5 Incontinence and female urology

Urinary incontinence (UI) is the complaint of any involuntary leakage of urine.¹ It results from a failure to store urine during the filling phase of the bladder due to dysfunction of the bladder smooth muscle (detrusor), urethral sphincter, or anatomical abnormalities (congenital or acquired). Urine loss is either urethral or extraurethral (i.e. due to ectopic ureter or vesicovaginal fistula).

There is wide variation in the reported prevalence of UI worldwide. It affects about 3.5 million people in the UK. The prevalence is approximately twice as common in females compared to males and increases with age (Table 5.1).² International studies show a gradual increase in the prevalence of female UI during adulthood to 30%, stabilizing between the ages of 50 and 70y old, before rising again.³ Approximately 50% of women suffer stress UI, 11% urgency UI, and 36% mixed UI.³

Stress urinary incontinence (SUI): involuntary urinary leakage on effort, exertion, sneezing, or coughing.¹ It is due to hypermobility of the bladder base, pelvic floor and/or intrinsic urethral sphincter deficiency. When confirmed on urodynamic testing, it is termed urodynamic stress incontinence. It was further categorized by Blaivas⁴ (using videourodynamics) into:

Urgency urinary incontinence (UUI): involuntary urine leakage accompanied by or immediately preceded by urgency (a sudden, strong desire to void).¹ Previously called ‘urge’ urinary incontinence, it is due to an overactive detrusor muscle. The urodynamic diagnosis is termed ‘detrusor overactivity incontinence’. It is a component of the overactive bladder syndrome (see OAB  p. 148).

Mixed urinary incontinence (MUI): involuntary leakage associated with urgency and also with exertion, effort, sneezing, or coughing.¹ It contains symptoms of both SUI and UUI.

Overflow incontinence: is leakage of urine when the bladder is abnormally distended with large residual volumes. Typically, men present with chronic urinary retention (with a degree of detrusor failure) and dribbling incontinence. This can lead to back pressure on the kidneys and renal failure in 30% of patients. BOO must be corrected; detrusor failure can be managed with clean intermittent self-catheterization (CISC) or indwelling catheter.

Nocturnal enuresis: the complaint of loss of urine occurring during sleep.¹ The prevalence in adults is about 0.5%⁵ and 7–10% in children aged 7y old.⁶ Nocturnal enuresis can be further classified into primary types (never been dry for longer than a 6-month period) or secondary (the re-emergence of bedwetting after a period of being dry for at least 6–12 months; see  p. 694). In an adult male, nocturnal incontinence may be an indicator of high-pressure chronic retention (see  p. 120).

Post-micturition dribble: involuntary loss of urine immediately after the individual has finished passing urine, usually after leaving the toilet in men or after rising from the toilet in women.¹ In men, it is due to pooling of urine in the bulbous urethra after voiding.

A recent standardization report by the International Urogynaecology Association and the International Continence Society on female pelvic floor dysfunction⁷ recommend new definitions, including:

Urodynamic studies can help determine the underlying aetiology for UI.

Detrusor overactivity: a urodynamic observation characterized by involuntary bladder muscle (detrusor) contractions during the filling phase of the bladder, which may be spontaneous or provoked and can consequently cause UI. The underlying cause may be neuropathic where there is a relevant neurological condition or idiopathic where there is no defined cause. It leads to the symptoms of urgency incontinence and overactive bladder (OAB).

The pathogenesis of detrusor overactivity is most likely to be multifactorial. Theories include:

Low bladder compliance: characterized by a decreased volume-to-pressure relationship where there is a high increase in bladder pressure during filling due to alterations in elastic properties of the bladder wall or changes in muscle tone (secondary to myelodysplasia, SCI, radical hysterectomy, interstitial or radiation cystitis).

In females, there may be functional abnormalities of urethral hypermobility and/or ISD. These are the main causes of SUI.

Urethral hypermobility: due to a weakness of pelvic floor support, causing a rotational descent of the bladder neck and proximal urethra during increases in intra-abdominal pressure. If the urethra opens concomitantly, there will be urinary leaking.

