OVERACTIVE
BLADDER
DR.PREKSHA JAIN
DR. PRACHI DIXIT

CONTENTS
• Introduction
• Nerve supply
• Physiology of Micturition
• Urinary continence
• Definition Overactive bladder
• Etiology
• Pathophysiology
• Symptoms
• Diagnosis
• Treatment
• Differential diagnosis

Introduction
• Bladder- Detrusor, Trigone, Bladder neck
• Urethra- Proximal, Mid, Distal, Submucous & Mucous layers
• Supports to Bladder neck & urethra -
1. INTRINSIC: Rhabdosphincter, Cavernous plexus, Urethral
smooth muscles, Sympathetic activity, Estrogen
2. EXTRINSIC: Pubococcygeus, Pubourethral ligaments &
condensed endopelvic fascia, Urogenital diaphragm, uterus
& cervix, Exercise

Nerve supply of Vesicourethral unit

Micturition Reflex
Filling of bladder
Stimulation of stretch receptors
Afferent impulses via Pelvic nerve
Sacral segments of spinal cord
Efferent impulses via pelvic nerve
Contraction of detrusor Relaxation of sphincter
Flow of urine into urethra & stimulation of stretch receptors
Efferent impulses via pelvic nerve
Inhibition of pudendal nerve & relaxation external sphincter

• Once it begins it is self regenerative
• Initial contraction increases sensory impulses from bladder &
urethra. These further increase in reflex bladder contraction
• Cycle is repeated until force of bladder contraction reaches
maximum.
• HIGHER CENTRES FOR MICTURITION-
1. Inhibitory Areas: mid brain, Frontal cerebral cortex
2. Facilitatory Areas: Pons & posterior hypothalamus

Physiology of Micturition
STORAGE PHASE:
• Fills at rate of 0.5- 5 ml/min.
• Intravesical pressure 10 cm of water even with 500ml volume.
• Intravesical pressure kept lower by-
1. Proximal urethral musculature
2. Detrusor stretching reflex contraction of neck
3. Spinal centres inhibit cholinergic system
4. Stimulation of β (relax detrusor) & α (contracts) adrenergic
5. External sphincter

• VOIDING PHASE:
• Stimulation of stretch receptors
Untrained bladder Trained
At spinal level Hypothalamus & Frontal lobes
Controls spinal reflex arcInvoluntary voiding
Voluntary inhibited Voiding

Process of micturition
Abdominal ms contracts & pelvic floor relax
Drop in intraurethral pressure, sympathetic blockade, obliteration of post urethro vesicle
angle
Detrusor contracts
Funneling of proximal urethra
Urine leaks into upper urethra
EUS opens & Voiding occurs
Distal end of urethra closes, milking back last drop into bladder
Post UrV angle restored & EUS closes

Urinary Continence
• Intraurethral pressure > Intravesical at rest & stress
20-50 cm of water 10 cm of water

Pathophysiology of Continence
• Maintained by: (at rest)
1. Apposition of longitudinal mucosal folds
2. Submucous vascular plexus (washer effect)
3. Rhabdosphincter & levator ani
4. Abundance of collagen & elastic tissue
5. Tonic contraction of prox. urethra & bladder neck
• In stress-
1. Intra abdominal pressure at bladder neck
2. Reflex contraction of external sphincter
3. Kinking of urethra
1/3rd each

Urinary incontinence
• Objectively demonstrable involuntary loss of urine so
as to cause hygienic &/ or social inconvenience for day
to day activity.
• Pathophysiology- Intravesical > intraurethral pressure
Due to- childbirth, surgery, ageing
Injury to supports of bladder neck

Classification
URETHRAL
• Genuine Stress
Incontinence
• Overactive Bladder
• Mixed
• Overflow incontinence
• Functional (DIAPPERS)
• Congenital
• Others (UTI)
EXTRAURETHRAL
• Congenital- Ectopic
ureter
• Acquired- Fistulae

Definitions (Abnormal storage)
• INCONTINENCE- Involuntary leakage of urine.
• STRESS URINARY INCONTINENCE- Involuntary leakage due to
sudden rise in intra-abdominal pressure.
• GENUINE STRESS INCONTINENCE- Involuntary loss of urine when
intravesical pressure exceeds intraurethral pressure in absence of
detrusor overactivity. (Following urodynamic assessment only)
• URGENCY- Sudden compelling desire to pass urine which is difficult
to defer
• URGE INCONTINENCE- Involuntary loss of urine associated with
urgency

• FREQUENCY- no. of voids per day from waking up until falling
asleep at night. (pollakisuria)
• NOCTURIA- interruption of sleep one or more time because of
need to micturate. (It excludes last void before going to bed &
includes first void after waking up in morning)
• NOCTURNAL ENURESIS- Involuntary loss of urine that occurs
during sleep.
• OVERACTIVE BLADDER- urgency, usually with frequency and
nocturia, with or without incontinence, in the absence of UTI or
other obvious pathology

