This document discusses the anatomy, physiology, and dysfunction of the urinary bladder and micturition process. It begins with an overview of bladder anatomy, including its parts and innervation. It then covers the normal physiology of bladder filling and emptying, controlled by the brain, spinal cord, and peripheral nerves. Different types of bladder dysfunction are described, such as overactive bladder, dysfunctional voiding, underactive bladder, and detrusor-sphincter dyssynergia. Evaluation of voiding disorders and urodynamic studies are also mentioned. In summary, the document provides a comprehensive review of the structure and function of the urinary bladder and the potential sites of dysfunction.

1. BLADDER INNERVATION
PHYSIOLOGY OF MICTURITION
VOIDING DYSFUNCTION
DR. LOKANATH REDDY
JUNIOR RESIDENT
DEPT. OF PAEDIATRICS
KASTURBA MEDICAL COLLEGE, MANIPAL

2. HEADINGS
 Introduction
 Anatomy
 Physiology of micturition
 Bladder innervation
 Voiding dysfunction- evaluation and management
 Urodynamic studies
 Nocturnal enuresis

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
enuresis, incontinence 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. URINARY BLADDER ANATOMY
 The bladder is the most anterior element of the pelvic
viscera. Situated in the pelvic cavity when empty, but
expands superiorly into the abdominal cavity when full.
 The urinary bladder is abdominal at birth, positioned at
the extraperitoneal area of the lower abdominal wall.
Around the 5th or 6th year of age the bladder gradually
descends into the area of the true (minor) pelvis.

5. URINARY BLADDER ANATOMY
It has 4 parts
 Apex
 Base
 Superior surface
 Inferolateral surfaces

6. URINARY BLADDER ANATOMY
 The mucosal lining on the base of
the bladder is smooth and firmly
attached to the underlying smooth
muscle coat of the wall-unlike
elsewhere in the bladder where the
mucosa is folded and loosely
attached to the wall. The smooth
triangular area between the openings
of the ureters and urethra on the
inside of the bladder is known as the
trigone.

7. URINARY BLADDER ANATOMY
Ureterovesical Junction
 As the ureter approaches the bladder, 2 to 3 cm from the
bladder, a fibromuscular sheath (of Waldeyer) extends
longitudinally over the ureter and follows it to the trigone.
 The ureter pierces the bladder wall obliquely, travels 1.5 to
2 cm, and terminates at the ureteral orifice. As it passes
through a hiatus in the detrusor (intramural ureter), it is
compressed and narrows considerably.
 The intravesical portion of the ureter lies beneath the
urothelium, it is backed by a strong plate of detrusor
muscle. With bladder filling, this arrangement is thought to
result in passive occlusion of the ureter, like a flap valve.

8. URINARY BLADDER ANATOMY
 This anatomic arrangement helps prevent reflux during
bladder filling by fixing and applying tension to the
ureteral orifice. As the bladder fills, its lateral wall
telescopes outward on the ureter, thereby increasing
intravesical ureteral length.
 Vesicoureteral reflux is thought to result from
insufficient submucosal ureteral length and poor
detrusor backing.
 Chronic increases in intravesical pressure resulting from
bladder outlet obstruction can cause herniation of the
bladder mucosa through the weakest point of the hiatus
above the ureter and produce a “Hutch diverticulum”
and reflux.

9. URINARY BLADDER ANATOMY
Detrusor muscle

10. URINARY BLADDER ANATOMY
Transitional epithelium : Allows expansion of bladder without
significant rise in intravesical pressure

11. URINARY BLADDER ANATOMY

12. PHYSIOLOGY OF MICTURITION
FILLING
 The walls of the ureters contain smooth muscle arranged in spiral,
longitudinal, and circular bundles, but distinct layers of muscle are
not seen.
 Regular peristaltic contractions occurring one to five times per
minute move the urine from the renal pelvis to the bladder, where it
enters in spurts synchronous with each peristaltic wave.
 The ureters pass obliquely through the bladder wall and, although
there are no ureteral sphincters as such, the oblique passage tends
to keep the ureters closed except during peristaltic waves,
preventing reflux of urine from the bladder.
 Expected bladder capacity = [30+ (age in yrs x 30)] ml

