Detrusor overactivity

Detrusor overactivity is defined as a urodynamic observation characterized by involuntary contractions during the filling phase which maybe spontaneous or provoked [2]. It is the second commonest cause of urinary incontinence in women and accounts for 30-40% of cases. The incidence is higher in the elderly and after failed incontinence surgery. The actual cause of detrusor overactivity is unknown and in the majority of cases it is idiopathic, occurring when there is a failure of adequate bladder training in childhood or when the bladder escapes voluntary control in adult life. Often emotional or other psychosomatic factors are involved. In some cases detrusor overactivity may be secondary to an upper motor neurone lesion, especially multiple sclerosis. In such cases it is known as neurogenic detrusor overactivity. In men detrusor overactivity may be secondary to outflow obstruction and will be cured when the obstruction is relieved. However, outflow obstruction in women is rare.

Low compliance is said to exist when there is a sustained rise in detrusor pressure without actual detrusor contractions during bladder filling. There are a variety of causes, including radical pelvic surgery, radiotherapy, recurrent urinary tract infections and interstitial cystitis; but the symptoms associated with phasic detrusor overactivity and with low compliance may be indistinguishable without cystometry (Figs 49.28 and 49.29).

Low Compliance Bladder
Fig. 49.28 Cystometrogram recording showing phasic detrusor instability.
Cystometrogram Picture
Fig. 49.29 Cystometrogram recording showing low compliance.

pathophysiology of detrusor overactivity

The pathophysiology of detrusor overactivity remains elusive. In vitro studies have shown that the detrusor muscle in cases of idiopathic detrusor overactivity contracts more than normal detrusor muscle. These detrusor contractions are not nerve mediated and can be inhibited by the neuropeptide vasoactive intestinal polypeptide [154]. Other studies have shown that increased a-adrenergic activity causes increased detrusor contractility [155]. There is evidence to suggest that the pathophysiology of idio-pathic and obstructive detrusor overactivity is different. From animal and human studies on obstructive overactivity it would seem that the detrusor develops postjunc-tional supersensitivity possibly due to partial denervation [156], with reduced sensitivity to electrical stimulation of its nerve supply but a greater sensitivity to stimulation with acetylcholine [157]. If outflow obstruction is relieved the detrusor can return to normal behaviour and reinnervation may occur [158].

Relaxation of the urethra is known to precede contraction of the detrusor in a proportion of women with detrusor overactivity [159]. This may represent primary pathology in the urethra which triggers a detrusor contraction, or may merely be part of a complex sequence of events which originate elsewhere. It has been postulated that incompetence of the bladder neck, allowing passage of urine into the proximal urethra, may result in an uninhibited contraction of the detrusor. However, Sutherst and Brown [160] were unable to provoke a detrusor contraction in 50 women by rapidly infusing saline into the posterior urethra using modified urodynamic equipment.

More recently Brading and Turner [161] have suggested that the common feature in all cases of detrusor overactivity is a change in the properties of the smooth muscle of the detrusor which predisposes it to overactive contractions. They hypothesize that partial denervation of the detrusor may be responsible for altering the properties of the smooth muscle leading to increased excitability and increased ability of activity to spread between cells, resulting in coordinated myogenic contractions of the whole detrusor [162]. They dispute the concept of neurogenic detrusor overactivity, that is, increased motor activity to the detrusor, as the underlying mechanism in detrusor overactivity proposing that there is a fundamental abnormality at the level of the bladder wall with evidence of altered spontaneous contractile activity consistent with increased electrical coupling of cells, a patchy denerva-tion of the detrusor and a supersensitivity to potassium [163]. Other authorities suggest that the primary defect in the idiopathic and neurogenic bladders is a loss of nerves accompanied by hypertrophy of the cells and an increased production of elastin and collagen within the muscle fascicles [164].

clinical symptoms

Most women with an overactive bladder exhibit a multiplicity of symptoms, including urgency, urgency incontinence, stress incontinence, enuresis, frequency and especially nocturia and sometimes incontinence during sexual intercourse. There are no specific clinical signs and the diagnosis can only be made urodynamically when there is a failure to inhibit detrusor contractions during cystometry.

Treatment for detrusor overactivity aims to re-establish central control or to alter peripheral control via bladder innervation (Table 49.13). The fact that so many different types of treatment are available for this condition shows that none is universally successful. Various behavioural interventions (habit retraining) have been successfully used to treat idiopathic detrusor overactivity and have been shown to improve symptoms in up to 80% of women [165, 166]. Unfortunately, these types of therapy are time consuming and require the patient to be fairly intelligent and highly motivated. In addition, there is a high relapse rate and patients do not seem to respond as well on a second occasion. However, it is always appropriate to instruct patients with detrusor overactivity regarding the use of bladder drill, often as an adjunct to drug therapy. The regimen suggested by [167] is commonly employed and is described as follows.

1 Exclude pathology.

2 Explain rationale to the patient.

Table 49.13 Treatment of detrusor overactivity

Psychotherapy Bladder drill Biofeedback Hypnotherapy Acupuncture

Drug therapy

Inhibit bladder contractions anticholinergic agents musculotrophic relaxants tricyclic antidepressants Improve local tissues Oestrogens

Reduce urine production DDAVP (synthetic vasopressin)

Intravesical therapy Capsaicin Resiniferatoxin Botulinum toxin

Neuromodulation Cystoplasty Clam ileocystoplasty Detrusor myectomy


Maximum electrical stimulation Acupuncture

Transcutaneous electrical neuromuscular stimulation (TENS)

3 Instruct to void every 1.5 h during the day; she must not void between these times, she must wait or be incontinent.

4 Increase voiding interval by half an hour when initial goal achieved, and continue with 2-hourly voiding and so on.

5 Give normal volume of fluids.

6 Keep fluid balance chart.

7 Give encouragement.

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