Bladder innervation, physiology of micturition
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Bladder innervation, physiology of micturition, voiding dysfunction

Bladder innervation, physiology of micturition, voiding dysfunction

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    Bladder innervation, physiology of micturition Bladder innervation, physiology of micturition Presentation Transcript

    • BLADDER INNERVATION PHYSIOLOGY OF MICTURITION VOIDING DYSFUNCTION DR. LOKANATH REDDY JUNIOR RESIDENT DEPT. OF PAEDIATRICS KASTURBA 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 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
    • 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.
    • 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)
    • 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 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
    • 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.
    • 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.
    • 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
    • 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 URINE CONTINENCE DAY TIME URINE CONTINENCE DAY TIME FECAL CONTINENCE NIGHT TIME FECAL CONTINENCE
    • 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 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
    • 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 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
    • 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 PHASES 1. Ia – small rise, Initial filling 2. Ib – long, nearly flat, subseuent filling 3. 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 Oxybutinin Bladder training Response Normal Reassure
    • 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 failure TYPES: 1. Bladder sphincter dyssynergia 2. Synergic low pressure incontinent bladder 3. Completely denervated bladder Evaluation: 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