OVERACTIVE BLADDER SYNDROMEPRACTICAL VIEW

By

Hassaan Ali GadAssistant lecturer of urology and Andrology

Aswan University hassaan.ali@aswu.edu.eg

OUTLINE

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 defer urgency

Patient considers that he/she voids too often by dayNormal 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 urgency

Urge urinaryincontinence (UUI)

OAB with UUI OAB “wet”

OAB without UUI OAB “dry”

Time from first sensation of urgency to voiding Warning 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 relaxes

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 hypothesisMost 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 hypothesisStructural 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

WomenUTIBladder cancerDiabetesMultiple sclerosisSUIRecent pelvic surgeryNeurogenic bladderProlapseUrethral obstructionAtrophic vaginitisPostsurgical incontinence

Treatment of OAB

Treatment of OAB

First-Line Treatments - Behavioral therapySecond-Line Treatments -Medication -Combined therapy: behavioral and pharmacologic

therapyThird-line Treatments:

– Botulinum A-toxin– Neuromodulation

Additional Treatments: -Augmentation cystoplasty or urinary diversion

Behavioral Modifications

Dietary ChangesFluid ManagementPelvic Muscle Exercises (Kegel exercises)BiofeedbackBladder Retraining.

Anticholinergic AgentsOxybutyninOxybutynin transdermalTolterodineSolifenacin Trospium chlorideDarifenacin

Medication

Darifenacin Trospium chloride

Solifenacin Tolterodine Oxybutynin

Tertiary amine Quaternary amine

Tertiary amine Tertiary amine Tertiary amine Chemical stracture

More M3 selective

Non selective Non selective Non selective Non selective Receptor

Poor 20% Poor 10% Good 90% Good 75% Poor 15% Oral bioaviablity

13- 19hours 12- 20hours 45- 86hours 2hoursER 9hrs

2hourspatch8hrsER 12hrs

Half-life

7.5-15 mg/Day

20-40 mg/Day 5-10 mg/Day 1-2 mg Twice Day

5 mg 3 times Day

Dosing

•Dry mouth Constipation

•Dry mouth•Constipation

•Dry mouth•Constipation

•Dry mouth•Constipation• Blurred vision• Drowsiness

•Dry mouth•Constipation• Blurred vision• Drowsiness

Side effects

Oxybutynin Transdermal

Translucent matrix-type patch Twice-weekly application

Intravesical BTX InjectionBotox can suppress ACh release from cholinergic

terminalsBotox can inhibit aberrant sensory neurotransmitter Botox can treat OAB in both sensory and motorResponse rate in non-neurogenic OAB about 60-80%

with duration of response around 6-12 months. Risk of urinary retentionAnd Patients may need to self catheterise

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

Sacral NeuromodulationSacral 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 eachCheaper ?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