Abnormal sensory symptoms
• Increased bladder sensation
• Reduced
• Absent
• HESITANCY- delay in initiating micturition
• RETENTION- inability to pass urine despite persistent effort.
• INTERMITTENCY- urine flow that stops & starts on one or more
occasions during voiding.
Abnormal emptying

Others
• OVERFLOW INCONTINENCE: involuntary release of urine from
overtly full bladder, often in absence of urge to urinate
• PAINFUL BLADDER SYNDROME: Chronic inflammatory condition
resulting in painful voiding
• Urge incontinence two types
1. Motor- overactive bladder
2. Sensory- unable to control escape of urine once there is urge
to void. Can be controlled with adequate encouragement.
Infection may be present. Cystometry is normal

Overactive Bladder
• Definition – symptom complex of urgency, usually with
frequency and nocturia, with(wet) or without(dry)
incontinence, in the absence of UTI or other obvious pathology.
• Prevalence – 16.9% in North America, increases with age
• Overall 12-15%
• Detrusor overactivity - Ach induced stimulation of muscarinic
receptors (urodynamic diagnosis)
• 64% of OAB have detrusor overactivity.
• 83% of patients with detrusor overactivity have OAB.

Etiology
• Idiopathic
• Psychosomatic
• Following surgery for incontinence
• Neurogenic- Multiple sclerosis, diabetic neuropathy,
spinal injuries, parkinsonism, CVA

Pathophysiology
• OUTFLOW OBSTRUCTION HYPOTHESIS-
Lead to partial denervation & in AchEsterase.
Supersensitivity to Ach.
Instability of membrane potential
Facilitation of Spinal reflex mediated by C-fibres. NGF & tachykinins
• NEUROGENIC HYPOTHESIS-
When cause is Idiopathic.
Increased α adr activity causes increased detrusor contractility.

Incompetent bladder neck
Urine in proximal urethra
Detrusor overactivity
Incontinence
• URETHRAL REFLEX-

• MYOGENIC HYPOTHESIS-
Common in all cases of detrusor overactivity
Alteration of properties of smooth muscles
Loss of nerves & hypertrophy of cells with collagen & elastin.
Increased excitability & cell to cell propagation
Coordinated myogenic contractions of whole detrusor
• UROTHELIAL AFFERENT HYPOTHESIS-
C- fibres afferent activation in the urothelium & suburothelial
myofibroblasts.
Bladder distension releases NO (inhibitory)& prostanoids
(stimulatory)in urothelium
Supported by use of Capsaicin & Resiniferatoxin intravesically

Symptoms
• Urgency
• Frequency
• Nocturia
• Nocturnal enuresis
• SIGNS- vulval excoriation, urogenital atrophy, residual
urine & stress incontinence

Diagnosis
• History & QOL Questionnaire & Urgency severity scales
• Physical examination
• Pelvic examination with bladder full – Stress test, Q-tip,
cystocele, levator ani & anal sphincter function
• Simple (primary care level) Tests-
1. Voiding Diary
2. Urinalysis
3. Post Void Residual volume
4. Cough stress test
5. Pad test

Advanced Testing
• Urodynamics-
1. Uroflowmetry
2. Filling Cystometry
3. Urethral pressure profile
4. Leak point pressure
5. Voiding cystometrogram
• Imaging tests- USG,
Fluoroscopy, Functional
neuroimaging, MRI
• Neurophysiologic test-
1. Pudendal nerve terminal
motor latency
2. Sacral reflexes
3. Somatosensory evoked
potentials
4. EMG
5. Emerging techniques-
PET

Urodynamics
• I/c-
1. Diagnosis is uncertain/mixed disorder
2. Surgery is being considered
3. Failure of multiple surgical corrections
4. Elevated PVR
5. Neurological condition
6. Frequency/voiding difficulties/nocturia
7. Marked pelvic organ prolapse

UROFLOWMETRY
• Volume of urine voided plotted over time
• Flow rate- 15-25ml/sec
• Peak flow rate
• Time to peak flow

CYSTOMETRY
• Assess bladder & urethral function during filling phase
• Single channel & multi channel
• Steps conducting multichannel urodynamic study-
1. Insert pressure & filling bladder catheter. 2nd in vg/ rectum
2. Infuse saline @ 50-100ml/min. Record volume & pressure
3. Note the point at which any leakage occurs.
4. Record first desire to void & strongest desire to void &
maximum cystometric capacity
5. If no detrusor overactivity, do provocative test.
• Pdet = Pves - Pabd

Normal findings in cystometry
• Residual volume 0-50ml
• First sensation of urination 150-200ml
• Strong desire to void >250ml
• Cystometric Capacity 400-600ml
• Intravesical pressure on filling & standing 0-15 cm of
water

