Overactive Bladder Syndrome (OAB)

1. Clinical Overview

Summary

Overactive bladder (OAB) is a symptom syndrome characterised by urinary urgency, usually accompanied by increased daytime frequency and nocturia, with or without urgency urinary incontinence, in the absence of urinary tract infection (UTI) or other obvious pathology. [1] The International Continence Society (ICS) defines OAB primarily by the presence of urgency - a sudden, compelling desire to pass urine that is difficult to defer. [2]

OAB represents a storage-phase dysfunction of the lower urinary tract and can occur with ("OAB wet") or without ("OAB dry") incontinence episodes. The condition is highly prevalent, affecting 10-15% of the adult population, with significant impact on quality of life, mental health, and healthcare costs. [3]

Pathophysiological Basis

The underlying mechanism in most cases is detrusor overactivity (DO) - involuntary detrusor muscle contractions during the filling phase of the bladder cycle, demonstrated on urodynamic studies. [4] However, OAB is diagnosed clinically based on symptoms, while DO is a urodynamic diagnosis requiring invasive testing.

Key Facts

Clinical Pearls

• Urgency is the cardinal symptom: Without urgency, the diagnosis of OAB should be questioned
• "Latchkey incontinence": Classic scenario - patient leaks urine when putting key in door, triggered by anticipation of voiding
• Always exclude UTI first: Dipstick urinalysis or midstream urine (MSU) culture essential before diagnosing OAB
• Avoid oxybutynin in elderly: High rates of cognitive impairment and anticholinergic burden - prefer selective agents like solifenacin or mirabegron
• OAB is a diagnosis of exclusion: Must exclude infection, malignancy, stones, and neurological causes
• Bladder diary is diagnostic gold standard: 3-day voiding diary confirms frequency (> 8 voids/day) and functional bladder capacity
• Combination therapy: Antimuscarinic + β3-agonist combination superior to monotherapy in refractory cases [5]

Diagnostic Criteria (ICS 2002/2019)

Essential symptom:

• Urinary urgency (sudden compelling desire to void, difficult to defer)

Usually accompanied by:

• Increased daytime frequency (> 8 micturitions/24 hours)
• Nocturia (≥1 void per night)
• Urgency urinary incontinence (involuntary leakage accompanied by or immediately preceded by urgency)

Exclusion criteria:

• Urinary tract infection
• Bladder pathology (stones, tumour)
• Significant post-void residual (> 200mL suggests retention)

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2. Epidemiology

Prevalence

Overactive bladder is a highly prevalent condition affecting millions worldwide, with significant underdiagnosis due to patient reluctance to report symptoms and physician failure to enquire. [6]

Incidence

• Annual incidence: 4-6% in adults aged > 40 years [7]
• Progression from OAB dry to OAB wet: ~20-30% over 5 years
• Spontaneous resolution: 10-15% per year (lower in elderly)

Demographics

Age:

• Incidence and prevalence increase progressively with age
• Most rapid increase after age 50 years
• Multifactorial: bladder ageing, comorbidities, medications, neurological changes

Sex:

• Women have slightly higher overall prevalence (12-17% vs 10-13% in men)
• In men, OAB often coexists with benign prostatic hyperplasia (BPH)
• In women, OAB may coexist with stress urinary incontinence (mixed incontinence)

Ethnicity:

• Limited data, but some studies suggest higher prevalence in Caucasian and Hispanic populations compared to Asian populations
• May reflect cultural differences in reporting and healthcare access

Risk Factors

Modifiable Risk Factors

• Obesity: Weight loss of 5-10% can improve symptoms [8]
• Fluid intake: Excessive (> 3L/day) or restricted (less than 1L/day) intake worsens symptoms
• Caffeine and alcohol: Bladder irritants; reduction improves symptoms in 30-40%
• Smoking: Associated with chronic cough and increased intra-abdominal pressure
• Constipation: Chronic straining and pelvic floor dysfunction

Impact and Burden

Quality of Life:

• Significant impairment in physical, psychological, and social domains
• Sleep disturbance from nocturia (average 2-3 episodes/night in OAB wet)
• Social isolation and embarrassment leading to reduced activities