13. PHYSIOLOGY OF MICTURITION
EMPTYING
 Contraction of the circular muscle, which is called the
detrusor muscle, is mainly responsible for emptying the
bladder during micturition.
 Muscle bundles pass on either side of the urethra, and
these fibers are sometimes called the internal urethral
sphincter (smooth muscle) although they do not encircle
the urethra.
 Farther along the urethra is a sphincter of skeletal
muscle, the sphincter of the membranous urethra,
external urethral sphincter.

14. PHYSIOLOGY OF MICTURITION
BLADDER
INNERVATION
 Micturition is
fundamentally a
spinal reflex
facilitated and
inhibited by higher
brain centers and, like
defecation, subject to
voluntary facilitation
and inhibition
(Sympathetic)
(Somatic)
(Parasympathetic)

15. TYPES OF NERVES NERVE FIBRES ACTION COMMENTS
SYMPATHETIC HYPOGASTRIC
NERVES(L1,L2,L3)
INFERIOR
MESNTERIC
GANGLION
motor to internal
urethral sphincter,
inhibitory to
detrusor
No significant role in
micturition; along wit IUS prevent
reflux of semen into the bladder
during ejaculation
PARASYMPATHETIC PELVIC NERVES
(S2,S3,S4)
motor to detrusor
inhibitory to
internal urethral
sphincter
Stretch receptors present on the
wall of the urinary bladder
 Sensory fibers in the pelvic
nerve  intermediolateral column
of spinal cord  parasympathetic
nerves Muscarinic receptors 
emptying of urinary bladder
SOMATIC PUDENDAL NERVES
(S2,S3,S4)
Voluntary control of
External urethral
sphincter
This maintains the tonic contractions
of the skeletal muscle fibers of the
external sphincter, so that this
sphincter is contracted always.
During micturition this nerve is
inhibited, causing relaxation of the
external sphincter and voiding of
urine.
SENSORY HYPOGASTRIC,
PELVIC AND
PUDENDAL NERVES
Cortical sensation

16. PHYSIOLOGY OF MICTURITION
Cortical center
• Second frontal gyrus(paracental lobule)
• Inhibitory to pontine center
Brain stem center
• Pons- Barrington nucleus
• Facilitatory to micturition
Sacral spinal cord (Onuf nucleus)
• Parasympathetic (s2,S3,s4)
• Reflex evacuation

17. PHYSIOLOGY OF MICTURITION
 Afferents to Spinal cord  sphincter relaxation
 Afferents to Pons  Contraction of detrusor
 Spinal center: Reflex ill-sustained contractions of
detrusor – incomplete evacuation
 Pontine center: Coordinating center.
Synchronization and maintenance of sustained
contractions to complete evacuation.
 Cortical Center: Controls pontine center till a
suitable socially acceptable situation for micturition
is available.

18. PHYSIOLOGY OF MICTURITION
CORTICAL BLADDER:
Physiologic: Newborns and infants – periodic complete
evacuation.
Pathologic:
 Lesion in paracentral lobule (cerebral palsy, multiple
sclerosis, trauma, infarcts)
 Uncontrolled evacuation in socially unacceptable situations.
 Since pontine arc is intact evacuation is complete, no
residual urine and coordination is good, no detrusor
sphincter dyssynergia.
 No VUR, “Safe bladder.”
 Associated with dementia (frontal lobe).

