Detrusor Related Incontinence
What is Detrusor Related Incontinence?
The detrusor muscle is used to contract the bladder for urination. Detrusor instability, also known as
Overactive Bladder Syndrome, happens when this muscle doesn’t function properly. Involuntary
contractions occur for no reason, which can cause urinary incontinence.
Overactive bladder (OAB) syndrome is characterised by urgency, often with frequency and nocturia
(excessive urination at night) and sometimes leakage (urge incontinence). It is often but not always
associated with detrusor muscle overactivity. It can be idiopathic or neurogenic. Strictly speaking, the
term overactive bladder should be confined to cases where the condition is secondary to a known
cause, whilst overactive bladder syndrome should be used in cases which are idiopathic. In practice the
term is often used interchangeably. OAB can have a significant impact on quality of life. It seems to
affect more women than men. The risk of developing this condition increases with age. Patients with
Parkinson Disease, multiple sclerosis, diabetic neuropathy, spinal cord injury, or those who have
suffered a stroke also have an increased risk.
WHY and How
A variety of physical conditions and lifestyle habits can influence the chances of developing OAB. It is
often the result of a combination of factors where no single cause may be determined.
Within the body, OAB is often the result of spasms in the detrusor muscle, the main muscle of the
urinary bladder wall.
When the brain senses the bladder is about half full, it usually sends out nerve signals. These cause the
pelvic floor and sphincter muscles to relax while the detrusor contracts, squeezing out urine.
In people with OAB, detrusor muscle contractions occur at random. This leads to a sudden urge to
urinate, even when there's very little urine in the bladder. Depending on how the urinary sphincter
muscles reacts, urine leakage can occur.
Nerve damage and neurocognitive disorders have long been known to cause OAB symptoms by
interfering with nerve signalling.
Some definitions of OAB include neurological causes. Others refer to the symptoms as the result of
nervous system conditions affecting the bladder.
Common OAB causes include:
-pelvic organ prolapse
-stretched or weakened pelvic muscles
-low estrogen levels, especially after menopause
-giving birth via the vagina
-bladder abnormalities such as bladder stones or tumors
-Parkinson's disease, stroke, and multiple sclerosis
-decreased thinking ability or related diseases, including Alzheimer's disease
-hip surgery or hip problems
-stretched or weakened bladder muscles
-incomplete bladder emptying
-structural problems with the bladder
Common OAB risk factors include:
-being overweight or excess belly fat
-frequent or chronic urinary tract infections
-long-term dehydration or overhydration
-medications that cause a clear increase in urination or fluid intake
Management and Prevention
● Lifestyle changes:
1) Trial of reduction in caffeine intake. Staying hydrated but not overhydrated.
2) Modification of high or low fluid intake.
3) Many foods and drinks worsen OAB symptoms. Making a few dietary changes will often reduce
symptoms greatly. Caffeine, alcohol, and salty foods can act as a diuretic, increasing urine
output and trips to the bathroom. Spicy and acidic foods irritate the bladder lining, causing
discomfort and typically increasing the need for more bathroom visits. Dehydration also allows
bladder irritants closer contact with the bladder lining, making their effect more intense.
4) If the body mass index is over 30, weight loss.
5) Treating chronic constipation through medication or diet
6) Bladder training:
This is first-line treatment and should be for a minimum of six weeks. It typically involves pelvic muscle
training, including Kegels, scheduled voiding intervals with stepped increases and suppression of urge
with distraction or relaxation techniques.
7) Treating urinary and bladder infections
8) Quitting smoking to reduce coughing
9) Regular exercise
● Drug treatment:
1) Anticholinergic drugs: anticholinergics (antimuscarinic drugs) – have a direct relaxant effect on
urinary smooth muscle. They reduce involuntary detrusor contractions and increase bladder
capacity. Anticholinergic drugs have been shown to improve symptoms in OAB syndrome and
allow a modest improvement in quality of life.
2) Intravaginal oestrogens: these can be used to treat OAB syndrome in postmenopausal women
who have vaginal atrophy.
3) Mirabegron is an agonist of beta-3 receptors in detrusor smooth muscle, designed to promote
detrusor relaxation. It is recommended for people in whom antimuscarinic drugs are contra-
indicated or clinically ineffective, or who have unacceptable side-effects.
● Botulinum toxin A:
Injection of the bladder wall with botulinum toxin A is the first-line invasive option. It may be used if
there is idiopathic OAB that has not responded to conservative treatment. The patient must be prepared
to perform intermittent catheterisation if the effects wear off between injections. Urinary tract
infections are a recognised risk. The duration is variable.
● Nerve stimulation:
Sacral nerve stimulation is effective in treating symptoms of OAB, including urinary urge incontinence,
urgency and frequency in patients who do not respond to botulinum toxin A.
Percutaneous posterior tibial nerve stimulation (PTNS) is also effective in reducing symptoms in the
short term and medium term for patients with OAB syndrome and should be offered to patients who do
not want the first- or second-line options.
● Surgical treatment:
Surgery is only indicated for intractable and severe idiopathic OAB. Augmentation cystoplasty is the
most frequently performed surgical procedure for severe urge incontinence.
In patients whose condition is refractory to non-surgical treatment, open augmentation cystoplasty is an
Laparoscopic augmentation cystoplasty (including clam cystoplasty) is also indicated for OAB syndrome.
Potential advantages of a laparoscopic approach are less intraoperative blood loss, quicker recovery,
less pain, a shorter stay in hospital and smaller scars.
Urinary diversion may be considered if augmentation cystoplasty is neither appropriate nor acceptable
to the patient.