Prolapse and disorders of the urinary tract

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Prolapse and disorders of the urinary tract

Ajay Rane and Jay Iyer

Uterovaginal prolapse

The position of the vagina and uterus depends on various fascial supports and ligaments derived from specific thickening of areas of the fascial support (Figs 21.121.4). There has been a paradigm shift in our understanding of the anatomy of pelvic floor supports and with it the pathophysiology of development of pelvic organ prolapse. There are three levels of pelvic organ support that are clinically relevant and conceptually easier to grasp. The uterosacral ligaments responsible for providing level I support to the upper vagina and the cervix (and by extension to the uterus) have a broad attachment over the second, third and fourth sacral vertebrae arising posteriorly from the junction of the cervix and the upper vagina running on each side lateral to the rectum towards the sacral attachments. The other important structure is the arcus tendineus fasciae pelvis (ATFP; see Figs 21.3 and 21.5) also known as the ‘white line’ – a condensation of pelvic cellular tissue on the pelvic aspect of the obturator internus muscle. The ATFP runs from the ischial spines to the pubic tubercle and its terminal medial end is known as the iliopectineal ligament (Cooper’s ligament), well known to general surgeons that operate on inguinal and femoral hernias. Extending medially from the white lines are condensed sheets of pelvic cellular tissue suspending the anterior and posterior vaginal walls and the organs underlying these, namely the urinary bladder and the rectum providing level II support. The anterior support to the bladder was previously referred to as the pubovesicocervical fascia or ‘bladder pillars’, whereas the posterior support to the rectum was termed the rectovaginal fascia.

Level III support is provided by the perineal body posteriorly and the pubourethral ligaments anteriorly. The perineal body is a complex fibromuscular mass in to which several structures insert. It is bordered cephalad by the rectovaginal septum (Dennonviller’s fascia), caudad by the perineal skin, anteriorly by the wall of the anorectum, and laterally by the ischial rami. The three-dimensional form has been likened to the cone of the red pine (Pinus resinosa) and it forms the keystone of the pelvic floor a 4 cm × 4 cm fibromuscular structure providing support not just to the lower third of the vaginal wall (part of the genital hiatus) anteriorly but also to the external anal sphincter posteriorly. Attaching laterally to the perineal body are the superficial and deep perineal muscles.

The anterior vaginal wall is supported by the pubovesicocervical fascia, which extends from the ATFP on one side to the ATFP of the other providing a hammock-like level II support. The posterior vaginal wall is supported by the fibrous tissue of the rectovaginal septum that is well defined only in the midline; laterally the hammock-like supports arise from the ATFP.

The uterus is supported indirectly by the supports of the vaginal walls but directly by the uterosacral ligaments. The round and broad ligaments provide weak if any support to the vagina and uterus. Indirect support of the lower third of the vagina and uterus is provided by the intact levator ani (pelvic floor). The role of the latter has always been in doubt, but the puborectalis portion of the levator ani plays a significant role in the distension of the genital hiatus in labour and delivery making it very prone to injury. Injury to this muscle has been postulated to be the cause for vaginal prolapse later in life.

Definitions

Vaginal prolapse

Prolapse of the anterior vaginal wall may affect the urethra (urethrocele), and the bladder (cystocele, Fig. 21.6). On examination, the urethra and bladder can be seen to descend and bulge into the anterior vaginal wall and, in severe cases, will be visible at or beyond the introitus of the vagina. An urethrocele is the result of damage to level III (anterior) support, i.e. the pubourethral ligaments. Cystoceles usually result due to a loss of level II support and usually due to a midline defect in pubovesicocervical fascia. A rectocele is formed by a combination of factors: a herniation of the rectum through a defect in the rectovaginal fascia as well as a lateral detachment of the level II support from the ATFP. This can usually be seen as a visible bulge of the rectum through the posterior vaginal wall. It is often associated with a deficiency and laxity of the perineum. This is the classical level III defect (posterior) affecting the perineal body.

An enterocele is formed by a prolapse of the small bowel through the rectouterine pouch, i.e. the pouch of Douglas, through the upper part of the vaginal vault (Fig. 21.6). The condition may occur in isolation, but usually occurs in association with uterine prolapse. An enterocele may also occur following hysterectomy when there is inadequate support of the vaginal vault. This represents damage to level I support.

Symptoms and signs

Symptoms generally depend on the severity and site of the prolapse (Table 21.1).

