Dr hassaan...(OAB)

3/29/2015 hassaan.ali@aswu.edu.eg

OUTLINE
3/29/2015
Introduction… Definition and Prevalence.
Bladder Anatomy and Physiology.
 Etiology and Pathophysiology OAB.
Diagnosis and evaluation of OAB.
Treatment of OAB.

Definition of OAB
• The International Continence Society (ICS)
defines OAB as:
• The presence of “urinary urgency, usually
accompanied by frequency and nocturia, with
or without urge incontinence, in the absence
of UTI or other pathology.”
• OAB is defined based on symptoms and
Known as( Overactive Bladder Syndrome)

Sudden compelling desire to pass urine that is difficult to deferurgency
Patient considers that he/she voids too often by day
Normal is < 8 times per 24 hours
Frequency
Waking to urinate during sleep hours considered a clinical problem if
frequency is greater than twice a night
Nocturia
Involuntary leakage accompanied by or immediately preceded by urgencyUrge urinary
incontinence (UUI)
OAB with UUIOAB “wet”
OAB without UUIOAB “dry”
Time from first sensation of urgency to voidingWarning time
Terminology

It affects
approximately 17%
of the adult
Women < Men
prevalence increase
with age
Dry OAB < wet OAB
PREVALENCE

Bladder Anatomy and Physiology

L1
L2
L3
Sympathetic nerve supply
Sympathetic
chain
Hypogastric
ganglion
Hypogastric
nerve internal
sphincter relaxes
Urethra
External sphincter
Parasympathetic nerve supply
S2
S3
S4
S2
S3
S4
Pelvic nerve
contraction of the
detrussor muscle
Pudendal nerve
external sphincter
Somatic nerve supply
Bladder Anatomy and Physiology

ETIOLOGY OAB
The knowledge of OAB is incomplete.
The etiology of OAB is complex and poorly
understood.
Neurological hypothesis.
The myogenic hypothesis.
Increased sensitivity of afferent nerves.

Neurological hypothesis
Most of the time the bladder control is modulated in
an inhibitory fashion by the dienchephalic and
cerebral cortex.
• damage to the brain can induce DO by reducing
suprapontine inhibition.
• damage to axonal pathways in the spinal cord
allows the expression of primitive spinal bladder
reflexes.
• synaptic plasticity leads to reorganization of
sacral activity, with the emergence

The myogenic hypothesis
Structural deformation of detrusor muscle,
 Increased production of (NGF) → → growth and
maintenance of sympathetic and sensory
neurones,
 Partial denervation (denervation superactivity),
 Metabolic effects (free radicals, lipid
peroxidases).
 Detrusor hypertrophy (↑metabolic demands,
↓ blood flow → ischamia and anoxia neurones).

Increased sensitivity of afferent
nerves
Low Ph, increased urine osmolality →
release of mediators as: nitric oxide and
neurokinin A → sensitization of submucosal
afferents.
Sensitization of C-fiber (unmyelinated)
afferents.

Clinical Evaluation

Clinical Evaluation
The diagnosis of OAB is symptom based and involves:
 Careful history,
 physical exam,
Urinalysis.
Urodynamics, cystoscopy and diagnostic renal and
bladder ultrasound should not be used in the initial
workup of the uncomplicated patient.
Urodynamic study or cystoscopy
 Refractory or complicated cases of OAB
 Prior to invasive surgery.

Urodynamic study

Urodynamic findings:
-Cystometry: spontaneous bladder
contractions during the filling phase → → ↑
intravesical pressure.
 Ambulatory urodynamic monitoring is better
than the conventional filling cystometry, as
motor overactivity of the detrusor is more
frequently detected.

Differential Diagnosis of OAB
Men
 Benign prostatic
hyperplasia (BPH)
 Prostate cancer
 Diabetes
 Postsurgical
incontinence
 Bladder outlet
obstruction (BOO)
 Urethral stricture
 Neurogenic bladder
 Bladder stones
Women
UTI
Bladder cancer
Diabetes
Multiple sclerosis
SUI
Recent pelvic surgery
Neurogenic bladder
Prolapse
Urethral obstruction
Atrophic vaginitis
Postsurgical incontinence

Treatment of OAB

Treatment of OAB
 First-Line Treatments
- Behavioral therapy
Second-Line Treatments
-Medication
-Combined therapy: behavioral and pharmacologic
therapy
Third-line Treatments:
– Botulinum A-toxin
– Neuromodulation
Additional Treatments:
-Augmentation cystoplasty or urinary diversion

Behavioral Modifications
Dietary Changes
Fluid Management
Pelvic Muscle Exercises (Kegel exercises)
Biofeedback
Bladder Retraining.

Anticholinergic Agents
Oxybutynin
Oxybutynin transdermal
Tolterodine
Solifenacin
Trospium chloride
Darifenacin
3/29/2015
Medication
hassaan.ali@aswu.edu.eg

DarifenacinTrospium
chloride
SolifenacinTolterodineOxybutynin
Tertiary amineQuaternary
amine
Tertiary amineTertiary amineTertiary amineChemical
stracture
More M3
selective
Non selectiveNon selectiveNon selectiveNon selectiveReceptor
Poor 20%Poor 10%Good 90%Good 75%Poor 15%Oral
bioaviablity
13 -19hours12 -20hours45 -86hours2hours
ER 9hrs
2hours
patch8hrs
ER 12hrs
Half-life
7.5-15
mg/Day
20-40 mg/Day5-10 mg/Day1-2 mg Twice
Day
5 mg 3 times
Day
Dosing
•Dry mouth
Constipation
•Dry mouth
•Constipation
•Dry mouth
•Constipation
•Dry mouth
•Constipation
• Blurred
vision
•Dry mouth
•Constipation
• Blurred
vision
Side effects

Oxybutynin Transdermal
Translucent matrix-type patch Twice-weekly application

Intravesical BTX Injection
Botox can suppress ACh release from cholinergic
terminals
Botox can inhibit aberrant sensory neurotransmitter
 Botox can treat OAB in both sensory and motor
Response rate in non-neurogenic OAB about 60-80%
with duration of response around 6-12 months.
Risk of urinary retention
And Patients may need to
self catheterise

Intradetrusor onabotulinumtoxinA 100 units
diluted in 10ml saline in 30 injection sites

Sacral Neuromodulation
Sacral nerve stimulation InterStim®:
Implanted neurostimulation of sacral nervesS3:
Stimulation of the sacral roots has effectively
suppressed the hyperactivity, relying on the known
reflex response of the detrusor muscle to stimulate the
somatic component of the sacral plexus (which aborts
and inhibits detrusor contractilit

Pre-tibial sacral nerve root stimulation
New less invasive way of stimulating sacral
nerve roots
12x weekly sessions of 30 minutes each
Cheaper
?effectiveness

Additional Treatments:
Indwelling catheters (including
transurethral, suprapubic, etc.) are not
recommended as a management
strategy for OAB because of the adverse
risk/benefit balance except as a last
resort in selected patients.
In rare cases, augmentation
cystoplasty or urinary diversion for
severe, refractory, complicated OAB
patients may be considered.

Resources
• American Urological Association (AUA)
• www.auanet.org
• International Continence Society (ICS)
• www.icsoffice.org
• Society for Urodynamics & Female Urology
(SUFU)
• www.sufuorg.com
• American Urogynecological Society (AUGS)
• www.augs.org

THANK YOU

Dr hassaan...(OAB)

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