OVERACTIVE BLADDER (OAB)

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. Urge
incontinence is one of the most common types of urinary
incontinence.
ETIOLOGY:
1.Neurological causes:
a. Neurologic injuries
Spinal cord injury
Stroke
b.Neurologic diseases
Multiple sclerosis
Dementia
Parkinson disease
Medullary lesions
Diabetic neuropathy
2.Nonneurogenic causes:
Detrusor hyperactivity can also occur in the
absence of a neurogenic etiology.
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 .
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.
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.
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.
.
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
The parasympathetic nervous system (PNS) causes
contraction of the detrusor, while the muscles of
the pelvic floor and external sphincter relax.

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 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
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.
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)
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.
 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
.
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
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
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
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
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
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
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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