Economic Burden:

• Direct costs: medications, consultations, pads/continence products, interventions
• Indirect costs: lost productivity, caregiver burden
• UK costs estimated at £200-300 per patient per year [9]
• US costs estimated at $65 billion annually

Comorbidities:

• Falls and fractures (especially in elderly rushing to toilet at night)
• Urinary tract infections (incomplete emptying, catheter use)
• Skin breakdown and pressure ulcers (incontinence-associated dermatitis)
• Depression and anxiety
• Sexual dysfunction

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3. Pathophysiology

Normal Bladder Function

To understand OAB, one must first understand normal micturition:

Filling Phase (Storage):

1. Bladder fills with urine from ureters
2. Detrusor muscle relaxes (β3-adrenoceptor stimulation)
3. Internal urethral sphincter contracts (α1-adrenoceptor stimulation)
4. External urethral sphincter maintains tone (pudendal nerve, voluntary)
5. First sensation to void: ~150-200mL
6. Normal desire to void: ~300-400mL
7. Strong desire to void: ~400-500mL
8. Cortical inhibition prevents involuntary contractions

Voiding Phase:

1. Voluntary decision to void
2. Relaxation of pelvic floor and external sphincter
3. Detrusor contraction (parasympathetic, muscarinic M3 receptors)
4. Internal sphincter relaxes
5. Sustained detrusor contraction until bladder empty
6. Post-void residual: less than 50mL normal

Neural Control

Sympathetic (T10-L2):

• Hypogastric nerve
• β3-adrenoceptors → detrusor relaxation
• α1-adrenoceptors → internal sphincter contraction
• Promotes storage

Parasympathetic (S2-S4):

• Pelvic nerve
• Muscarinic receptors (M2 and M3) → detrusor contraction
• Promotes voiding

Somatic (S2-S4):

• Pudendal nerve
• External urethral sphincter (voluntary control)

Central Control:

• Pontine micturition centre (brainstem): coordination of voiding
• Periaqueductal grey: relay station
• Prefrontal cortex: voluntary inhibition and social continence

Pathophysiology of OAB

The fundamental abnormality in OAB is loss of cortical inhibition or increased afferent signalling leading to involuntary detrusor contractions during filling. [10]

1. Myogenic Mechanisms

Detrusor Overactivity:

• Spontaneous detrusor smooth muscle contractions
• Increased excitability of detrusor myocytes
• Altered gap junction communication
• Increased sensitivity to acetylcholine
• Partial denervation leading to supersensitivity

Ischaemia:

• Bladder ischaemia (reduced blood flow) → hypoxia → afferent nerve sensitisation
• Common in elderly, diabetics, and those with atherosclerosis

2. Neurogenic Mechanisms

Afferent Hypersensitivity:

• Increased C-fibre afferent activity (normally "silent" fibres activated)
• Upregulation of sensory receptors (TRPV1, P2X3)
• Enhanced transmission of urgency signals

Central Disinhibition:

• Loss of cortical/pontine inhibition
• Seen in: stroke, Parkinson's disease, multiple sclerosis, dementia
• Disruption of "guarding reflex"

Spinal Mechanisms:

• Spinal cord lesions (e.g., trauma, myelopathy)
• Loss of supraspinal control → reflex bladder activity

3. Urothelial Dysfunction

Urothelium as Sensory Organ:

• Urothelium releases mediators (ATP, acetylcholine, prostaglandins, nitric oxide)
• Mediators activate suburothelial afferents
• In OAB: increased mediator release → enhanced afferent signalling [11]

Bladder Inflammation:

• Low-grade inflammation and mast cell activation
• Release of histamine, prostaglandins, nerve growth factor (NGF)
• NGF sensitises bladder afferents

4. Autonomic Dysfunction

Increased Sympathetic Activity:

• Stress and anxiety increase sympathetic tone
• May paradoxically worsen OAB symptoms

Altered Receptor Expression:

• Upregulation of muscarinic M2/M3 receptors
• Changes in β3-adrenoceptor density and function

Aetiological Classification

Detrusor Overactivity (Urodynamic Diagnosis)