Intrinsic sphincter deficiency: describes an intrinsic malfunction of the sphincter, regardless of its anatomical position, which is responsible for type III SUI (described by McGuire). Causes include inadequate urethral compression (previous urethral surgery, ageing, menopause, radical pelvic surgery, anterior spinal artery syndrome) or deficient urethral support (pelvic floor weakness, childbirth, pelvic surgery, menopause). In males, the urethral sphincter may be damaged after prostatic or pelvic surgery (TURP, radical prostatectomy) or radiotherapy.

Theories for the pathogenesis of SUI include:

Aim: to establish the type of incontinence (stress, urgency or mixed). Enquire about LUTS (storage or voiding symptoms); triggers for incontinence (cough, sneezing, exercise, position, urgency); frequency, severity, and degree of bother of symptoms. Establish risk factors (abdominal/pelvic surgery or radiotherapy, neurological disorders, obstetric and gynaecology history, medications). Enquire about bowel function and symptoms of sexual dysfunction and pelvic organ prolapse in women (see  p. 170) A validated patient-completed questionnaire is helpful to assess initial symptoms and patient-reported outcome following intervention (ICIQ-UI short form,^1,5 ICIQ-FLUTS,² ICIQ-MLUTS,³ SF36 QoL⁴) (Fig. 5.1).

‘Red flag’ symptoms which require further specific investigation are incontinence associated with pain, haematuria, recurrent UTI, significant voiding or obstructive symptoms, and a previous history of pelvic surgery/radiotherapy.

Perform a chaperoned pelvic examination in the supine, standing, and left lateral position with a Sim’s speculum. Ask the patient to cough or strain and inspect for anterior and posterior vaginal wall prolapse, uterine or vaginal vault descent, and urinary leakage (stress test). Internal pelvic examination can be performed to assess the strength of voluntary pelvic floor muscle strength and for bladder neck mobility. Inspect the vulva for oestrogen deficiency (causing vaginal atrophy), which may require topical oestrogen treatment. Calculate of body mass index (BMI) as a tool to counsel patients as higher BMIs are associated with incontinence.

Examine the abdomen for a palpable bladder (indicating urinary retention if the patient has recently passed urine). A neurological examination should include assessment of gait, anal reflex, perineal sensation, and lower limb function. DRE should be performed to exclude constipation, a rectal mass, and to test anal tone.

‘Red flag’ signs requiring further investigation include (new) neurological deficit, haematuria, urethral, bladder or pelvic masses, and suspected fistula.

Bladder diaries: record fluid intake, the frequency and volume of urine voided, incontinent episodes, pad usage, and degree of urgency over a 3-day period.

Urinalysis ± culture: treat any infection and reassess symptoms.

Flow rate and post-void residual (PVR) volume: patients need to void 150mL of urine for an accurate result. A reduced flow rate suggests BOO or reduced bladder contractility. The volume of urine remaining in the bladder after voiding (PVR) is also informative (<50mL is normal; >200mL is abnormal; 50–200mL requires clinical correlation). PVR is measured with transabdominal USS.

Pad testing: weighing of perineal pads to estimate urine loss after a specific time or provocation test. It is performed with a full bladder. A pad weight gain >1g is positive for a 1h test and a pad weight gain >4g is positive for a 24h test. This is not standardized and not always reliable.

Blood tests, imaging (USS) and cystoscopy: indicated for complicated cases with persistent or severe symptoms, haematuria, bladder pain, voiding difficulties, recurrent UTI, abnormal neurology, previous pelvic surgery or radiation therapy, or suspected extraurethral incontinence.

Sphincter electromyography (EMG): measures electrical activity from striated muscles of the urethra or perineal floor and provides information on synchronization between the bladder muscle (detrusor) and external urethral sphincter.

This accounts for up to 50% of reported UI in women and causes the symptoms of involuntary urinary leakage on effort (e.g. lifting), exertion (e.g. running), sneezing, and coughing. It is associated with an intrinsic loss of urethral strength and/or urethral hypermobility.

