 15% will gain continence at a rate of 15% per year. • By adolescence 0.5-1% continue to have enuresis. ENURESIS INCONTINENCE Complete evacuation of bladder Incomplete evacuation of bladder Bed soaking wet not Always functional Organic causes
  • 51. NOCTURNAL ENURESIS ENURESIS intermittent nocturnal incontinence a. MONO SYMPTOMATIC Without any lower urinary tract symptoms b. NON-MONO SYMPTOMATIC With lower urinary tract symptoms – daytime incontinence, urgency, holding maneuvers c. PRIMARY Previously dry for < 6 mnths/ Never been dry d. SECONDARY Previously dry for =/> 6 months(minimum)
  • 52. NOCTURNAL ENURESIS ETIOLOGY Maturational delay: • Most common cause • Spontaneous cure rates increase with age. • Developmental delay, Anxiety, stress. • Boys > girls.
  • 53. NOCTURNAL ENURESIS ETIOLOGY ADH: (circadian rhythm, more secretion at night and peak from 4am-8am) • Loss of circadian rhythm • Impaired response of kidneys to ADH.
  • 54. NOCTURNAL ENURESIS ETIOLOGY Bladder capacity: • Imbalance between the bladder capacity and nocturnal urine production. • If bladder capacity is less, may lead to enuresis.
  • 55. NOCTURNAL ENURESIS ETIOLOGY Genetics: • 1 parent – 40% ,Both– 70% chance • Linked with chromosomes 8,12,13 & 22 • ENUR 1 gene on long arm of chr-13 • Autosomal dominant • modulated by environmental factors and other genes.
  • 56. NOCTURNAL ENURESIS ETIOLOGY  Sleep factor: Inadequate arousal– impair vasopressin secretion– polyuria. Co-morbid conditions: - Constipation -ADHD
  • 57. NOCTURNAL ENURESIS INVESTIGATIONS Less than 5% - organic causes Uncomplicated enuresis - no further evaluation  Clinical & Neurological Examination Urine R/E: Rule out infection, proteinuria and glycosuria in all children Voiding dairy: Urine output (frequency,volume), fluid intake – 2 days, day time accidental voiding , bladder symptoms, bowel habits- 7 days
  • 58. NOCTURNAL ENURESIS USG abdomen and MCU: For suspected neurological and urological dysfunction. Screening test: Uroflowmetry + pelvic floor and abdominal muscle EMG Cystometry: Invasive and only in suspected functional voiding disorder
  • 60. NOCTURNAL ENURESIS TREATMENT Supportive measures • Timely treatment - prevent psychological damage to the child and provide relief to the family • Assess the level of motivation of the child and parents • General advice to all enuretic children • Active treatment after the age of 6 years.
  • 61. NOCTURNAL ENURESIS TREATMENT Supportive measures • Caffeinated drinks like coffee, tea and soda should be avoided in evening. • Adequate fluid intake : - 40% morning - 40% afternoon - 20% evening.
  • 62. NOCTURNAL ENURESIS TREATMENT Supportive measures • Dry bed training : a) emptying bladder before retiring to bed b) encourage bed time resolution c) keeping wet and dry night charts d) rewarded for active co-operations
  • 63. NOCTURNAL ENURESIS TREATMENT Supportive measures • Bladder training exercises: - for those with smaller functional bladder capacity - Recent trials show these are not effective.
  • 64. NOCTURNAL ENURESIS TREATMENT Supportive measures • Motivational therapy : - reassurance - emotional support - positive reinforcement - Gift technique
  • 65. NOCTURNAL ENURESIS TREATMENT Supportive measures • Behavioral modification - Good bladder and bowel habits • Stool softener • Supportive parent, motivated child and Paediatrician with time n patience.
  • 66. NOCTURNAL ENURESIS TREATMENT Supportive measures • Alarms: - To elicit a conditioned response - Awakening to the sensation of full bladder. - Best for children >7yrs of age. - Use at least for 6 months (min 2 -3 moths trial) - Continue till 14 consecutive dry nights are achieved.
  • 67.
  • 68. NOCTURNAL ENURESIS Pharmacotherapy: Treatment initiated Continue for 2 weeks Assess efficacy and adjust dose If child dry Maintain for 3 to 6 months Gradually wean over 3 to 4 weeks
  • 69. Medications for Enuresis DRUG DOSE DURATION AGE FOR USE DDAVP nasal spray 10 – 40 mcg/ day Until 4 weeks dry Any if supervised Oxybutynin 5 – 20 mg/day 3 -6 months > 6 years Imipramine 0.9 – 1.5 mg/kg/day (25 – 50 mg) 3 -6 months > 7 years Tolterodine 1 mg twice daily Until uninhibited blader improves 5 – 10 years
  • 71. NEUROGENIC BLADDER • Neurogenic bladder dysfunction is usually congenital • Results from neural tube defects and other spinal anomalies • Acquired and traumatic lesions of spinal cord are less common
  • 72. NEUROGENIC BLADDER Causes: – Spinal dysraphism • Meningocoele • Meningomyelocoele • Spina bifida occulta • Sacral agenesis
  • 73. NEUROGENIC BLADDER Causes: – Spinal trauma • Sacrococcygeal teratoma – Spinal tumours – Degenerative disorders • Autonomic neuropathy • Transverse myelitis
  • 74. NEUROGENIC BLADDER Effects: -Socially unacceptable incontinence -Renal failure Types: 1. Bladder sphincter dysynergia 2. Synergic low pressure incontinent bladder 3. Completely denervated bladder
  • 76. NEUROGENIC BLADDER Treatment: – Constipation- laxatives – Crede’s maneuver- suprapubic massage causes reflex bladder contraction and should be avoided. – CIC: Improves the outcome significantly by maintaining low intravesical pressures – Oxybutinin: decreases detrusor overactivity – Antibiotics: before CIC in dilated upper tract.
