This document discusses overactive bladder (OAB). It defines OAB as a clinical syndrome of urgency, usually with frequency and nocturia. It can occur with or without urge incontinence. The prevalence of OAB increases with age and it affects both men and women. Treatment progresses from behavioral modifications and oral medications to minimally invasive procedures like botulinum toxin injections or sacral nerve stimulation for refractory cases. More invasive treatments like augmentation cystoplasty or urinary diversion are reserved for cases that fail less invasive options.
2. Introduction, Definition and Prevalence.
Bladder Anatomy and Physiology.
Etiology and Pathophysiology OAB.
Diagnosis and evaluation of OAB
Treatment of OAB.
3. The International Continence Society (ICS)
• 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 based on symptoms and it is a clinical syndrome.
• While detrusor overactivity (DO) is a urodynamic
observation, characterized by involuntary detrusor
contractions during the filling phase.
• OAB and DO are different terms.
4.
5. urgency Sudden desire to pass urine that is difficult to defer
Frequency Patient considers that he/she voids too often by day
Normal is < 8 times per 24 hours
Nocturia Waking to urinate during sleep hours considered a clinical
problem if frequency is greater than twice a night
Urge urinary
incontinence
(UUI)
Involuntary leakage accompanied by or immediately
preceded by urgency
OAB "wet“ OAB with UUI
OAB "dry" OAB without UUI
6. • When I want to go,
I have to rush
because I think I
may wet myself"
7. • Overall OAB prevalence is 11.8% in adults.
• prevalence increase with age.
• Both genders have similar rates of OAB, but
"OAB wet" is more prevalent in women and
"OAB dry" is more prevalent in men.
• OAB wet common in women due to the
relative weakness of the bladder neck and
urethral sphincter mechanism in women,
especial after pregnancy.
8. • Normal filling requires
Parasympathetic inhibition and sympathetic
stimulation - Reduces detrusor tone.
• Normal emptying requires
Sympathetic inhibition and parasympathetic
stimulation - increase detrusor tone.
9.
10. • The etiology of OAB is complex and poorly
understood.
Neurological hypothesis.
The myogenic hypothesis.
11. • DO arises from generalized, nerve-mediated
excitation of the detrusor muscle.
• Normaly the bladder control is modulated in an
inhibitory fashion by the 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..
12. Overactive detrusor contractions result
from a combination of
1. Increased spontaneous excitation within
smooth muscle of the bladder.
2. Enhanced propagation of this activity to
affect an excessive proportion of the
bladder wall.
13. • Bladder inflammation.
• Chronic bladder outlet obstruction
• Central nervous system disorders
• Pregnancy
• Vaginal delivery
• Postmenopausal status
• Older age (risk increase with age)
• Although the most common cause is idiopathic.
14. There are two types of OAB
• Complicated
1. Poor response to OAB medications
2. Extremely severe OAB symptoms
3. Young age
4. Recurent UTI
5. Pelvic surgery
6. Pelvic radiation
7. Poorly controlled DM
• Uncomplicated
have non of above characteristics
15. Diagnosis of OAB is symptom based and involves:
□ Careful history.
□ physical exam.
□ Urinalysis.
□ Frequency volume chart.
□ Post-micturation residue.
16. History should cover the following:
1. Presence or absence , severity, and effect on quality of life
for each of the OAB symptoms including urgency, frequency,
incontinence. Other LUTS should also be assessed.
2. Presence or absence of dysuria and hematuria.
3. Nature and volume of fluid intake.
4. Neurologic disease.
17. 5. Obstetric and gynecologic history, previous surgery/
radiotherapy, bowel symptoms.
6. Other medical issues (e.g., closed-angle glaucoma and
cognitive impairment can limit treatment options).
7. Drug history
There are many medications that can exacerbate the symptoms
of OAB (diuretics, alpha agonist)
18.
19.
20. • Abdominal and vaginal examinations should be performed
and, if indicated a rectal examination should also be
undertaken.
• The presence of pelvic organ prolapse, e.g a cystocele, may
cause urinary urgency and frequency as it drags on the
trigone and causes sensation of bladder fullness.
21. Physical examination
• Bimanual examination will rule out pelvic masses, e.g
ovarian cysts and uterine enlargement, which can also
cause urinary symptoms.