External urethral sphincter damage (from pelvic fracture, prostatectomy, pelvic surgery, or radiotherapy).

Neurological disorders causing sphincter weakness (SCI, multiple sclerosis, spina bifida).

Approximately 30% of women will report symptoms of MUI, with involuntary urinary leakage associated with urgency and also with exertion, effort, sneezing, or coughing. The underlying aetiologies and evaluation remain the same as for SUI and UUI, but also consider further investigation to rule out pathologies such as bladder cancer, stones, and interstitial cystitis. The aim of management is to treat the predominant symptoms first.

The injection of bulking materials into bladder neck and periurethral muscles is a minimally invasive surgical technique used to increase outlet resistance (Table 5.2). The main indication is for female stress incontinence secondary to demonstrable ISD in the presence of normal bladder muscle function. There is also evidence of benefit in urethral hypermobility.

The aim is to achieve urethral muscosal apposition and closure of the lumen. In women, 2–4 injections are recommended (depending on agent) while in men, 3–4 circumferential injections are administered. Overall success rates are variable, depending on both the agent and patient selection (reported in ranges of 50–80%).¹²³⁴ Results tend to deteriorate with time and repeat treatments are often needed.

Overall success rates are variable, depending on both the agent and patient selection, with reported ranges of 10–80%.¹²³⁴⁵ Results tend to deteriorate with time (i.e. the success of Durasphere^® decreases from 80% at 1y to 12% at 3y).⁵ Patients should be counselled on outcomes and the need for repeat treatments. As the results are not durable, periurethral bulking agents are not commonly used as a first-line intervention.

Retropubic suspension procedures are used to treat female stress incontinence predominantly caused by urethral hypermobility. The aim of surgery is to elevate and fix the bladder neck and proximal urethra in a retropubic position in order to support the bladder neck and regain continence. There is a lower chance of clinical benefit in the presence of significant ISD.

Surgery is considered after conservative methods have failed. There are three main operations, all of which can be performed open via a Pfannenstiel or lower midline abdominal incision to approach the bladder neck and develop the retropubic space. Burch colposuspension can also be performed laparoscopically. Better results are seen in patients with pure stress incontinence and primary repair (as opposed to ‘re-do’ surgery).

This is the most widely used technique with the best durability. Patients that are selected require good vaginal mobility as the vaginal wall is elevated and attached to the lateral pelvic wall where the formation of adhesions over time will secure its position. It is also considered an option for patients with concurrent SUI and anterior vaginal wall prolapse. This operation involves exposing the paravaginal fascia and approximating it to the iliopectineal (Cooper’s) ligament of the superior pubic rami. Initial success rates for open repair are about 85–90% at 1y and 70% at 5y.¹ Success rates when used for recurrent incontinence are 83% at 1y.² Overall success rates are slightly higher for open repair over the laparoscopic approach.^3,4 Open repair has a shorter operating time and the laparoscopic approach is more costly, but has a shorter hospital stay.

A variant of the Burch procedure. Sutures are placed by the vaginal wall and paravaginal fascia and then passed through the obturator fascia to attach to part of the parietal pelvic fascia below the tendinous arch (arcus tendoneus fascia). It aims to disperse tension on the paravesical tissues laterally to reduce the risk of prolapse. Cure rates are up to 85%, although it is considered less effective than the Burch colposuspension.

Sutures are placed on ither side of the urethra around the level of the bladder neck and then tied to the hyaline cartilage of the pubic symphysis. Short-term success is about 90%,¹ however, this declines over time and is now considered less effective than the Burch procedure. Complications include a 3% risk of osteitis pubis which typically presents up to 8 weeks post-operatively with pubic pain radiating to the thigh. Treatment is with simple analgesia, bed rest, and steroids.