Definition:

• Involuntary detrusor contractions during filling cystometry
• May be spontaneous or provoked (coughing, position change)

Types:

• Phasic DO: Transient contractions with return to baseline
• Terminal DO: Contraction at capacity leading to voiding
• Sustained DO: Prolonged high-pressure contractions

Correlation with OAB:

• Only 60-70% of patients with OAB symptoms have demonstrable DO on urodynamics
• Some with urgency have normal urodynamics (detrusor overactivity sensory urgency)
• Urodynamics NOT required for routine OAB diagnosis [12]

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4. Clinical Presentation

Cardinal Symptom: Urgency

Definition (ICS):

• Sudden, compelling desire to pass urine which is difficult to defer

Patient Descriptions:

• "I have to run to the toilet"
• "When I need to go, I need to go NOW"
• "I can't hold it"
• "I worry I won't make it in time"

Triggers:

• Sound of running water
• Cold weather
• Putting key in door ("latchkey incontinence")
• Arriving home
• Handwashing
• Anxiety

Associated Symptoms

OAB Subtypes

OAB Dry (~60%):

• Urgency, frequency, nocturia
• No incontinence episodes
• Better prognosis
• May progress to OAB wet

OAB Wet (~40%):

• All symptoms of OAB dry PLUS urgency incontinence
• Greater impact on quality of life
• Higher treatment-seeking behaviour
• More likely to have demonstrable detrusor overactivity on urodynamics

Clinical Scenarios

Typical Presentations:

Scenario 1: Young Woman

• 35-year-old woman
• Voids 12-15 times/day
• Wakes 2-3 times/night
• Sudden urges, occasionally leaks small amounts
• No leakage with coughing/sneezing
• Impact: avoids long journeys, knows location of every toilet

Scenario 2: Elderly Man

• 72-year-old man with BPH
• Poor stream, hesitancy (obstructive symptoms)
• Frequency, urgency, occasional incontinence
• Nocturia ×4/night
• Falls risk from rushing to toilet

Scenario 3: Patient with MS

• 45-year-old woman with multiple sclerosis
• Neurogenic bladder
• Severe urgency and incontinence
• Incomplete emptying (mixed storage and voiding dysfunction)
• Requires intermittent self-catheterisation

Distinguishing OAB from Other Causes of Incontinence

Symptom Severity Assessment

Patient-Reported Outcome Measures:

• OAB-q (Overactive Bladder Questionnaire): Symptom bother and quality of life
• ICIQ-OAB (International Consultation on Incontinence Questionnaire): 4-item symptom score
• PPBC (Patient Perception of Bladder Condition): Single-item global assessment (1-6 scale)

Bladder Diary (Gold Standard):

• 3-day (minimum) or 7-day voiding diary
• Records:
  • Time of each void
  • Voided volume (measured)
  • Urgency episodes (scale 0-4)
  • Incontinence episodes
  • Pad usage
  • Fluid intake (type and volume)
• Provides objective data on:
  • Functional bladder capacity (average voided volume)
  • Voiding frequency
  • Nocturia episodes
  • Total urine output (polyuria?)
  • Fluid intake patterns

Severity Classification:

• Mild: Bothersome but does not interfere with daily activities
• Moderate: Interferes with daily activities and quality of life
• Severe: Severely affects quality of life; patient housebound or using pads continuously

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5. Clinical Examination

Objectives

Clinical examination in OAB aims to:

1. Exclude underlying pathology (masses, neurological disease)
2. Assess for concurrent stress incontinence
3. Identify red flags requiring urgent investigation
4. Assess pelvic floor function

Abdominal Examination

Pelvic/Genital Examination

In Women:

• Inspection: Atrophic vaginitis (oestrogen deficiency), skin changes from incontinence
• Speculum: Exclude pelvic organ prolapse (cystocele, rectocele, uterine prolapse)
• Bimanual: Pelvic masses, uterine size
• Pelvic floor assessment: Tone, voluntary contraction ability (for pelvic floor exercises)
• Cough stress test: Ask patient to cough with full bladder - if leakage occurs, suggests concurrent stress incontinence (mixed incontinence)