19. PHYSIOLOGY OF MICTURITION
SPINAL/UMN/HYPER REFLEXIC BLADDER
 Transection above the level of cord and below the level
of pons (transverse myelitis, trauma)
 Acute spinal shock stage: Bladder remains toneless with
large volume of urine.
 Post spinal shock stage:
 Bladder tone recovers, Spinal arc is established 
Hypertonic bladder with small capacity which empties
suddenly and reflexly with the help of spinal center
(Automatic bladder)

20. PHYSIOLOGY OF MICTURITION
 Residual urine due to incomplete evacuation
 Detrusor sphincter dyssynergia
 VUR – infections, renal damage “Unsafe bladder”

21. PHYSIOLOGY OF MICTURITION
LMN/AREFLEXIC BLADDER:
 Lesion in at/below spinal level (anterior horn cell,
nerve)
 No spinal reflex – areflexic, huge capacity bladder
 Overflow incontinence
 High residual volume - infections

22. PHYSIOLOGY OF MICTURITION
SENSORY DENERVATED BLADDER
 Afferent sensory limb is lost (tabes dorsalis, diabetic
neuropathy), not seen in children
 No bladder sensation
 Overflow incontinence
 Can void with straining in a timetable fashion, but
emptying is incomplete.

23. PHYSIOLOGY OF MICTURITION
MOTOR PARALYTIC BLADDER
 Efferent motor limb is damaged
 Bladder sensation is present but cannot void
 Can void with manual compressions
 Rare in clinical settings
 May be seen transiently in Guillain Barrie
Syndrome, poliomyelitis.

24. PHYSIOLOGY OF MICTURITION
AUTONOMOUS BLADDER
 Combined involvement of both sensory and motor
limbs (Cauda equina lesions, spina bifida)
 Local vesical plexus takes over the control and
functions as autonomous bladder
 Continuous dribbling
 Incomplete evacuation
 High residual volumes

25. 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

26. MATURATION SEQUENCE
NIGHT TIME URINE CONTINENCE
DAY TIME URINE CONTINENCE
DAY TIME FECAL CONTINENCE
NIGHT TIME FECAL CONTINENCE

27. VOIDING DYSFUNCTION
 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.

28. TERMINOLOGY
1. DECREASED DAYTIME
VOIDING FREQUENCY
</= 3 voidings/day
2. INCREASED DAYTIME
VOIDING FREQUENCY
>/= 8 voidings/day
3. POLYURIA > 2 lit/m2
4. EXPECTED BLADDER
CAPACITY
[30+ (age in yrs x 30)] ml

29. TERMINOLOGY
1. URINARY
INCONTINENCE
uncontrollable leakage
of urine
a. CONTINUOUS continuous leakage of
urine , not in discrete
portions
malformation or
iatrogenic damage
b. INTERMITTENT leakage in discrete
portions during
day/night
night = nocturnal
enuresis
c. URGE
INCONTINENCE
associated with urgency overactive bladder
d. VOIDING
POSTPONEMENT
In the presence of
habitual holding
maneuvers

30. TERMINOLOGY
OVERACTIVE BLADDER Urgency
UNDERACTIVE BLADDER
(LAZY BLADDER)
Low voiding frequency + to
increase intra abdominal
pressure to void
DYSFUNCTIONAL VOIDING Habitual contraction of
urethral sphincter during
voiding in neurologically
normal children
DETRUSOR-SPHINCTER
DYSSYNERGIA
Dysfunctional voiding in
neuropathic setting
MAXIMUM VOIDED VOLUME Largest voided volume, as
documented in bladder dairy

31. VOIDING DYSFUNCTION
Classification:
According to the International Children's Continence
Society
 Overactive bladder – filling phase defect
 Dysfunctional voiding – voiding phase defect
 Underactive bladder
 Giggle incontinence
 Detrusor-sphincter dyssynergia

32. VOIDING DYSFUNCTION
OVERACTIVE BLADDER
 Frequent episodes of urgency countered by contractions
of pelvic floor muscles and holding maneuvers (squatting,
crossing legs, sitting on heels).
 Symptoms are due to underlying detrusor overactivity
(filling phase defect).
 Bladder capacity is small. Voiding pattern is normal with
appropriate relaxation of pelvic floor muscles.
 Associated with constipation. It triggers detrusor
contraction by stimulation of stretch receptors in bladder
wall by extrinsic fecal mass or by colonic contractions via
shared neural pathways.