Widely practised first-line surgical treatment for female SUI. Tapes can be inserted under general or local anaesthetic as day cases. They are less invasive than colposuspension with fewer complications. They are placed via a retropubic route (TVT) or a transobturator route (TOT, TVTO). The bladder should be empty and catheterized. All techniques use cystoscopy to detect bladder perforation during sling placement. Post-operatively, patients may temporarily require CISC until post-void residuals are less than 100–150mL.

A small midline anterior vaginal incision is made over the mid-urethra. The TVT tape has long trocars on each end. These are inserted either side of the urethra and perforate through the endopelvic fascia. They are then pushed up behind the symphysis pubis and out onto the lower abdominal wall in the midline, just above the pubic bone (i.e. trocar passes from bottom upwards). Once the tape is positioned loosely (tension-free) over the mid-urethra, its covering is removed and the ends cut flush to the abdomen. Vaginal epithelium is closed over the top.

A midline anterior vaginal incision is made for dissection around the urethra. Two small incisions are made lateral to the labia majora at the level of the clitoris. In the Monarc Subfascial Hammock (AMS), the curved handle device is placed through the skin incision and turned downwards, passing through the anterior part of the obturator foramen and exiting alongside the urethra on each side (i.e. trocar passes from outside to inside). The tape is attached to the end of each handle and brought back out to the skin surface. It is positioned loosely around the mid-urethra and the ends cut flush with the skin. In TVTO, the tape is passed in a reverse route (i.e. trocar passes from inside to outside).

Examples of self-retaining mini tapes inserted via a single vaginal incision are the MiniArc^® (AMS) and GYNECARE TVT SECUR^TM. The short-term success rates are around 80–90%,^7,8 although results may not be sustained over time.⁸

Most commonly, a segment of rectus fascia measuring 10–20cm in length is harvested via a Pfannenstiel approach and non-absorbable long sutures placed on both ends. The sling is placed under the mid-urethral and the sutures placed through the endopelvic fascia up to the remaining rectus fascia where the suture ends are tied using the minimal amount of tension needed to prevent urethral movement. Autologous slings have been shown to have a better outcome as compared to colposuspension, but at the expense of higher complications (UTI, voiding dysfunction, and urge incontinence).⁹ Autologous retropubic slings are not commonly used as first-line surgical procedures for SUI.

There are many new male continence slings and devices available, but follow-up data are limited. Examples include:

The artificial urinary sphincter (AUS) (AMS800^TM; Fig. 5.5) is a closed pressurized system with three components. The inflatable cuff is commonly placed around the bulbar urethra or alternatively, the bladder neck (in both women and men). A pressure-regulating balloon is placed extraperitoneally in the abdomen. An activating pump is placed in the scrotum or labia majora. The cuff provides a constant circumferential pressure to compress the urethra. To void, the pump is squeezed, which transfers fluid to the reservoir balloon, thereby deflating the cuff. The cuff then automatically refills within 3min. Voiding takes place in the interval taken for the cuff to refill. The reservoir balloon pressure can be 61–70mmHg for bulbar urethral placement or 71–80mmHg for bladder neck placement.

Used for moderate to severe SUI, secondary to urethral sphincter deficiency in patients with normal bladder capacity and compliance. In men, it is used for sphincter damage due to radical prostatectomy, TURP, pelvic radiotherapy, pelvic fracture, and following complicated urethral reconstruction. In women, it is used after other treatments for incontinence have failed. It can be used for neuropathic sphincter weakness (e.g. SCI, spina bifida). If there is combined bladder overactivity and sphincter weakness, treat the bladder first (i.e. lower bladder pressures with anticholinergics, intravesical botulinum injections, augmentation), which, in some cases, will be enough to achieve continence. If incontinence persists, proceed with AUS at a later date.

Contraindications to AUS: bladder neck stenosis, poor patient manual dexterity or cognition, active infection.

Patients should undergo urodynamics, cystoscopy, and upper tract imaging to evaluate voiding function and identify anatomical abnormalities that might affect the efficacy of the AUS. Good manual dexterity is required to manipulate the pump and sufficient cognitive function to operate the AUS themselves several times daily.