In Men:

• External genitalia: Phimosis, meatal stenosis
• Digital rectal examination (DRE): Prostate size, consistency, nodules (BPH vs cancer)
• Anal tone: Neurological assessment

Neurological Examination

Essential if neurogenic OAB suspected:

Red Flag Findings

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6. Investigations

First-Line Investigations (All Patients)

Post-Void Residual Measurement:

• Bladder scan (ultrasound): Non-invasive, immediate
• In-out catheterisation: Gold standard, invasive
• Normal: less than 50mL
• Borderline: 50-200mL (repeat measurement)
• Abnormal: > 200mL (suggests incomplete emptying, overflow risk)

Blood Tests

Usually not required unless specific indications:

Second-Line Investigations (Specialist)

Not required for routine diagnosis but indicated in specific scenarios:

1. Urodynamic Studies

Indications:

• Failed conservative and pharmacological management (considering invasive treatment)
• Mixed incontinence (OAB + stress incontinence) - planning surgery
• Neurogenic bladder
• Previous failed continence surgery
• Unexplained symptoms

Components:

• Filling cystometry: Bladder filled with saline; detects involuntary contractions (detrusor overactivity)
• Pressure-flow studies: Assesses voiding phase; detects obstruction
• Leak point pressure: Measures pressure at which incontinence occurs

Findings in OAB:

• Detrusor overactivity (DO): Involuntary contractions > 5cmH₂O during filling
• Present in 60-70% of patients with OAB symptoms
• Absence does not exclude OAB (normal urodynamics in 30-40%)

Limitations:

• Invasive, uncomfortable
• Not physiological (artificial filling)
• Poor test-retest reliability
• Does NOT change management in most cases [12]

2. Cystoscopy

Indications:

• Haematuria (visible or non-visible in age > 40)
• Recurrent UTIs
• Suspected bladder cancer (risk factors: smoking, occupational exposure)
• Persistent symptoms despite treatment
• Suspected interstitial cystitis / bladder pain syndrome
• Before Botox injection (assess bladder, exclude cancer)

Findings:

• Normal in idiopathic OAB
• May reveal: bladder tumour, stones, chronic cystitis, interstitial cystitis (Hunner's lesions, glomerulations)

3. Imaging

Renal Ultrasound:

• Indications: Haematuria, recurrent UTIs, abnormal renal function, hydronephrosis
• Assesses: Kidney size, hydronephrosis, bladder wall thickness, post-void residual

CT Urogram:

• Indications: Haematuria, suspected upper tract pathology
• Assesses: Kidney masses, urothelial tumours, stones

MRI Spine:

• Indications: Suspected spinal cord pathology, neurological signs, cauda equina symptoms
• Assesses: Cord compression, demyelination (MS), spinal tumours

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7. Management

Management of OAB follows a stepwise approach from conservative to invasive therapies. [13]

General Principles

1. Exclude pathology first: UTI, cancer, stones, neurological disease
2. Start conservative: Lifestyle + bladder training (6-12 weeks trial)
3. Add pharmacotherapy: If conservative fails
4. Specialist treatments: For refractory cases
5. Individualise treatment: Consider age, comorbidities, cognitive status, patient preference

Step 1: Conservative Management (First-Line)

Lifestyle Modifications

Fluid Management:

• Avoid excessive fluids (polyuria worsens frequency)
• Avoid severe restriction (concentrated urine irritates bladder)
• Reduce evening fluids to minimise nocturia
• Monitor with bladder diary

Bladder Training

Principle: Gradually increase time between voids to improve bladder capacity and cortical control.

Protocol:

1. Baseline assessment: 3-day bladder diary to establish current voiding interval
2. Set initial target: Current interval + 15-30 minutes
3. Schedule voids: Void at scheduled times whether or not urgency present
4. Urgency suppression: When urgency occurs before scheduled time:
   • Stop and stand still (do not rush)
   • Perform pelvic floor contraction (5-10 quick squeezes)
   • Distraction techniques (mental arithmetic, breathing)
   • Wait for urgency to subside, then walk normally to toilet
5. Gradual progression: Increase interval by 15-30 minutes every 1-2 weeks
6. Goal: Void every 3-4 hours; functional capacity 300-400mL

Duration: Minimum 6 weeks (often 12 weeks for full benefit)

Success Rate: 50-80% report improvement [15]

Pelvic Floor Muscle Training (PFMT)

Mechanism: Strengthens external urethral sphincter and improves cortical inhibition of detrusor.