• For women with an atrophic vagina and symptoms of
OAB, estrogen deficiency may be a contributing factor to
their symptoms.
22. Urinalysis
• It should be done to exclude an underlying urinary tract
infection.
Post-micturition residual
• This can be performed to rule out overflow incontinence or
incomplete bladder emptying, which can cause symptoms of
OAB.
24. • Bladder diaries are useful tool when assessing patients
with urinary symptoms and facilitates history taking.
• Bladder diary done for a minimum of 3 days and the
patient continue his normal eating/drinking patterns as
well as daily activities.
• A record of how much fluid intake , how much urine
output , and how often patient empty his bladder on a
daily basis as well as any leakage occurs and number and
degree of wetness of pads.
26. • It is common practice to prescribe conservative
management and oral pharmacotherapy without a
urodynamic diagnosis.
• Before urodynamic tests are requested, the reasons for
"failure" of drug therapy should be explored:
1. Insufficient duration or poor patient compliance.
2. Insufficient dose, Presence of dry mouth symptoms is
a useful for deciding whether dose is adequate.
3. Idiosyncrasy of response; some people appear to find
better efficacy with certain agents.
4. Side effects.
27. Urodynamic indicated when
1) Conservative and drug therapy fail adequately to
manage OAB.
2) Complicated cases of OAB.
3) Before invasive surgery.
28. Urodynamic Evaluation
• Detrusor overactivity is involuntary detrusor contractions,
There is a rise in Pves with no associated rise in Pabd, and
therefore the subtracted Pdet looks identical to the Pves.
30. □Men
■ Benign prostatic
hyperplasia (BPH)
■ Prostate cancer
■ Bladder outlet
obstruction (BOO)
□Women
■ UTI
■ SUI
■ Prolapse
■ Atrophic vaginitis
■Both
■Postsurgical incontinence
■Neurogenic bladder
■Recent pelvic surgery
■Diabetes ■Bladder Stone
■Bladder cancer ■Urethral
stricture
31. □ Non invasive Treatment
• Behavioral therapy
• Oral Medication ( anticholinergic or beta 3 agonist).
• Combined therapy: behavioral and pharmacologic therapy.
• Estrogen for postmenopausal women.
• Role of alpha blocker.
□ Minimally invasive Treatments:
• Botulinum A-toxin.
• Neuromodulation (post tibial nerve , sacral nerve stimulation)
• Interruption of innervation (central subarachnoid block or sacral
rhizotomy, Peripheral motor and/or sensory block)
□ Highly invasive Treatments:
• Augmentation cystoplasty.
• Urinary diversion.
32. □ Dietary Changes and fluid Management
□ Timed voiding
□ Bladder training
□ Pelvic floor therapy
• Pelvic floor training ( Kegel exercises).
• Biofeedback ( auditory or visual feedback).
• Pelvic floor electrical or magnetic stimulation.
33. • Voiding by routine schedule with constant interval
between void(every 2 -3 hours).
• This help to empty the bladder before
incontinence occurs and decrease urgency and
frequency.
• Voiding interval may be changed throughout the
day to match patients' incontinence pattern.
34. It involves two processes
1. Modification of voiding interval by Gradual
increase of voiding interval by 15- 60 min every 1-2
week until an acceptable voiding interval is achieved
without incontinence. (initial interval determined by
pre-ttt voiding diary).
2. Urge control (bladder inhibition)
35. • It consists of Intermittent voluntary maximal
contraction of pelvic floor muscles
• Each contraction is held 6-8 seconds and
followed by brief period of relaxation.
• A common regimen is set of 10 contraction 3
times per day.
• Continence improved 6 -12 weeks after PFME.
38. ■ Mechanism of action
Act by competitively inhibit muscarinic receptor in
bladder wall - Reduce detrusor over activity.
■ Side effects
Due to inhibit muscarinic receptors outside the bladder
1. Eye
2. Salivary glands
3. Intestines
4. Heart
5. Brain
Blurry vision
Dry mouth
Constipation
Tachycardia
Impairs cognition and memory
(more with tertiary amines)
39. ■ Contraindications
1. Urinary retention
2. Intestinal obstruction
3. Uncontrolled narrow angle glaucoma
4. Myasthenia gravis
■ Duration
□ It improve symptoms within 1 week but max benefit is
achieved by 3 months.