AUS can function well for many years (10y). Overall long-term success (continued continence, no device malfunction) is 70–90%; revision rates are 20–30%.¹

Recurrent incontinence due to:

Erosion: occurs in 5%, most commonly at 3–4 months, with 75% occurring in the first year. Presents with pain and swelling of scrotum, labia or perineum, incontinence, and bloody discharge. Increased risk after pelvic radiotherapy.

Infection: primary implant infection rates are 1–5%. With infection or erosion, remove the entire device and wait 3–6 months before reinsertion.

Other: haematoma (scrotum or labia); late urinary retention which may signify obstruction from urethral stricture or bladder neck contracture (higher risk with previous pelvic irradiation). Always ensure that the AUS is deactivated (i.e. the cuff is deflated) prior to urethral instrumentation or catheterization.

Overactive bladder (OAB) is a symptom syndrome that includes urgency, with or without urge incontinence, usually with frequency and nocturia. The symptoms are usually caused by bladder (detrusor) overactivity, but can be due to other forms of voiding dysfunction (Fig. 5.6). Seventeen percent of the population aged >40y in Europe have symptoms of OAB.¹ The prevalence increases with age.

Patient management involves a multidisciplinary team approach (urologists, urogynaecologists, continence nurse specialists, physiotherapists, and community-based health care workers). Pelvic floor muscle training (PFMT), biofeedback, acupuncture, and electrical stimulation therapy (which strengthens the pelvic floor and sphincter by increasing tone through sacral neural feedback systems) may provide some benefit.

This involves modifying fluid intake, avoiding stimulants (caffeine, alcohol), and bladder training (delayed micturition for increasing periods of time by inhibiting the desire to void). If this fails, consider medication.

Acetylcholine acts on muscarinic receptors (M3 ± M2 subtypes) on the bladder smooth muscle (detrusor) to cause involuntary contractions and provoke the symptoms of bladder overactivity. These receptors are the targets of anticholinergic (antimuscarinic) drugs which inhibit contractions and increase bladder capacity. Approximately 50% of patients will benefit from medication.

Uncontrolled narrow angle glaucoma, myasthenia gravis, BOO, bowel disorders (i.e. active ulcerative colitis, bowel obstruction).

Dry mouth, constipation, blurred vision, urinary retention, cognitive impairment, skin rash with transdermal patches.

(see also  p. 624)

Sacral nerve stimulation involves electrical stimulation of the bladder’s nerve supply to suppress reflexes responsible for involuntary bladder muscle (detrusor) contraction.^*

The aim is to increase functional bladder capacity, decrease maximal detrusor pressure, and protect the upper urinary tract (also see  pp. 602–7).

Augmentation enterocystoplasty (‘Clam’ ileocystoplasty): relieves intractable frequency, urge, and UUI in 90% of patients. The bladder dome is cut open (bivalved) and a detubularized segment of ileum is anastomosed, creating a larger bladder volume.

Autoaugmentation (detrusor myectomy): detrusor muscle is excised from the entire dome of bladder, leaving the underlying bladder endothelium intact. A large epithelial bulge is created which augments bladder capacity. Less commonly performed now as limited long-term efficacy. Most benefit in patients with idiopathic detrusor overactivity.

Urinary diversion: a non-continent urinary outlet, reserved for intractable cases only. Typically, both ureters are anastomosed and connected to a short ileal pouch which is brought out cutaneously as a stoma.

Botulinum toxin-A (BTX-A): injected at multiple sites as a bleb under the bladder mucosa or into detrusor, sparing the trigone (see  pp. 152–3; 604–7; 590–1). This treatment is off licence.

Botulinum toxin (BTX) is a neurotoxin produced by a Gram-positive, rod-shaped, anaerobic bacterium, Clostridium botulinum. There are seven subtypes. Subtypes A and B are used in urology; however, BTX-A is the more potent with longer duration of action.