Protocol:

• 8-12 contractions, 3 times daily
• Mix of slow (hold 10 seconds) and quick contractions
• Duration: Minimum 3-6 months
• Biofeedback or supervised physiotherapy improves compliance and effectiveness

Evidence: More effective for stress incontinence, but beneficial in mixed incontinence and OAB [16]

Step 2: Pharmacotherapy (Second-Line)

Indicated if conservative measures fail after 6-12 weeks.

Antimuscarinic Agents (Anticholinergics)

Mechanism: Block muscarinic M3 receptors on detrusor muscle, reducing involuntary contractions.

Efficacy:

• 60-70% report improvement in symptoms [17]
• Reduce urgency episodes by 50-60%
• Reduce incontinence episodes by 50-70%
• Reduce frequency by 1-2 voids/day

Side Effects (Anticholinergic):

• Dry mouth (most common, 20-40%)
• Constipation (10-15%)
• Blurred vision (accommodation difficulties)
• Cognitive impairment (especially oxybutynin in elderly) [18]
• Urinary retention (rare, less than 2%)
• Tachycardia (antimuscarinic effect on heart)

Contraindications:

• Urinary retention
• Gastric retention / uncontrolled narrow-angle glaucoma
• Myasthenia gravis
• Relative: Dementia, cognitive impairment (anticholinergic burden)

Prescribing Tips:

• Start with solifenacin 5mg OD or tolterodine MR 4mg OD
• Avoid oxybutynin IR (immediate-release) in elderly
• Trial for 4-6 weeks before assessing efficacy
• If inadequate response, increase dose or switch agent
• Warn patients about dry mouth (most common SE)
• Consider anticholinergic burden in elderly (use tools like Anticholinergic Cognitive Burden Scale)

β3-Adrenoceptor Agonists

Efficacy:

• Similar to antimuscarinics (60-70% improvement)
• Non-inferior to solifenacin in RCTs

Side Effects:

• Hypertension (small increase, ~1-2mmHg) - monitor BP
• Tachycardia
• Nasopharyngitis
• Headache
• No dry mouth or cognitive effects

Contraindications:

• Severe uncontrolled hypertension (> 180/110mmHg)
• End-stage renal failure

Prescribing Tips:

• First-line alternative to antimuscarinics, especially in:
  • Elderly (no cognitive effects)
  • Patients with dry mouth intolerance
  • Glaucoma, constipation
• Monitor blood pressure at baseline and follow-up
• Start at 25mg in elderly or renal impairment

Combination Therapy

Antimuscarinic + β3-Agonist:

• Evidence supports solifenacin 5mg + mirabegron 50mg combination [5]
• Superior to monotherapy in refractory cases
• Consider if monotherapy partially effective
• Monitor for cumulative side effects

Topical Oestrogen (Women)

Indication: Postmenopausal women with vaginal atrophy and OAB symptoms

Mechanism: Restores urogenital tissues; may improve symptoms

Evidence: Modest benefit in OAB symptoms; better evidence for recurrent UTI prevention

Options:

• Vaginal oestrogen cream (0.01% oestriol)
• Vaginal pessary
• Vaginal ring

Step 3: Invasive / Specialist Treatments (Third-Line)

Indicated for refractory OAB (failed conservative and at least 2 pharmacological agents).

1. Intradetrusor Botulinum Toxin A (Botox)

Mechanism: Inhibits acetylcholine release at neuromuscular junction → detrusor relaxation; also affects afferent signalling.