33. VOIDING DYSFUNCTION
DYSFUNCTIONAL VOIDING
 Voiding phase defect
 Staccato voiding: Bursts of pelvic floor muscle
activity during voiding causing interruption in the
urine flow. Prolonged flow duration and
incomplete voiding.
Uroflowmetry Demonstrating Staccato Voiding Pattern

34. VOIDING DYSFUNCTION
 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.
 Underactive bladder: Under active detrusor muscle.
Long term result of dysfunctional voiding with
detrusor decompensation. No detrusor contraction
during voiding. Large post residual volume with
recurrent UTIs.

35. VOIDING DYSFUNCTION
 Hinman syndrome: Non –neurogenic neurogenic
bladder. Severe bladder sphincter dyssynergia.
Trabeculated bladder develops a high pressure
state with B/L VUR and large PVR akin to a
neurogenic bladder without any obvious
neurological abnormality. May lead to renal
failure.
 Dysfunctional elimination syndrome: Co existence
of significant constipation along with dysfunctional
voiding.

36. VOIDING DYSFUNCTION
OTHER DISORDERS
 Voiding postponement: Postpones imminent micturition
until overwhelmed by urgency. Overactivity of urethral
sphincter is a behavioral maladjustment as it is
associated with other behavioral problems in these
children.
 Giggle incontinence: Involuntary voiding during sudden
laughter in school girls and adolescents. Instability of
bladder with inappropriate detrusor contraction.

37. VOIDING DYSFUNCTION
 Vesico-vaginal entrapment: Vaginal reflux of urine
from voiding in a knees-closed position can cause
dampness when the child assumes an upright
posture after voiding or postvoid dribbling.
 Pollakiuria: Child voids extremely frequently at 30-
60 min interval. No dysuria, pain or incontinence
and nocturia is unusual. No organic cause. Stress
related. Reassurance and psychiatric evaluation
in persistent cases.

38. DD for CHILDHOOD URINARY INCONTINENCE
 Voiding dysfunction.
 Cystitis.
 Anatomical: Bladder outlet obstruction (posterior urethral
valves). Ectopic ureter and fistula, Sphincter abnormality
(epispadias, exstrophy; urogenital sinus abnormality)
 Neuropathic- neurogenic bladder.
 Traumatic.
 Iatrogenic.
 Behavioral.

39. VOIDING DYSFUNCTION
EVALUATION OF VOIDING DISORDERS
History :
 Perinatal history
 Developmental milestones, attentiveness, academic performance at
school, behavioral issues – ADHD.
 Toilet-training process (delayed or prolonged, never achieved)
 Family issues (family stressors that include move, separation/divorce,
death, new siblings)
 History of sexual abuse – dysfunctional elimination syndrome.
 Child's current voiding and bowel pattern- Urinary stream, Constipation.
 H/O Recurrent UTI.
 Family h/o – bladder dysfunction, enuresis.
 Prior surgeries
 Medications

40. VOIDING DYSFUNCTION
 List of questions regarding bladder and bowel pattern

41. VOIDING DYSFUNCTION
Physical examination
 Abnormal maneuvers – Vincent’s curtsy sign – voiding
postponement.

42. VOIDING DYSFUNCTION
 Abdominal examination: Abdominal masses, a palpable
bladder, or stool-filled colon.
 Back and spine examination: Significant scoliosis/ kyphosis and
asymmetry of the buttocks, legs, or feet, as well as other signs
of occult neurospinal dysraphism in the lumbosacral area
(lipomeningocele, intradural lipoma, diastematomyelia, tight filum terminale,
dermoid cyst-sinus, aberrant nerve roots, anterior sacral meningocele,
cauda equina tumor,
 Look for naevus, small dimple, tuft of hair, dermal vascular malformation, or
subcutaneous lipoma
Abnormal Gluteal Cleft

43. VOIDING DYSFUNCTION
 Neurological examination: perineal sensation(s2,s3,s4)
and lumbosacral reflexes (L1,L2,L3) (standing on toes,
anal reflex, anal tone and bulbocavernosus reflex).
 Genitalia: location and size of the urethral meatus. In
girls, labial adhesions should be ruled out.
Urine analysis: Glycosuria, bacteriuria, proteinuria,
hyposthenuria and pyuria.