Children with NDO associated with myelomeningocele⁵ and with IDO⁶ have been safely and successfully treated with BTX-A. There is also emerging, but limited, evidence for a role in symptomatic benign prostatic enlargement and chronic pelvic pain syndromes (BPS/IC).

BTX-A acts by inhibiting the release of acetylcholine (ACh) and other neurotransmitters from presynaptic cholinergic nerve terminals, resulting in regionally decreased muscle contractility and muscle atrophy at the site of BTX-A injection. The chemical dennervation that results is a reversible process.

UI occurs in <1% after TURP and 0.5% after open prostatectomy (OP) performed for benign prostate disease.¹ Following radical prostatectomy (RP) for malignant disease, UI tends to improve over 12–18 months post-surgery.² The overall incidence in open RP is 710–15%,^2,3 with similar risks reported for laparoscopic RP.⁴ Early results from robotic-assisted laparoscopic RP suggest slightly earlier recovery of continence and improved overall continence rates.⁵

Earlier recovery of continence after open RP is achieved using a perineal approach, nerve sparing techniques, and sphincter and bladder neck preserving procedures.

The main cause of post-radical prostatectomy incontinence is sphincter dysfunction. The proximal sphincter mechanism is removed at prostatectomy (TURP, OP, RP). Post-prostatectomy continence, therefore, requires a functioning distal (external) urethral sphincter mechanism and low bladder pressure during bladder filling. Direct damage to the external sphincter can occur during prostatectomy (at TURP, it occurs particularly during resection between 11 and 2 o’clock positions when the reference point for the position of the distal sphincter, the verumontanum, cannot be seen). Damage to the innervation of the sphincter can also occur during prostatectomy. Urodynamic studies before and after RP show that maximal urethral closure pressure (MUCP) and functional urethral length (the length of urethra over which the sphincter functions to maintain high pressures) are lower. Nerve-sparing RP (where the neurovascular bundles are specifically identified and preserved) produces better continence rates and longer functional urethral lengths and MUCPs.

A substantial proportion of men also have OAB before prostatectomy and this may remain so after surgery, contributing to UI.

Wait for up to 12 months for spontaneous improvement. Act sooner if symptoms are severe.

PFMT does not appear to convey benefit. In the Men After Prostate Surgery (MAPS) study, four sessions of PFMT administered by a trained physiotherapist or continence nurse over a 3-month period had no impact on continence^* or QALY 12 months post-prostatectomy when compared with no intervention. In the radical prostatectomy group, 76% of incontinent men receiving PFMT remained wet compared with 77% not receiving such training; in the TURP group, 65% of incontinent men receiving PFMT remained wet compared with 62% not receiving such training.⁶

VVF is an abnormal communication between the bladder and vagina. In 10%, there is a coexisting ureterovaginal fistula.

In developing countries, the majority are due to obstructed or prolonged childbirth, causing tissue pressure necrosis between the vagina and bladder. In developed countries, 75% follow hysterectomy (0.1–0.2% risk; Fig. 5.6).^1,2 Other causes include pelvic surgery or radiotherapy, pessary erosion, advanced pelvic malignancy (cervical carcinoma), pelvic endometriosis, inflammatory bowel disease, trauma, childbirth (5%), low oestrogen states, infection (urinary TB), and congenital abnormalities.

Immediate or delayed onset of urinary leakage from the vagina post-operatively; abdominal pain or distension; prolonged bowel ileus (due to leak of urine into the peritoneal cavity as well as through the vagina); suprapubic pain; haematuria.

Small, uncomplicated VVF may resolve with urethral catheterization (9 anticholinergics and antibiotics) or electrocoagulation of the tract (9 fibrin sealant). A coexisting ureterovaginal fistula will require ureteric stent or catheter. Most cases proceed to surgery.

Overall surgical success for simple VVF repair is 90%. Early repair (within 2–3 weeks) is advocated in selected cases, but traditionally, surgery is delayed 3–6 months (or 6–12 months following radiation therapy). The main principles are to excise the fistula, tension-free closure, and interposition of healthy tissue.