40. • Tertiary amine , metabolize in liver to N-
Desethyloxybutynin which responsible for most
side effects.
Adult dose
• Immediate Release = 2.5 - 5 mg 3 times/day.
• Extended release= 5 - 30 mg once a day.
• Side effects - dry mouth, constipation, headache It
is Approved for pediatric use (age 6 or older)
Transdermal Patch available
41. • Teriary amine ,metabolize in liver
Adult dose
• Immediate Release 1-2 mg twice per day.
• long acting 2-4 mg Once per day.
Side effects
• Similar to oxybutynin in addition to allergic reaction
and hallucinations are reported.
42. • Tertiary amine, selective M3 inhibitor, metabolize
by liver.
• Highly selective for bladder than salivary glands
which may reduce dry mouth.
• Has long half life (48 hour) so used once per day.
• Adult dose
• 5 - 10 mg once daily dose
• Main side effects - constipation and less dry
mouth.
43. • Tertiary amine , M3 selective , metabolize by liver
• Adult dose
• 7.5 mg or 15 mg once a day.
• Main side effects - constipation and dry mouth.
44. • Quaternary amine , Not metabolize by liver.
• 60 % Excreted unchanged in the urine.
• Low oral bioavailability only 10 %.
• Adult dose
o 20 mg Twice per day.
o Extended release 60 mg once per day.
o Can be used in children older than 6 years with dose
20mg once per day.
• Theoretically harder to pass through blood/brain
barrier with less cognitive side effects.
45.
46. • Mechanism of action
Stimulate beta 3 adrenergic receptors causes relaxation of detrusor muscle
and Increase bladder capacity.
• Adult dose
25 or 50 mg per day
• Side effects
1. Hypertension
2. Headache
3. Tachycardia
4. Urinary retention
5. Very low rate of dry mouth and constipation.
• Contraindications
Sever uncontrolled hypertension
47. Role of estrogen in EUA Guidelines 2015
• Offer Vaginal Estrogen therapy for post-menopausal
women with urinary incontinence especially if other
symptoms of vulvovaginal atrophy are present.
• Don't offer oral estrogen replacement due to it's systemic
side effects.
48. 1) Botulinum A-toxin Intravesical injection.
□ Inhibit detrusor contraction by inhibit release of Ach at
neuromuscular Junction.
□ FDA approved in ttt of OAB refractory to Antimuscarinic
medications.
Side effects
Increase risk of UTI and Urinary retention that required
catheterization.
Contraindications
UTI, Pregnancy , myasthenia gravis.
51. □indication
-OAB refractory to less invasive ttt.
-Urinary incontinence due to reduce bladder capacity.
□Types
• Augmentation Enterocystoplasty
• Autoaugmentaton
• Urinary diversion as ileal conduit, catheterizable Stoma.
□ Mechanism
Increase bladder capacity and lower intravesical pressure.
□Efficiancy
• 80% become dry however 10-40% requires CIC.
• Less in Autoaugmentaton due to limited bladder capacity.
• Less in preoperative radiation .
52. • Offer bladder training as a first-line therapy to adults
with urgency urinary incontinence or mixed urinary
incontinence.
• Offer antimuscarinic drugs for adults with urgency
urinary incontinence.
• Consider using transdermal oxybutynin if oral
antimuscarinic agents cannot be tolerated due to dry
mouth.
• Use antimuscarinic drugs with caution in elderly
patients who are at risk of, or have, cognitive
dysfunction.
53. • Offer bladder wall injections of onabotulinum
toxin A (100 units) to patients with urgency
urinary incontinence refractory to antimuscarinic
therapy.
• If available, offer sacral nerve modulation to
patients, who have urgency urinary incontinence
refractory to conservative therapy.
54. • Only offer augmentation cystoplasty to patients
with detrusor overactivity incontinence who have
failed conservative therapy, in whom the
possibility of botulinum toxin and sacral nerve
stimulation has been discussed.
• Only offer urinary diversion to patients who have
failed less invasive therapies for the treatment of
urinary incontinence and who will accept a stoma.
• Do not offer Auto augmentation as a treatment
for urinary incontinence.