The document discusses overactive bladder (OAB) and its treatment. It defines OAB as a condition caused by involuntary bladder contractions resulting in urgency and frequent urination. Common causes include neurological issues, bladder problems, medications, and idiopathic factors. Treatment involves pharmacotherapy using anticholinergic drugs to suppress contractions, bladder retraining, or surgery in severe cases. Lifestyle changes like limiting caffeine and bladder retraining exercises can also help manage symptoms.

1. OVERACTIVE BLADDER (OAB)
Dept of Urology
Govt Royapettah Hospital and Kilpauk Medical College
Chennai
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2. MODERATORS:
Professors:
 Prof. Dr. G. Sivasankar, M.S., M.Ch.,
 Prof. Dr. A. Senthilvel, M.S., M.Ch.,
Asst Professors:
 Dr. J. Sivabalan, M.S., M.Ch.,
 Dr. R. Bhargavi, M.S., M.Ch.,
 Dr. S. Raju, M.S., M.Ch.,
 Dr. K. Muthurathinam, M.S., M.Ch.,
 Dr. D. Tamilselvan, M.S., M.Ch.,
 Dr. K. Senthilkumar, M.S., M.Ch.
Dept of Urology, GRH and KMC, Chennai.
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3. DEFINITION:
Overactive bladder (OAB) is a condition caused by sudden
involuntary contraction (overactivity) of the bladder detrusor
muscles.
According to the International Continence Society (ICS), OAB is
characterized as urinary urgency, with or without urge
incontinence, usually with frequency and nocturia, in the absence
of causative infection or pathological conditions.
Other terms used include detrusor instability and
detrusor hyperreflexia.
Urge incontinence is characterized by a strong
sudden need to urinate, immediately followed by bladder
contraction, resulting in an involuntary loss of urine.
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Dept of Urology, GRH and KMC, Chennai.

4. ETIOLOGY:
1.Neurological causes:
a. Neurologic injuries
Spinal cord injury
Stroke
b.Neurologic diseases
Multiple sclerosis
Dementia
Parkinson disease
Medullary lesions
Diabetic neuropathy
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Dept of Urology, GRH and KMC, Chennai.

5. 2.Nonneurogenic causes:
Contractions can be spontaneous or induced by
rapid filling of the bladder, postural changes, or
even walking or coughing.
Nonneurogenic origins of detrusor
hyperactivity include
local genitourinary conditions such as
infection, bladder cancer, bladder stones,
bladder inflammation, or bladder outlet
obstruction .
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Dept of Urology, GRH and KMC, Chennai.

6. 3.Medications:
Diuretics can cause symptoms of urge
incontinence because of increased bladder
filling, stimulating the detrusor.
Bethanecol can also cause urge
incontinence through its stimulation of
bladder smooth-muscle contraction.
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Dept of Urology, GRH and KMC, Chennai.

7. 4.Idiopathic:
A specific cause cannot be identified in only
rare cases.
5.Cardiologic:
Heart failure or peripheral venous and
vascular disease can also contribute to OAB.
During the day, such individuals have excess fluid
collect in dependent positions (feet and ankles).
When they recline to go to sleep, much of this fluid
becomes mobilized and increases renal output,
thereby increasing urine output. Many of these
patients describe increased nocturia that
manifests as OAB. 7
Dept of Urology, GRH and KMC, Chennai.

8. Pathophysiology
A normal bladder operates through a
complex coordination of musculoskeletal,
neurologic, and psychological functions that
allow filling and voiding of the bladder
contents.
The prime effector of continence is the
synergic relaxation of detrusor muscles and
contraction of bladder neck and pelvic floor
muscles.
. 8
Dept of Urology, GRH and KMC, Chennai.

9. In bladder filling, sympathetic nerve fibers
that originate from the Th11 to L2
segments of the spinal cord, which
innervate smooth-muscle fibers around the
bladder neck and proximal urethra, cause
these fibers to contract, allowing the
bladder to fill
As the bladder fills, sensory stretch
receptors in the bladder wall trigger a CNS
response
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Dept of Urology, GRH and KMC, Chennai.

10. The PNS fibers, as well as those responsible for
somatic (voluntary) control of micturition
(urination), originate from the S2 to S4 segment
of the spinal cord in the sacral plexus.
The somatic fibers innervate the external
sphincter and are responsible for the voluntary
control of continence in the face of a pressing
desire to void.
The parasympathetic nervous system (PNS)
causes contraction of the detrusor, while the
muscles of the pelvic floor and external
sphincter relax.
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Dept of Urology, GRH and KMC, Chennai.

11. The normal adult bladder accommodates
300-600 mL of urine;
A CNS response is usually triggered when
the volume reaches 400 mL.
However, urination can be prevented by
cortical suppression of the PNS or by
voluntary contraction of the external
sphincter
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Dept of Urology, GRH and KMC, Chennai.

12. Any disruption in the integration of musculoskeletal and
neurologic responses can lead to loss of control of normal
bladder function and to urge incontinence.
In addition, physiologic changes associated with aging,
such as decreased bladder capacity and changes in
muscle tone, favor the development of OAB when
precipitating factors intervene.
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Dept of Urology, GRH and KMC, Chennai.