Transvaginal approach: most commonly used. The vaginal flap technique involves incision of the fistula tract and closure with two layers of sutures. Interpositional tissue grafts may be mobilized between the bladder and vagina (Martius fat pad graft from labia majora; peritoneal flap; gracilis flap) prior to the advancement of a vaginal flap and closure of the vaginal wall.

Abdominal approach: more often used for complex cases, patients with a VVF high in the vagina or associated ureteric injury. The bladder is bisected to the level of the fistula tract which is then completely excised. The bladder is closed and an interpositional (omental) graft created. In complex cases, urinary diversion procedures may be needed.

Suprapubic and urethral catheters are placed for 2 weeks and MCUG performed prior to catheter removal. Offer oestrogen replacement to post-menopausal women. Avoid tampons or sexual intercourse for 3 months.

Post-operative complications: vaginal bleeding; infection; bladder pain; dyspareunia due to vaginal stenosis; graft ischaemia; ureteric injury; fistula recurrence.

UI steadily increases with advancing age (particularly ≥70y). It affects about 10–20% of women and 7–10% of men >65y old and living at home. These figures escalate if older people are institutionalized.

Prevalence for both sexes: residential home, 25%; nursing home, 40%; long-stay hospital ward, 50–70%.¹

Delirium.

Infection.

Atrophic vaginitis or urethritis.

Pharmaceuticals (opiates and calcium antagonists cause urinary retention and constipation; anticholinergics cause increased PVR and retention; A-adrenergic antagonist cause reduced urethral resistance in women).

Psychological problems (depression; neurosis; anxiety).

Excess fluid input or output (diuretics; congestive cardiac failure (CCF); nocturnal polyuria).

Restricted mobility.

Stool impaction (constipation).

This is unrelated to comorbid illness and persists over time. There are several types, including UUI, SUI, and incontinence associated with impaired bladder emptying (due to underactive bladder, urethral or bladder outlet obstruction). In addition, functional incontinence is associated with factors outside of the urinary tract such as permanent immobility, cognitive impairment, and environmental changes.

Seek out any transient causes and correct before arranging complex assessment and investigation. This can immediately improve function and quality of life and may be sufficient to restore continence, even if there is coexisting urinary tract dysfunction. Elicit full drug history; comorbid conditions; psychological, cognitive, functional, social, and environmental status.

Include mini-mental state evaluation and direct observation of patient dexterity and mobility (Barthel Index). Include abdominal assessment (distended bladder), DRE (impacted faeces), vulval inspection (POP; atrophic vaginitis), and neurological testing.

Urodynamics should be reserved for patients considered fit for surgery and where the results will alter clinical treatment. Renal tract USS can be undertaken where clinically indicated (i.e. large PVR, impaired renal function, haematuria, UTI).

Biofeedback, electrical stimulation of pelvic floor, and behavioural methods are appropriate only if cognition is intact. PFMT (good results if used in conjunction with anticholinergics). Treat any atrophic vaginitis (0.01% estriol cream topically). Optimize mobility and bring the toilet closer to the bed. Try timed and prompted voiding. Absorbent appliances include bed pads and body worn pad products (disposable or reuseable); body worn external urine collection devices (close fitting penile sheath); pessary for POP; indwelling catheters where UI is due to obstruction and/or no alternative intervention suitable.

Ensure that BOO and significant post-void bladder residuals are adequately treated before considering treatment of OAB symptoms. Antimuscarinic drugs with fewer effects on cognitive function and good efficacy in older patients include solifenacin and trospium chloride.

Where conservative treatments have failed, surgery can be considered for selected cases.

An epithelialized outpouching of urethral mucosa with a single connection (ostium) entering the urethral lumen. Affects women in the 3^rd to 5^th decades of life, with an incidence of 1–6%. The UK incidence has increased from 74 cases in 1998–1999 to 174 in 2009–2010, likely due to improved detected cases.¹ Some report a predilection in Afro-Caribbean races.