Procedure:

• Cystoscopy (local or general anaesthetic)
• 20 injections of 100 units onabotulinumtoxinA into detrusor (sparing trigone)
• Day case procedure

Efficacy:

• 70-80% report improvement
• Reduces urgency incontinence episodes by 50-80%
• Duration: 6-9 months (repeat injections needed)

Side Effects:

• Urinary retention (5-10%) - may require intermittent self-catheterisation
• UTI (20-30%)
• Incomplete emptying (increased PVR)
• Haematuria (transient)
• Systemic botulism (rare)

Patient Selection:

• Must be able to perform intermittent self-catheterisation (ISC) if retention occurs
• Counsel about risk of retention and need for repeat injections
• Urodynamics often performed before Botox

2. Sacral Neuromodulation (SNM)

Mechanism: Implanted device delivers electrical stimulation to S3 nerve root, modulating bladder reflex pathways.

Procedure:

• Stage 1 (Trial): Temporary lead placed percutaneously; external stimulator worn for 1-2 weeks
• If > 50% improvement → Stage 2 (Permanent)
• Stage 2: Permanent lead and implantable pulse generator (IPG) placed in buttock

Efficacy:

• 60-70% achieve > 50% symptom reduction
• Durable long-term (5-10 years)

Indications:

• Refractory OAB (failed conservative, pharmacotherapy, and Botox)
• Patients unwilling or unable to perform ISC (alternative to Botox)
• Urge-predominant mixed incontinence

Side Effects:

• Pain at IPG site (10-15%)
• Lead migration (5-10%)
• Infection (3-5%)
• Need for revision surgery (15-20% over 5 years)

Cost: High (device + surgery); NHS England approved for refractory OAB

3. Percutaneous Tibial Nerve Stimulation (PTNS)

Mechanism: Stimulation of posterior tibial nerve (S2-S4 afferents) modulates bladder reflexes.

Procedure:

• Needle electrode inserted near medial malleolus
• 30-minute sessions, weekly for 12 weeks
• Maintenance sessions monthly thereafter

Efficacy:

• 60% report improvement
• Less invasive than SNM
• Lower cost

Side Effects:

• Minimal (discomfort at needle site)
• Time commitment (weekly sessions)

4. Augmentation Cystoplasty (Surgery)

Indication: Severe refractory OAB; neurogenic bladder (rare in idiopathic OAB)

Procedure: Bowel segment (ileum) used to augment bladder capacity

Complications: High morbidity (mucus production, UTI, stones, malignancy risk); requires ISC

Rarely Used: Reserved for end-stage neurogenic bladder; not routine for OAB

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8. Complications

Complications of Untreated OAB

Complications of Treatment

Antimuscarinic Side Effects

• Dry mouth, constipation, blurred vision
• Cognitive impairment (especially oxybutynin in elderly) - increases dementia risk with long-term use [18]
• Urinary retention

Mirabegron Side Effects

• Hypertension (monitor BP)
• Tachycardia

Botox Complications

• Urinary retention (5-10%) - requires ISC
• UTI (20-30%)
• Incomplete emptying

Sacral Neuromodulation Complications

• Device infection, lead migration, pain at site
• Need for surgical revision (15-20%)

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9. Prognosis & Outcomes

Natural History

• Chronic relapsing-remitting condition in most cases
• Spontaneous resolution: 10-15% per year (lower in elderly)
• Progression from OAB dry to OAB wet: 20-30% over 5 years
• Most patients require long-term management

Treatment Outcomes

Factors Affecting Prognosis

Better Prognosis:

• Younger age
• OAB dry (vs OAB wet)
• Recent onset (less than 2 years)
• Absence of neurological disease
• Good response to conservative management

Poorer Prognosis:

• Elderly age
• Neurogenic OAB
• Severe symptoms at baseline
• Comorbidities (diabetes, obesity)
• Cognitive impairment (poor adherence to bladder training)

Patient Adherence

Medication Adherence:

• 50% discontinue antimuscarinics within 12 months
• Reasons: Side effects (dry mouth), lack of efficacy, cost, forgetfulness
• Strategies to improve adherence:
  • Set realistic expectations
  • Start low, titrate dose
  • Review at 4-6 weeks
  • Switch agents if side effects problematic

Quality of Life Improvements

Studies show significant improvements in:

• SF-36 (generic quality of life)
• OAB-q (disease-specific quality of life)
• Reduced pad usage
• Improved sleep quality
• Return to social activities

