30 HOW TO TREAT : URINARY INCONTINENCE IN WOMEN
30 HOW TO TREAT : URINARY INCONTINENCE IN WOMEN
13 SEPTEMBER 2024 ausdoc . com . au
Typically , the sensation of urinary urgency precedes leakage , and is usually associated with urinary frequency and nocturia . These symptoms may occur in the absence of urinary infection or other obvious pathology . In women , urgency urinary incontinence occurs when patients attempt to defer urination .
OAB is considered neurogenic if associated with a neurological condition but is otherwise regarded as idiopathic . Neurogenic OAB can be caused by afferent nerve sensitisation or damaged central inhibitory pathways , which can result in unmasking of primitive voiding reflexes and uninhibited detrusor contractions . In neurogenic OAB , there may be poor warning before leakage occurs . In OAB , involuntary contractions of the detrusor muscle during filling overwhelm the urethral closure mechanisms , leading to incontinence even when the bladder is not full .
Risk factors for OAB are listed in box 4 .
Mixed urinary incontinence
Stress urinary incontinence and urge urinary incontinence coexist in 33 % of patients . 23 It may be difficult to ascertain on history which component is the dominant cause of the incontinence . Urodynamics study may be useful to elucidate the main problem and to guide treatment .
Overflow incontinence
Overflow incontinence occurs when the bladder cannot empty adequately and patients develop severe chronic urinary retention . Bladder filling beyond a certain volume results in the intravesical pressure exceeding the bladder outlet pressure , and a variable volume of urine leaks out . 24
Chronic retention can result either from inadequate bladder contractility or bladder outlet obstruction . The increased intravesical pressure in chronic retention can also overcome the natural mechanism to prevent vesicoureteric reflux , resulting in hydronephrosis and renal damage . 24
Less common causes of incontinence
Three less common causes are described . These include , first , a urethral diverticulum . This is a rare and benign condition where the urethra develops an epithelium-lined outpouching , causing incontinence via post-micturition dribbling . 25
The second is a duplex / ectopic ureter . This is a unilateral congenital defect where the ureter implants in the sphincter or even directly in the vaginal wall rather than in the normal location . 26
The third is a urinary fistula . This is an abnormal opening between the urinary bladder and an adjacent structure , either the vagina or ureter , usually as a result from iatrogenic injury from pelvic surgeries , though an obstetric injury is more common in developing countries . 27
SYMPTOMS AND SIGNS
LOWER urinary tract symptoms ( LUTS ) can be divided into storage and voiding symptoms ( see box 5 ). 28
Box 1 . Physiology of the lower urinary tract ( LUT )
• Efferent pathways of the LUT : — Three sets of peripheral nerves make up the efferent pathways of the bladder : the sympathetic , parasympathetic and the somatic nervous systems . 4 — Activation of sympathetic nerves releases noradrenaline that relaxes the bladder body and contracts the bladder outlet and urethra , contributing to low pressure urine storage in the bladder . 5 — Activation of the parasympathetic nerves contracts the bladder body , contributing to voiding . 6 — The sacral somatic nerves in the pudendal nerve innervate the pelvic floor and the external urethral sphincter muscles . Activation of these nerves results in urine storage and voluntary relaxation of the pelvic floor to initiate voiding .
• Afferent pathways of the LUT : — In the storage phase , the bladder accommodates urine and maintains continence through inhibition of detrusor reflex activity ; this prevents involuntary bladder smooth muscle contractions and promotes normal urethral sphincter behaviour with sphincters closed at rest . — In the voiding phase , the bladder contracts and the sphincters relax . — Dysfunction in the sensory afferent signals that feed into the reflex pathways can lead to conditions like bladder pain syndrome or overactive bladder
( OAB ).
• Storage phase : — The intrinsic properties of the bladder smooth muscle and stroma , together with the absence of parasympathetic efferent activity , allow the bladder to fill .
• Bladder distention also triggers the sympathetic reflex , which promotes urethral outlet closure and inhibits centrally mediated bladder contraction . 6
• The bladder neck and proximal urethra are maintained in a closed position at rest because of coaptation ( apposition of the lumenal surface ) that is sympathetically mediated , leading to passive stress continence .
• The proximal urethra is normally well supported and does not descend during exertion .
• Pelvic supports of the urethra contribute to active urethral compression during exertion . — The guarding reflex , facilitated by external urethral sphincter via activated pudendal motoneurons , results in increased outlet resistance , contributing to the maintenance of urinary continence as the bladder fills .
• Voiding phase : — When circumstances are appropriate for voiding , voiding is heralded by external sphincter relaxation , the first component of a normal detrusor reflex voiding event .
• The external sphincter stays open , and the spinal cord excites a sustained detrusor contraction until complete bladder emptying .