UD are single or multiple (10%) and located in the distal, middle (most common), or proximal urethra, usually seen as a midline anterior vaginal cystic swelling.

The classical ‘three Ds’ (dysuria, post-void dribble, and dyspareunia) are only found in 23% of patients.² Patients report a wide array of symptoms, including urinary frequency, urgency, urethral discharge, recurrent UTI, incontinence, pain, obstructive symptoms, urinary retention, vaginal mass, and haematuria. Twenty percent of patients are asymptomatic.

Skene’s gland cysts or abscess, Gartner’s duct cysts, vaginal wall inclusion cysts, vaginal leiomyoma, ectopic ureterocele, urethral carcinoma, and endometrioma.

History: voiding symptoms, dyspareunia, and urethral or vaginal discharge. It is common to have coexisting detrusor overactivity or SUI.

Examination: a midline anterior vaginal wall mass may be visualized or palpable in 80%² (Fig. 5.12). Gentle pressure can express urethral discharge in up to 40%.²

Symptomatic UD requires surgery. The aims are dissection and excision of the diverticulum, identification and closure of the connection to the urethra (ostium), and a three-layered watertight closure ± an interpositional flap (Martius fat pad). Some advocate marsupialization for small distal third UD. A urethral catheter is placed for up to 14 days ± cystourethrogram prior to catheter removal (depending on the complexity of the repair).

The concomitant insertion of a pubovaginal sling or tape for SUI remains controversial. Many authors advocate initial UD surgery and reassessment of symptoms before proceeding with incontinence surgery.²

Contemporary series report overall success rates for primary and redo surgery of 70–97%. Success rates for primary surgery are approximately 89%.²

Anterior wall prolapse: is herniation of the bladder (cystocele) or urethra (urethrocele) through the anterior vaginal wall due to weakened pubocervical ligaments.

Posterior wall prolapse: is protrusion of the rectum through the posterior vaginal wall due to weakened perirectal fascia (rectocele) or protrusion of peritoneum (small intestine or omentum) into the vagina (enterocele).

Middle compartment prolapse: includes uterine prolapse (descent of the uterus secondary to weak cardinal or uterosacral ligaments), vault prolapse (descent of the vaginal cuff after hysterectomy) and procidentia (prolapse of the entire uterus).

Approximately 50% of women develop prolapse after childbirth (20% is symptomatic). Lifetime risk of requiring POP or incontinence surgery is 711% with 29% requiring repeat procedures.¹ Fifty percent are anterior, 30% posterior, and 20% uterine or vault prolapse.

Congenital: secondary to connective tissue abnormalities (spina bifida, exstrophy, Ehlers–Danlos syndrome).

Acquired (multifactorial): related to previous vaginal surgery (prolapse repair, colposuspension, hysterectomy); vaginal delivery; older age (decreased oestrogen levels), obesity, constipation, and chronic straining.

Pelvic organ prolapse quantification (POPQ) is a validated system which allows standardized and accurate prolapse description by measuring distances between defined anatomical points and the hymen (Fig. 5.14; Tables 5.4 and 5.5). An alternative is the Baden–Walker classification (Table 5.3).²

Repair may be with absorbable interrupted buttress sutures, with an onlay mesh strip cut to size or with pre-designed mesh (i.e. AMS Elevate^® and Gynecare Prolift^®).There is controversy as to whether SUI should be treated at the same time as prolapse. This will be addressed by RCT CUPIDO.

Interrupted sutures are placed in remnant fascia, excise surplus vaginal skin, and close. Gynecare Prolift^® is a tension-free vaginal mesh system using a trocar delivery system to guide placement of a pre-shaped mesh. AMS Elevate^® has pre-shaped mesh which is positioned with a slim needle device and then held in place by self-fixing tips and also supports the middle compartment.

If there is coexisting SUI, options include prolapse repair and insertion of a tension-free vaginal tape or alternatively, a primary colposuspension (15% risk of posterior wall prolapse).

Repair with suture or mesh as above.