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10. Special Populations

Elderly Patients

Considerations:

• High prevalence (30-35% in > 65 years)
• Multiple comorbidities and polypharmacy
• Anticholinergic burden: Avoid oxybutynin; prefer mirabegron or selective antimuscarinics
• Falls risk from nocturia
• Cognitive impairment common - bladder training less effective
• Functional incontinence often coexists

Management:

• Start with conservative measures (timed voiding, fluid management)
• Mirabegron first-line pharmacotherapy (avoid anticholinergics if dementia/cognitive impairment)
• Address comorbidities (constipation, mobility, medications)
• Consider bedside commode or urinal for nocturia

Neurogenic OAB

Common Causes:

• Multiple sclerosis (MS)
• Parkinson's disease
• Stroke
• Spinal cord injury
• Spina bifida

Differences from Idiopathic OAB:

• Often mixed storage + voiding dysfunction
• Higher risk of incomplete emptying (monitor PVR)
• May require urodynamics before treatment
• Higher rates of detrusor-sphincter dyssynergia (DSD)

Management:

• Antimuscarinics or mirabegron as per idiopathic OAB
• Botox highly effective (but higher retention risk)
• ISC often required
• Multidisciplinary care (neurology, urology, continence nurse)

Pregnancy and Postpartum

Pregnancy:

• Frequency and nocturia common in pregnancy (physiological)
• True OAB less common
• Conservative management only (avoid medications)

Postpartum:

• OAB symptoms may persist post-delivery
• Pelvic floor trauma from childbirth
• PFMT first-line
• Pharmacotherapy if conservative fails (safe in breastfeeding: limited data; avoid if possible)

Men with BPH

Overlap:

• OAB symptoms common in BPH (secondary detrusor overactivity)
• Distinguish storage (OAB) vs voiding (obstruction) symptoms

Management:

• α-blockers (e.g., tamsulosin) for voiding symptoms
• Antimuscarinics or mirabegron for storage symptoms
• Combination α-blocker + antimuscarinic effective but risk of retention - monitor PVR
• Finasteride / dutasteride (5α-reductase inhibitors) if large prostate
• Consider TURP if refractory

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11. Evidence & Guidelines

Major Guidelines

Key Clinical Trials

Antimuscarinic Trials:

• STAR study: Solifenacin vs placebo (reduction in urgency incontinence episodes) [17]
• OBJECT study: Fesoterodine vs tolterodine (similar efficacy)

β3-Agonist Trials:

• SCORPIO study: Mirabegron vs placebo (effective for OAB symptoms)
• BESIDE study: Combination solifenacin + mirabegron superior to monotherapy [5]

Botox Trials:

• EMBARK study: OnabotulinumtoxinA 100U vs placebo (significant reduction in incontinence episodes)

Neuromodulation Trials:

• SUmiT trial: Sacral neuromodulation vs extended release tolterodine (SNM superior at 6 months)

Levels of Evidence

• Bladder training: Level 1 (systematic reviews, RCTs)
• Antimuscarinics: Level 1
• Mirabegron: Level 1
• Botox: Level 1
• Sacral neuromodulation: Level 2
• PTNS: Level 2

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12. Patient / Layperson Explanation

What is Overactive Bladder?

Overactive bladder (OAB) is a common condition where your bladder squeezes (contracts) too often or at the wrong times, even when it's not full. This gives you a sudden, strong urge to pass urine that can be hard to control. You might also need to go to the toilet very frequently during the day and wake up several times at night. Some people leak urine when they get the urge (this is called urgency incontinence).

What Causes It?

In most people, we don't know exactly why it happens. Your bladder muscle may be too sensitive or overactive. It can be more common as you get older, if you are overweight, drink a lot of caffeine, or have conditions like diabetes. Sometimes it happens after a stroke or in people with conditions like multiple sclerosis or Parkinson's disease.

What Are the Symptoms?

• Sudden strong urge to urinate (the main symptom)
• Going to the toilet more than 8 times a day
• Waking up at night to urinate (often 2-3 times or more)
• Sometimes leaking urine when you get the urge
• Feeling like you might not make it to the toilet in time

How Is It Diagnosed?