44. VOIDING DYSFUNCTION
USG abdomen:
 Rule out structural anomalies of kidneys and urinary tract.
 Dilatation of upper urinary tract, bladder size, wall
thickness, evidence of cystitis.
 PVR (Post void residue) determination: >5ml is significant in
a child within 5 min of voiding. should prompt further
evaluation and the institution of a double voiding regimen.
 Practical upper limit for detrusor thickness for all ages is
>2mm at bladder fullness of 50% of expected bladder
capacity
 A wall thickness of 5mm on empty bladder is abnormal.

45. VOIDING DYSFUNCTION
 Micturating Cystourethrogram(MCU):
 Presence/absence of reflux
 Delineates the posterior urethra
 Bladder instability
 Spinning top bladder
 Bladder wall irregularity (trabeculations)
 elongated bladder shape and filling of posterior urethra
 MRI LS spine: If neurogenic bladder suspected.

46. URODYNAMIC STUDIES
 Aim: Reproducing the patient’s voiding complaints and offer a
pathophysiologic explanation to the problem.
 Indications:
1. Neurogenic bladder
2. Nocturnal enuresis with diurnal symptoms especially in a
pubertal child
3. Abnormal voiding with fecal incontinence
4. Persistence of voiding difficulty after infection has been treated
5. Recurrent UTI
6. Prior to the surgery for persistent VUR
7. Anorectal anomalies with suspected voiding disorder
8. Bladder trabeculation or sphincter spasm noted during MCU

47. URODYNAMIC STUDIES
Classification:
 Non invasive:
 Uroflowmetry : Requires a potty-trained child who can
void into a container on command. The voided volume,
voiding time, and peak voiding velocity are
recorded.
 Urinary stream during voiding
 Post void residue : by USG immediately post voiding
 surface EMG : Surface electrodes during voiding

48. URODYNAMIC STUDIES
 Invasive: Require urethral catheterization and the
placement of a rectal catheter to measure abdominal
pressure and often needle electrodes for sphincter EMG.
 Risk of pain, hematuria, infection, and possible urinary
retention.
 Cystometry
 Urethral pressure studies
 Pressure-flow micturation studies
 Video-urodynamic studies
 Electrophysiologic studies

49. URODYNAMIC STUDIES
Clinical roles
 Characterization of detrusor function
 Evaluation of bladder outlet
 Evaluation of voiding function
 Diagnosis and characterization of neuropathy.

50. URODYNAMIC STUDIES
Patient preparation and precautions:
 Prior to UDS
 A working Diagnosis should be entertained
 History and physical examination
 3-day voiding diary
 UDS should be deferred in the presence of
 UTI
 Recent instrumentation (cystoscopy)
 Routine prophylactic antibiotics not necessary.

51. URODYNAMIC STUDIES
 High risk patients (cardiac valve , orthopedic
prosthesis, GU prosthesis, pacemakers) parental
antibiotic prophylaxis may be necessary.
 In children who are catheter dependent ideally
should have the catheter removed and be placed on
CIC for a period before UDS performed.
 The test should be done in private area, as few
observers as possible.

52. URODYNAMIC STUDIES
 Uroflowmetry/EMG :
 Determine the etiology of voiding dysfunction, these tests provide
the child with tangible evidence of the underlying voiding
dysfunction and may serve as forms of biofeedback in managing
the child's voiding dysfunction.
 With a uroflow , the practitioner can show the child whether he or
she is voiding with a normal stream (a bell shaped curve) or if
there is dysfunctional voiding (a staccato or fractionated stream).
In an EMG display, the child can identify his or her pelvic floor
muscles.
 A prolonged voiding pattern on the uroflow/EMG without
increased pelvic floor muscle activity in a male should raise the
suspicion of bladder outlet obstruction, a urethral stricture, or
posterior urethral valves.