13. In postmenopausal women, many of these
changes are related to estrogen deficiency.
Perhaps the most important age-related
change in bladder function that leads to
incontinence is the increased number of
involuntary bladder contractions (detrusor
instability)
13
Dept of Urology, GRH and KMC, Chennai.

14. Treatment
Medical Care
Overactive bladder (OAB) can be managed with
several different methods. If a specific cause of
incontinence is identified, it should be treated
appropriately
for example, urinary tract infection should be
treated with antibiotics.
If a recent cause of OAB is detected, it should be
treated appropriately; for example, detrusor
overactivity can be caused by atrophic urethritis,
and topical application of estrogen vaginal cream
can be used for treatment in women. 14
Dept of Urology, GRH and KMC, Chennai.

15. The choice of a particular treatment depends on the
severity of the symptoms and the extent that the
symptoms interfere with the patient's lifestyle.
The 3 main approaches to treatment include
1.Pharmacotherapy,
2.Retraining ,
3.Surgery.
Behavioral interventions such as
- Limiting bladder irritants (eg, caffeine, alcohol)
- Bladder retraining
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Dept of Urology, GRH and KMC, Chennai.

16. Anticholinergics
These drugs inhibit the binding of acetylcholine to the
cholinergic receptor, thereby suppressing involuntary
bladder contraction of any etiology. In addition, they
increase the volume of the first involuntary bladder
contraction, decrease the amplitude of the involuntary
bladder contraction, and may increase bladder capacity.
Oxybutynin
Inhibits action of acetylcholine on smooth muscle and
has direct antispasmodic effect on smooth muscles,
which in turn increase bladder capacity and decrease
uninhibited contractions.
Immediate release: 2.5-5 mg PO tid/qid
Extended release: 5-30 mg PO qd
Patch: 3.9 mg twice weekly 16
Dept of Urology, GRH and KMC, Chennai.

17. Tolterodine
Competitive muscarinic receptor antagonist for
overactive bladder (OAB). However, differs from other
anticholinergic types in that it has selectivity for urinary
bladder over salivary glands.
Exhibits a high specificity for muscarinic receptors. Has
minimal activity or affinity for other neurotransmitter
receptors and other potential targets, such as calcium
channels.
Adult
Immediate release: 1-2 mg PO bid
Long acting: 2-4 mg PO qd
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Dept of Urology, GRH and KMC, Chennai.

18. Trospium
Quaternary ammonium compound that elicits
antispasmodic and antimuscarinic effects.
Antagonizes acetylcholine effect on muscarinic
receptors. Parasympathetic effect reduces
smooth-muscle tone in the bladder. Indicated to
treat symptoms of OAB (e.g., urinary
incontinence, urgency, frequency).
20 mg PO bid on empty stomach 1 h
before 18
Dept of Urology, GRH and KMC, Chennai.

19. Darifenacin
Extended-release product that elicits competitive
muscarinic receptor antagonistic activity. Reduces
bladder smooth-muscle contractions.
Has high affinity for M3 receptors involved in bladder
and GI smooth muscle contraction, saliva production,
and iris sphincter function. Indicated for OAB with
symptoms of urge incontinence, urgency and frequency.
Swallow whole; do not chew, divide, or crush.
7.5 mg PO qd initially; after 2 wk, may increase to 15 mg
PO qd based on response
Moderate hepatic impairment (Child Pugh B) or potent
CYP-450 3A4 inhibitors: Do not exceed 7.5 mg PO qd
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Dept of Urology, GRH and KMC, Chennai.

20. Solifenacin
Competitive muscarinic-receptor antagonist
approved by the FDA in late 2004 for the
treatment of OAB with symptoms of urge urinary
incontinence, urgency, and urinary frequency
5 mg PO qd; if tolerated, may be increased to
10 mg PO qd
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Dept of Urology, GRH and KMC, Chennai.

21. Tricyclic antidepressants
Some agents in this class may decrease bladder
contractility.
Imipramine
Useful in facilitating urine storage by decreasing bladder
contractility and increasing outlet resistance.
10-25 mg PO qd/tid initial; increase gradually prn;
not to exceed 25-100 mg/d
Doxepin:
Increases concentration of serotonin and norepinephrine in the
CNS by inhibiting their reuptake by presynaptic neuronal
membrane.
These effects are associated with a decrease in symptoms of
depression.
30-150 mg/d PO hs or 2-3 divided doses; gradually
increase dose to 300 mg/d prn 21
Dept of Urology, GRH and KMC, Chennai.

22. Hormones
These agents are used to treat OAB due to
atrophic urethritis.
Estrogen
Detrusor overactivity can be caused by
atrophic urethritis; topical application of
estrogen vaginal cream should be considered
in women.
Apply 2-4 g qd
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Dept of Urology, GRH and KMC, Chennai.

23. THANK YOU
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Dept of Urology, GRH and KMC, Chennai.