Your doctor will ask about your symptoms and may ask you to keep a bladder diary for 3 days, writing down when you go to the toilet, how much you pass, and if you have any leaks. You'll have a urine test to rule out an infection. In most cases, that's all that's needed.

How Is It Treated?

Treatment starts simple and gets more involved if needed:

1. Lifestyle Changes:

• Cut down on caffeine (tea, coffee, cola) and alcohol
• Drink the right amount of fluids (not too much, not too little) - about 1.5-2 litres a day
• Lose weight if you are overweight
• Stop smoking

2. Bladder Training:

• This means gradually training your bladder to hold more urine
• You learn techniques to control the urge (like pelvic floor squeezes, distraction, breathing)
• You gradually increase the time between toilet visits
• It takes 6-12 weeks but works for many people

3. Medication: If lifestyle changes and bladder training don't work, your doctor may prescribe tablets:

• Antimuscarinic drugs (like solifenacin or tolterodine) relax the bladder muscle
• Mirabegron also relaxes the bladder but works differently
• Side effects can include dry mouth, constipation; mirabegron can slightly raise blood pressure
• You usually try medication for at least 4-6 weeks to see if it helps

4. Specialist Treatments: If tablets don't help, a specialist may offer:

• Botox injections into the bladder (lasts 6-9 months; sometimes causes difficulty emptying the bladder)
• Nerve stimulation (a small device that sends signals to nerves that control the bladder)

Will It Get Better?

Most people find significant improvement with treatment. It may take time to find the right combination of treatments. OAB is a long-term condition, so you may need ongoing treatment, but many people get their symptoms well controlled and can return to normal activities.

When Should I See a Doctor Urgently?

See a doctor urgently if you have:

• Blood in your urine
• Pain when passing urine
• Severe abdominal or back pain
• Numbness around your bottom or genitals
• Sudden weakness in your legs

You Are Not Alone

Overactive bladder affects about 1 in 6 adults. It's very common, but many people don't seek help because they feel embarrassed. Don't suffer in silence - talk to your doctor. Effective treatments are available.

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13. References

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3. Irwin DE, Milsom I, Hunskaar S, et al. Population-based survey of urinary incontinence, overactive bladder, and other lower urinary tract symptoms in five countries: results of the EPIC study. Eur Urol. 2006;50(6):1306-1315. doi:10.1016/j.eururo.2006.09.019

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7. Milsom I, Altman D, Cartwright R, et al. Epidemiology of urinary incontinence (UI) and other lower urinary tract symptoms (LUTS), pelvic organ prolapse (POP) and anal incontinence (AI). In: Abrams P, Cardozo L, Wagg A, Wein A, eds. Incontinence. 6th International Consultation on Incontinence, Tokyo, 2017. Bristol, UK: International Continence Society; 2017:1-141.

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14. Swithinbank L, Hashim H, Abrams P. The effect of fluid intake on urinary symptoms in women. J Urol. 2005;174(1):187-189. doi:10.1097/01.ju.0000162020.10447.31

15. Wallace SA, Roe B, Williams K, Palmer M. Bladder training for urinary incontinence in adults. Cochrane Database Syst Rev. 2004;(1):CD001308. doi:10.1002/14651858.CD001308.pub2

16. Dumoulin C, Cacciari LP, Hay-Smith EJC. Pelvic floor muscle training versus no treatment, or inactive control treatments, for urinary incontinence in women. Cochrane Database Syst Rev. 2018;10(10):CD005654. doi:10.1002/14651858.CD005654.pub4

17. Cardozo L, Lisec M, Millard R, et al. Randomized, double-blind placebo controlled trial of the once daily antimuscarinic agent solifenacin succinate in patients with overactive bladder. J Urol. 2004;172(5 Pt 1):1919-1924. doi:10.1097/01.ju.0000140729.07840.16

18. Gray SL, Anderson ML, Dublin S, et al. Cumulative use of strong anticholinergics and incident dementia: a prospective cohort study. JAMA Intern Med. 2015;175(3):401-407. doi:10.1001/jamainternmed.2014.7663