53. URODYNAMIC STUDIES
CYSTOMETRY
 The relation between
intravesical pressure and
volume can be studied by
inserting a catheter and
emptying the bladder, then
recording the pressure while
the bladder is filled with 50-
mL increments of water or air
 3 PHASES
1. Ia – small rise, Initial filling
2. Ib – long, nearly flat,
subseuent filling
3. II – sharp rise, Micturition
triggered

55. Step 1
• Suspect voiding disorder
• Recurrent UTI
• Enuresis with day time symptoms
• Prior surgery for PUV with pelvicalyceal dilatation
Step 2
• Rule out anatomical/neurological cause
• H/o fluid intake, constipation
• Examination of spine and urine stream
• Urinalysis
Step 3
• Frequency/volume/accidents charting
• MCU/USG abdomen

56. Abnormal
Unclear diagnosis
Urodynamic study
Suggestive of
dysfunctional voiding
Bladder training
Biofeed back
poor
Suggestive of detrusor
overactivity/instability
Oxybutinin
Bladder training
Response
Normal
Reassure

57. VOIDING DYSFUNCTION
Step 4
• CIC for underactive bladder(lazy bladder)
or large postvoid residue and poor response
to therapy

58. VOIDING DYSFUNCTION
 TREATMENT:
 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
 Encopresis: Child-parent psychological counselling.
 Overactive bladder:
 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

59. VOIDING DYSFUNCTION
 Double voiding in VUR
 Biofeedback therapy:
 Retraining children to develop relaxed voiding
 pelvic floor muscle therapy developed by keigel for postpartum
incontinence in adult females
 Maizels first applied biofeedback in children
 Dysfunctional voiding, recurrent UTI with poor bladder emptying
and VUR
 Types
 Uroflowmetry based – bell shaped urine flow curve (6 hrs)
 EMG based – sphincter tone traces (45-60 min)
 Limitations: Requires equipment and expertise

60. VOIDING DYSFUNCTION
 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

61. VOIDING DYSFUNCTION
 These include
 Deep breathing exercises
 Pelvic floor muscle relaxation exercises
 Motivation by frequent interaction
 Voiding diary – every 2 hrs and later increased
intervals
 Assessing reduction in no of UTIs and post void residues

62. VOIDING DYSFUNCTION
 Voiding diary

63. VOIDING DYSFUNCTION
 Combination Therapy:
 Biofeedback + alpha blockers (doxazocin-
0.5-1mg/day) in refractory cases of dyfunctional
voiding
 Clean intermittent cathetriasation(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

64. NEUROGENIC BLADDER
Causes:
 Spinal dysraphism
 lipomeningocele, intradural lipoma, diastematomyelia, tight filum
terminale, dermoid cyst-sinus, aberrant nerve roots, anterior sacral
meningocele, cauda equina tumor,
 naevus, small dimple, tuft of hair, dermal vascular malformation, or
subcutaneous lipoma
 Spinal trauma
 Spinal tumours
 Degenerative disorders

65. NEUROGENIC BLADDER
Effects: Socially unacceptable incontinence
Renal failure
TYPES: 1. Bladder sphincter dyssynergia
2. Synergic low pressure incontinent bladder
3. Completely denervated bladder
Evaluation: MRI LS spine, USG, MCU, DMSA

66. 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.
 Surgery: Bladder augmentation in low capacity bladder,
sphincterotomy, reimplantation of ureters in vesicoreteral
reflux.

67. NOCTURNAL ENURESIS
 Nocturnal Enuresis is a common problem often causing
considerable distress to the child and his family.
 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 of 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
Always functional Organic causes

68. NOCTURNAL ENURESIS
 Sex difference: Till eleven years of age boys >
girls(2:1), thereafter it is similar or slightly higher in
females.
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 months
d. SECONDARY Previously dry for =/> 6 months(minimum)

69. NOCTURNAL ENURESIS
 Importance: To differentiate uncomplicated primary
monosymptomatic enuresis from non-monosymptomatic enuresis
which needs further evaluation.
ETIOLOGY:
 Maturational delay: Most common cause, as spontaneous cure
rates increase with age and the sequence to dryness mimics the
pattern seen in normal children. Boys > girls
 ADH: ADH has a circadian rhythm with more secretion at night
and peak from 4am-8am. Loss of circadian rhythm/impaired
response of kidneys to ADH may cause nocturnal enuresis.
 Bladder capacity: Imbalance between the bladder capacity and
the amount of urine voided. If bladder capacity is less, may lead
to enuresis. This is determined as the largest volume voided after
measuring each void for 3 consecutive days and is compared to
the estimated bladder capacity for that age.