• This voluntary voiding is co-ordinated via the spinobulbospinal reflex , which relays through the pontine micturition centre in the brainstem . 7
• Disturbance of this reflex in the spinal cord or pons may lead to incontinence and poor emptying function ; this may cause severe symptoms and high bladder pressures causing leakage , vesicoureteric reflux and renal damage .
• These scenarios also jeopardise antibacterial defences , making severe infection more likely . 8
— Adequate contractility is required in addition to intact reflex activity .
• Diabetes and the ageing bladder may result in impaired emptying related to the quality of the detrusor muscle .
• Where contractile reserve is poor , the residual volume may rise .
• Inadequate emptying of the bladder is another risk factor for urinary tract infections .
• Pharmacology : — Muscarinic receptors ( M2 and M3 ) in the human bladder play a critical role in detrusor contraction . M3 receptors are responsible for cholinergic contractions . 9 — Anticholinergic medications are commonly used as treatment for OAB . — Activated α-adrenergic and β-adrenergic receptors lead to bladder relaxation :
• As an alternative to anticholinergic agents , mirabegron ( β3-receptor agonist ) can be used to treat OAB .
• For improvement in urine release , α-adrenergic receptor antagonists ( for example , tamsulosin ) can be used in conditions of functionally increased urethral resistance such as benign prostatic hyperplasia ( BPH ) in men , and in primary bladder neck obstruction in women .
• Poor detrusor reflex emptying is not improved by pharmacology . In severe spinal conditions , the patient may need to use a catheter to empty their bladder even when storage function is effectively improved by therapy .
Box 2 . Mnemonic for transient urinary incontinence ( DIAPERS )
• Delirium .
• Infection ( chronic urinary tract infection ).
• Atrophic vaginitis / urethritis .
• Pharmacologic .
• Excess urine production .
• Restricted mobility .
• Stool impaction or faecal loading .
Box 3 . Risk factors for SUI
• Pregnancy , vaginal delivery ,
12 , 13
hysterectomy .
• Strenuous activity , chronic cough , constipation . 13
• Previous pelvic surgery , pelvic
14 , 15
trauma , pelvic radiotherapy .
16 , 17
• Obesity , smoking .
• Family history . 18
• Increasing age . 19
ASSESSMENT
IN most cases , history , examination and investigations with MSU and urinary tract ultrasound including post-void residual volume will result in a diagnosis and treatment regimen . However , for complex cases or when initial conservative treatment fails , more comprehensive investigations may be needed .
Box 4 . Risk factors for OAB
• Central nervous system disease , such as cerebrovascular accident 20 or Parkinson ’ s disease .
• Spinal pathology , such as multiple sclerosis or spinal cord injury .
• Urethral obstruction , such as postoperatively following sling or pelvic organ prolapse ( POP ) surgery .
• In 60 % of women with SUI , OAB wet ( urgency AND urge incontinence with leakage on the way to the toilet ) coexists and will resolve when SUI is effectively treated . 21
— The same causative relationship exists with POP , where secondary OAB may resolve once the POP is treated . 22 When leakage occurs after surgery , it may take careful evaluation to determine whether the problem is related to the initial pathology or to a postoperative complication such as obstruction .
History
History-taking is critical to determine the severity and cause of the symptoms as well as the patient ’ s desire for treatment . It may be difficult for patients to discuss their bladder problem with the GP , or they may believe their symptoms are “ normal ” for their age and not feel they need to be proactive about the condition .
History-taking covers the duration of symptoms , the storage and voiding symptoms listed in box 6 , and risk factors for incontinence .
Examination
Examination in patients with UI aims to detect significant disease processes and modifiable contributing factors .
Table 1 contains a useful checklist for examination , table 2 lists basic investigations , and table 3 the advanced investigations and their indications .
MANAGEMENT
TREATMENTS include both non-surgical and surgical modalities . Non-surgical options are recommended as first line and include behavioural and lifestyle modification and medications . Surgical management may be required for those with inadequate control with conservative treatment .
Behavioural and lifestyle modification
Educate patients about the types of incontinence and possible lifestyle measures ( see table 4 ) to improve their symptoms and empower them .
Medications
Remind patients that medications will only work if they remain on the therapy and that medications are to be used in conjunction with lifestyle modifications .
HORMONE REPLACEMENT THERAPY Topical vaginal oestrogen for postmenopausal women with vulvovaginal atrophy is available as a 0.1 % oestriol cream and a 10mcg oestradiol pessary . Advise patients to start with daily applications for the first 1-2 weeks , followed by a maintenance dose of twice-weekly applications . Consult the patient ’ s oncologist before prescribing oestrogen in patients with a history of oestrogen-sensitive cancers .
ANTICHOLINERGICS In OAB , anticholinergics block the