  • 77. NEUROGENIC BLADDER Treatment: – Surgery: • Bladder augmentation in low capacity bladder • Urinary diversion for upper tract deterioration despite conservative measures Sphincterotomy in bladder outlet obstruction Reimplantation of ureters in vesicoreteral reflux.
  • 78. Case 1: A twelve year old male child presented with complaints of intermittent pain in the shaft of the penis of 3 years duration. associated with urgency and frequency.
  • 79.
  • 80.
  • 81. Case 1: Ultrasound had shown- evidence of cystitis, IVP had been interpreted as showing a trabeculated bladder. Cystoscopy reported normal. Uroflow EMG was advised to confirm / exclude dysfunctional voiding. Uroflow showed a bell shaped curve with a peak flow of 20mls/sec. What was striking was the complete silence of the external sphincter during voiding indicating good synergy between the detrusor and the external sphincter
  • 82. Case 1: Voiding dysfunction was therefore totally eliminated. Once dysfunctional voiding is identified on the Uroflow EMG remedial measures can be instituted. The simplest is double voiding – asking the child to go back, sit on the toilet and void again. This is efficacious for the preoccupied child who is busy with a computer game or a TV programme and tries to postpone voiding. For the older adolescent who has made a habit of not voiding in school and has thereby enlarged her bladder to an unusual capacity, timed voiding is the answer. these children should be encouraged to drink more fluids and to void at regular intervals.
  • 83. Case 2: A ten year old obese girl was brought with severe wetting and constipation refractory to anticholinergics and alpha blockers.
  • 84. Case 2: Micturiting Cystourethrogram showed vaginal pooling after voiding and a dribble on standing up. Uroflow EMG showed an interrupted pattern of voiding (staccato voiding) with low peak flow and pronounced detrusor activity.
  • 85. Case 2: She was advised 1) Anticholinergics to prevent unstable bladder contractions, 2) Diazepam at night to enable to relax chronically contracted external sphincter 3) Double voiding and relaxed voiding aiming to completely empty bladder and to eliminate dribbling 4) Posture on the toilet was reversed to eliminate vaginal voiding. Reverse posture is to spread the thighs wide apart, so that vaginal pooling is avoided 5) Weight reduction. 6) Treatment of constipation
  • 86. REFERENCES • Nelson Textbook of Pediatrics • Pediatric Nephrology – Srinastava & Bagga • Practical approach to a nocturnal enuresis & voiding dysfunction - IJPP 2012; 14(2) • Demystifying voiding dysfunction - IJPP 2007IJPP 2012; 14(2)

Editor's Notes

  1. Children with attention deficit hyperactivity disorder have a greater risk of incontinence and may be more challenging to treat
  2. Children with attention deficit hyperactivity disorder have a greater risk of incontinence and may be more challenging to treat
  3. part of the spinal cord is split, usually at the level of the upper lumbar vertebra.
  4. part of the spinal cord is split, usually at the level of the upper lumbar vertebra.
  5. Treat infections before start of anticholinergics
  6. Treat infections before start of anticholinergics
  7. Common problem often causing considerable distress to the child and his family
  8. Sex difference: Till eleven years of age boys > girls(2:1), thereafter it is similar or slightly higher in females.
  9. Functional capacity-volume of urine bladder can hold when awake or asleep(> in enuresis) largest volume voided after measuring each void for 3 consecutive days and is compared to the estimated bladder capacity for that age.
  10. Functional capacity-volume of urine bladder can hold when awake or asleep(> in enuresis) largest volume voided after measuring each void for 3 consecutive days and is compared to the estimated bladder capacity for that age.
  11. Functional capacity-volume of urine bladder can hold when awake or asleep(> in enuresis) largest volume voided after measuring each void for 3 consecutive days and is compared to the estimated bladder capacity for that age.
  12. enuretic children are often deep sleepers.Wake up signals from full bladder may switch deep sleep-light sleep but not full arousal.
  13. enuretic children are often deep sleepers.Wake up signals from full bladder may switch deep sleep-light sleep but not full arousal.
  14. Encouraged to drink more water during morning and hold urine for increased duration after feeling a desire to void.
  15. Encouraged to drink more water during morning and hold urine for increased duration after feeling a desire to void.
  16. Encouraged to drink more water during morning and hold urine for increased duration after feeling a desire to void.
  17.  (1-desamino-8-D-arginine vasopressin)
  18.  (1-desamino-8-D-arginine vasopressin)