• Bladder compliance after 60sec of reaching capacity
20- 100ml/cm of water
• Maximum detrusor pressure during voiding <50 cm of
water
• Peak urinary flow rate >15ml/sec
• No uninhibited detrusor contraction despite
provocation
• No stress or urge despite provocation

• Cystometrogram-
• Graphical registration of pressure changes in bladder in relation
to rise in the volume of urine.
• Segment 1, 2 & 3

URETHRAL FUNCTION TEST
1. Urethral pressure profilometry-
 catheter with microtip pressure transducer slowly pulled
along urethra measuring intravesical & urethral pressure.
 P ure – P ves = P clos
 <20cm of water poor prognosis after surgery
2. Fluoroscopic & cystoscopic assessment of bladder neck

3. Leak point pressure- urodynamic measure of the
minimum intra abdom or intravesical pressure to cause
incontinence .
1. Valsalva LPP
2. Cough LPP
Intrinsic sphincter deficiency found in women cutoff 60
cm water
Bulking agents (collagen) are used <100cm water LPP
when bladder is filled with 150ml

Voiding Cystometrogram
• Valsalva voiding, low preoperative flow rate & high detrusor
pressure during voiding are risk factors for postoperative
voiding dysfunction

Treatment
• General measures- Psychotherapy for psychosomatic
problems, treating other medical conditions
• Behavioral therapy-
o Limit fluid intake (1-1.5 litres/d)
o Reduce tea, coffee, alcohol
o Diuretics stopped
o Weight loss
o Bladder retraining : bladder drill, biofeedback,
hypnotherapy.
83% asymp 6mth
40% relapse in 3 yrs

Drug Therapy
• Inhibit bladder contractility,
• Increase bladder neck & urethral resistance.
• Antimuscarinic agents-
Reduce incontinence episodes per day
Reduce frequency, urgency
• Immediate release- Oxybutinin, tolterodine
• Extended release- Trospium, solifenacin
• Conjugated Estrogen- should not be prescribed
• Ephedrine, pseudoephedrine, phenylpropanolamine-
risks of complications , hemorrhagic cerebral vascular
accident

NATURE DRUGS & DOSES RELIEVES SIDE EFFECT CONTRAINDICATION
ANTI
CHOLINERGIC
M1 & M3
antagonist
Oxybutinin
5mg BD PO/
transdermal
patch 3.9mg
twice a wk
Frequency
Urgency
Dry mouth
Blurred vision
Constipation
Glaucoma
Myasthenia
Intestinal
obstruction
Ulcerative colitis
Urinary retention
ANTI
MUSCARINIC
M3 antagonist
Tolterodin
1-2mg PO BD
ANTI
MUSCARINIC
M3 anatgonist
Solifenacin
5-10 mg OD
Flatulence
Chest pain also
TCA Imipramine
50mg HS
Nocturia Sedation
Hip fracture
Orthostatic htn
Coronary Artery Dis
HTN
SYNTHETIC
ANTIDIURETIC
HORMONE
ANALOGUE
DDAVP
Intranasal
20-40µg HS
Nocturnal
enuresis
Fluid retention
Rhinitis
Nausea
Hyponatremia
Cardiac insufficiency

Other drugs
• Darifenacin- same as solifenacin
• Fesoterodine- Prodrug, active metabolite 5 hydroxy methyl
tolterodine
• Flavoxate (similar to oxybutinin)- 200mg TDS urinary frequency,
urgency, dysuria
• Propiverine- antichl & CCB, urgency frequency, urge incontinence,
M3 antagonist
• Trospium- cautiously in renal & hepatic, parasympatholytic,
reduces tone of smooth ms in bladder, not distributed to CNS
because of large molecular size & hydrophilicity
• Bumetanide- loop diuretic, decrease nocturia
• Furesemide- mid afternoon. Decrease night time urine
production

Refractory OAB
• Distressing symptoms continue despite conservative & drug therapy
• INTRAVESICAL THERAPY-
• Temporary effect & risk of voiding difficulties
• Capsaicin (in neurogenic DOA),
• Resiniferatoxin,
• Botulinum Toxin (idiopathic DOA)
• NEUROMODULATION-
• Peripheral – using posterior tibial nerve (similar effect as
antimuscarinics)
• Sacral neuromodulation- expensive, invasive
• Cutaneous sacral neuromodulation- less invasive

• SURGERY-
Denervation (interrupt nervous pathway)
Augmentation & clam cystoplasty (increase bladder capacity)
Urinary diversion (ileal conduit)
Detrusor myectomy
• RECENT DEVELOPMENTS-
Oxybutinin patch, gel
Mirabegron – β3 agonist
Solabegron – also in Irritable Bowel Synd , produces visceral
analgesia by releasing somatostatin & adipocytes

• THANK YOU..