70. NOCTURNAL ENURESIS
 Sleep factors: Inadequate arousal – enuretic children are often
deep sleepers. Wake up signals from full bladder may switch deep
sleep to light sleep but not full arousal. Obstructive sleep apnea
may contribute in obese children with primary mono-symptomatic
nocturnal enuresis.
 Genetics:
 1 parent affected – 40% chance
 Both parents – 70% chance
 Associated with chromosomes 8,12,13 & 22
 ENUR 1 gene on long arm of chr-13
 Autosomal dominant with reduced penetrance, modulated by
environmental factors and other genes.

71. NOCTURNAL ENURESIS
 Comorbid conditions: Associated with enuresis and may contribute to
resistance to therapy.
 Constipation
 ADHD
INVESTIGATIONS:
 Less than 5% - organic causes
 Uncomplicated enuresis - no further evaluation
 Urine R/E: to rule out infection, proteinuria and glycosuria in all
children
 Voiding dairy: Urine output and fluid intake – 2 days and
day time accidental voiding , bladder symptoms and bowel habits
– 1 week

72. NOCTURNAL ENURESIS
 USG abdomen and MCU: reserved for suspected
neurological and urological dysfunction.
 Screening test: Uroflowmetry + pelvic floor and
abdominal muscle EMG
 Cystometry: invasive and only in suspected
functional voiding disorder.

73. NOCTURNAL ENURESIS
TREATMENT:
 Aim is to prevent psychological damage to the child and to
provide relief to the family
 No single plan is ideal for any child
 Assess the level of motivation of the child and his parents
 General advice should be given to all enuretic children but
active treatment need not begin before the age of 6 years.
 Little evidence for withholding fluids in evening, random
awakening to void and negative reinforcement.
 Caffeinated drinks like coffee, tea and soda should be
avoided in evening.
 Adequate fluid intake : 40% morning, 40% afternoon and
20% in the evening.

74. NOCTURNAL ENURESIS
 Bladder training exercises: Those with smaller functional
bladder capacity. Encouraged to drink more water
during morning and hold urine for increased duration
after feeling a desire to void. Recent trials show these
are not effective.
 Motivational therapy : Reassurance and emotional
support. Positive reinforcement
 Behavioral modification : Good bladder and bowel
habits. Encourage to void frequently enough to avoid
urgency and daytime incontinence and to have a daily
bowel movement

75. NOCTURNAL ENURESIS
 Alarms: To elicit a conditioned response of
awakening to the sensation of full bladder. Best for
children >7yrs of age. Use at least for 6 months.
Continue till 14 consecutive dry nights are achieved.
 Pharmacotherapy: Last resort, 40% require
pharmacotherapy
 Desmopressin(DDAVP) nasal spray: 10-40 mcg/day,
until 4 weeks dry, any age if supervised

76. NOCTURNAL ENURESIS
 Oxybutinin: 5-20mg/day, 3-6 months, >6yrs SE:
drymouth, constipation, flushing, palpitations
 Tolterodine: 1mg BD, minimum side effects, 5-10 yrs
 Imipramine: Alter arousal sleep mechanisms. Before
bedtime 0.9-1.5mg/kg/day, 3-6 months, > 7 yrs
SE: Anxiety, palpitations, ruleout Long QT syndrome,
syncope
 Reboxetine: (NARI): without CVS toxic effects

77. REFERENCES
 Nelson textbook of pediatrics
 Campbell’s urology textbook
 The standardization of terminology of lower urinary
tract function in children and adolescence: Report
from the standardization committee of the
International children’s continence society : Tryggve
et al.
 Gray’s anatomy
 Ganong textbook of pysiology