bladder innervation, physiology of micturition
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Bladder innervation, physiology of micturition, voiding dysfunctionTRANSCRIPT
BLADDER INNERVATION PHYSIOLOGY OF MICTURITION
VOIDING DYSFUNCTIONDR. LOKANATH REDDYJUNIOR RESIDENT
DEPT. OF PAEDIATRICSKASTURBA MEDICAL COLLEGE, MANIPAL
HEADINGS
Introduction Anatomy Physiology of micturition Bladder innervation Voiding dysfunction- evaluation and
management Urodynamic studies Nocturnal enuresis
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.
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.
URINARY BLADDER ANATOMY
It has 4 parts Apex Base Superior surface Inferolateral
surfaces
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.
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.
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.
URINARY BLADDER ANATOMY
Detrusor muscle
URINARY BLADDER ANATOMY
Transitional epithelium : Allows expansion of bladder without significant rise in intravesical pressure
URINARY BLADDER ANATOMY
PHYSIOLOGY OF MICTURITIONFILLING 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
PHYSIOLOGY OF MICTURITIONEMPTYING 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.
PHYSIOLOGY OF MICTURITION
BLADDERINNERVATION 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)
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
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
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.
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).
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)
PHYSIOLOGY OF MICTURITION Residual urine due to incomplete evacuation Detrusor sphincter dyssynergia VUR – infections, renal damage “Unsafe
bladder”
PHYSIOLOGY OF MICTURITIONLMN/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
PHYSIOLOGY OF MICTURITIONSENSORY 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.
PHYSIOLOGY OF MICTURITIONMOTOR 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.
PHYSIOLOGY OF MICTURITIONAUTONOMOUS 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
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
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.
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
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
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
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
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.
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
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.
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.
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.
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.
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.
VOIDING DYSFUNCTION
EVALUATION OF VOIDING DISORDERSHistory :
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
VOIDING DYSFUNCTION
List of questions regarding bladder and bowel pattern
VOIDING DYSFUNCTION
Physical examination Abnormal maneuvers – Vincent’s curtsy
sign – voiding postponement.
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
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.
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.
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.
URODYNAMIC STUDIES
Aim: Reproducing the patient’s voiding complaints and offer a pathophysiologic explanation to the problem.
Indications: 1. Neurogenic bladder2. Nocturnal enuresis with diurnal symptoms especially in a
pubertal child3. Abnormal voiding with fecal incontinence4. Persistence of voiding difficulty after infection has been
treated5. Recurrent UTI6. Prior to the surgery for persistent VUR7. Anorectal anomalies with suspected voiding disorder8. Bladder trabeculation or sphincter spasm noted during
MCU
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
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
URODYNAMIC STUDIES
Clinical roles Characterization of detrusor function Evaluation of bladder outlet Evaluation of voiding function Diagnosis and characterization of
neuropathy.
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.
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.
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.
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 PHASES1. Ia – small rise, Initial
filling2. Ib – long, nearly flat,
subseuent filling3. II – sharp rise, Micturition
triggered
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
Abnormal
Unclear diagnosis
Urodynamic study
Suggestive of dysfunctional
voiding
Bladder training
Biofeed back
poor
Suggestive of detrusor overactivity/instability
OxybutininBladder training
Response
NormalReassure
VOIDING DYSFUNCTION
Step 4•CIC for underactive bladder(lazy bladder) or large postvoid residue and poor response to therapy
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
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
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
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
VOIDING DYSFUNCTION
Voiding diary
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
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
NEUROGENIC BLADDER
Effects: Socially unacceptable incontinence Renal failureTYPES: 1. Bladder sphincter dyssynergia
2. Synergic low pressure incontinent bladder
3. Completely denervated bladderEvaluation: 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. Surgery: Bladder augmentation in low capacity
bladder, sphincterotomy, reimplantation of ureters in vesicoreteral reflux.
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
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)
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.
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.
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
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.
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.
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
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
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
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