Overactive bladder:

Definition: 
Overactive bladder (OAB) is a symptom syndrome that includes urgency,
with or without urge incontinence, frequency, and nocturia.

The symptoms are usually caused by bladder (detrusor) overactivity, but can be due to other forms of voiding dysfunction. Roughly 17% of the population >40 years old in Europe has symptoms of OAB.
 

Conventional treatment:
Conservative
Patient management involves a multidisciplinary team approach (urologists,
gynecologists, continence nurse specialists, physiotherapists, and
community-based health care workers).

Treat underlying causes (urethral
obstruction, bladder stones, spinal disease, tumor).
 

TURP for bladder outlet obstruction due to BPH can provide symptomatic
relief in >66% of men.

Treatment of the SUI component includes
pelvic floor exercises, biofeedback, and high-frequency electrical stimulation
(which strengthens the pelvic floor and sphincter by increasing tone
through sacral neural feedback systems).
 

Behavioral modification

This involves modifying fl uid intake, avoiding stimulants (caffeine, alcohol),
and bladder training for urgency (delay micturition for increasing periods
of time by inhibiting the desire to void).

Medication
 

Most patients will benefi t from medication.
• Anticholinergic drugs act to inhibit bladder contractions and increase
capacity (oxybutynin, tolterodine, trospium chloride, solifenacin,
darifenicin, fesoteridine).

Oxybutynin also exerts a direct muscle effect
and can be administered directly into the bladder (intravesically) in
patients performing intermittent catheterization (5 mg in 30 mL normal
saline q8h after emptying the bladder).

• Contraindications include closed angle glaucoma.
 

• Side effects are dry mouth, constipation, and blurred vision.
 

• Tricyclic antidepressants (imipramine) exert a direct relaxant effect
on bladder muscle as well as produce sympathomimetic and central
effects.
 

• Desmopressin (DDAVP) is a synthetic vasopressin analog that acts
as an antidiuretic. It is used intranasally to alleviate nocturia in adults.
Oral DDAVP is effective for nocturnal polyuria.

• Baclofen is a GABA receptor agonist, used orally or via intrathecal
pump in patients with bladder dysfunction and limb spasticity.
 

Overactive bladder: options for failed
conventional therapy

Neuromodulation 

This involves electrical stimulation of the bladder’s nerve supply to suppress
refl exes responsible for involuntary bladder muscle (detrusor)
contraction.
The Interstim device stimulates the S3 afferent nerve, which then inhibits
detrusor activity at the level of the sacral spinal cord. An initial percutaneous
nerve evaluation is performed, followed by surgical implantation
of permanent electrode leads into the S3 foramen, with a pulse generator
that is programmed externally.
 

Surgery

The aim is to increase functional bladder capacity, decrease maximal
detrusor pressure, and protect the upper urinary tract.
 

Augmentation enterocystoplasty (“clamshell” ileocystoplasty)
 

This procedure is the gold-standard method of providing a high-volume
low-pressure storage system for the pathological bladder. It relieves
intractable frequency, urge, and UUI in 90% of patients.
The bladder dome is bivalved and a U-shaped detubularized segment of
ileum is patched into the defect, creating a larger bladder volume that can
store urine at lower pressures.
Many patients will void spontaneously but most will need to perform
intermittent catheterization periodically to empty completely.

Conduit diversion
 

This is a noncontinent urinary outlet in which the ureters are anastomosed
to a short ileal segment, which is brought out cutaneously as a stoma in
the right lower quadrant.
Ileocystoplasty: acts like an ileal conduit attached to the bladder, performed
in conjunction with bladder neck closure to provide conduit drainage
without the need for ureteral reconstruction.
 

Auto-augmentation (detrusor myectomy)
 

Detrusor muscle is excised from the dome of the bladder, leaving the
underlying bladder endothelium intact. A large epithelial bulge is created
which augments bladder capacity.

Intravesical pharmacotherapy
 

Botulinum toxin A (BTX-A) injection therapy acts by inhibiting calciummediated
release of ACh at the neuromuscular junction, reducing muscle
contractility. It is used predominantly for neuropathic bladder dysfunction,
but increasingly is being used for failed medical therapy of the OAB in
non-neuropaths. It is injected directly into detrusor muscle under cystoscopic
guidance (fl exible cystoscopy or rigid under regional or general
anesthetic) at 20–30 random sites, excluding the trigone (dose dependent
on supplier’s recommended dose schedule).

Repeat treatments are required (6–12 months between injections), and
ISC may be needed to empty residuals (5% of non-neuropaths).
Mild fl u-like reactions lasting a week or so can occur. Generalized
weakness, swallowing or breathing diffi culty are rarely reported. Allergic
reactions are uncommon