Table 21.1

Levels of supports, with diagnosis and co-relation with symptoms

Level of pelvic organ support Organ affected Type of prolapse Symptoms
Level I – uterosacral ligaments Uterus/vaginal vault (post-hysterectomy) Uterocervical/vault prolapse/enterocele Vaginal pressure, sacral backache, ‘something coming down’, dyspareunia, vaginal discharge
Level II – arcus tendineus fascia pelvis (ATFP) Urinary bladder Cystocele ‘Something coming down’, double voiding, occult stress incontinence, recurrent urinary tract infection
Rectum Rectocele ‘Something coming down’, difficult defecation, manual digitation
Level III – anterior (pubourethral ligaments) Urethra Urethrocele ‘Something coming down’, stress incontinence
Level III – posterior (perineal body) Lower third of the vagina/vaginal introitus/anal canal Enlarged genital hiatus Vaginal looseness, sexual dysfunction, vaginal flatus, needing to apply pressure to the perineum to evacuate faeces

image

There are some symptoms that are common to all forms of prolapse; these include:

Symptoms are often multiple and related to the nature of prolapse. It is important to note that the symptoms (and signs) of prolapse are worse at the end of the day. It is, therefore, of some value, to schedule examination of patients that have typical symptoms of prolapse without its obvious signs a little later in the day.

Urethrocele and cystocele

Typically patients complain of ‘something coming down’ per vaginum. At times there may be incomplete emptying of the bladder and this will be associated with double micturition, the desire to repeat micturition immediately after apparent completion of voiding. The patient may give a history of having to manually replace the prolapse into the vagina to void. Some patients may get recurrent urinary tract infections as a result of incomplete emptying of the bladder. Occasionally the patient may complain of occult stress incontinence, i.e. the involuntary loss of urine following raised intra-abdominal pressure that is not readily demonstrable on coughing but appears on reducing the prolapse.

The diagnosis is established by examination in the dorsal position. A single bladed Sim’s speculum can be used to visualize the anterior vaginal wall. When the patient is asked to strain, the bulge in the anterior vaginal wall can be seen and often appears at the introitus. It is important to culture a specimen of urine to exclude the presence of infection. The differential diagnosis is limited to cysts or tumours of the anterior vaginal wall, and diverticulum of the urethra or bladder.

Rectocele

The prolapse of the rectum through the posterior vaginal wall is commonly associated with a deficient pelvic floor, disruption of the perineal body and separation of the levator ani. It is predominantly a problem that results from over distension of the introitus and pelvic floor during parturition.

The symptoms of a rectocele include difficulty with evacuation of faeces with an occasional need to ‘manually digitate’. Needless to say the awareness of a reducible mass bulging into the vagina and through the introitus is often the presenting symptom.

Examination of the vulva usually shows a deficient perineum (measuring less than 3 cm in length) bringing the posterior fourchette in close apposition with the anterior anal verge. Patients can complain of vaginal looseness and sexual dysfunction as a result of this. Not uncommonly the symptom of vaginal ‘flatus’ can be uncovered on direct questioning.

Uterine prolapse

Descent of the uterus is initially associated with elongation of the cervix and descent of the body of the uterus. Mostly the affected portion of the cervix is supravaginal, i.e. above the level of the vaginal fornices. The symptoms are those of pressure in the vagina and, ultimately, complete protrusion of the uterus through the introitus. At this stage, the prolapsed uterus may produce discomfort on sitting, and decubitus ulceration may result in bleeding. Sometimes patients with minor degrees of prolapse or with congenital prolapse may have infravaginal cervical elongation, that often leads to confusion in staging the degree of prolapse as it may appear to be in a more advanced stage than it actually is.

Urinary tract infection may occur because of compression of the ureters and consequent hydronephrosis due to incomplete emptying of the bladder. Not unusually, patients experience dyspareunia but are not very forthcoming with this symptom.

Staging/grading of prolapse

Baden–Walker halfway system (Fig. 21.8 and Table 21.2)

This system was developed in an effort to introduce more objectivity into the quantification of pelvic organ prolapse. For example, measurements in centimetres are used instead of subjective grades. Nine specific measurements are recorded as indicated in Figure 21.9.

Table 21.2

Primary and secondary symptoms at each site used in the Baden–Walker halfway system

Anatomic site Primary symptoms Secondary symptoms
Urethral Urinary incontinence Falling out
Vesical Voiding difficulties Falling out
Uterine Falling out, heaviness, etc.  
Cul-de-sac Pelvic pressure (standing) Falling out
Rectal True bowel pocket Falling out
Perineal Anal incontinence Too loose (gas/faeces)

(Reproduced with permission from Baden WF, Walker T (1992) Surgical repair of vaginal defects. Lippincott, Williams & Wilkins, Philadelphia, p. 12.)

Pathogenesis

Prolapse may be:

• Congenital: Uterine prolapse in young or nulliparous women is due to weakness of the supports of the uterus and vaginal vault. There is a minimal degree of vaginal wall prolapse.

• Acquired: The commonest form of prolapse is acquired under the influence of multiple factors. This type of prolapse is both uterine and vaginal but it must also be remembered that vaginal wall prolapse can also occur without any uterine descent. Predisposing factors include:

image High parity: Uterovaginal prolapse is a condition of parous women. The pelvic floor provides direct and indirect support for the vaginal walls and when this support is disrupted by laceration or over distension it predisposes to vaginal wall prolapse. Instrumental delivery employing forceps/ventouse especially mid-cavity rotational forceps delivery may play a contributory role in the causation of urinary incontinence and prolapse in later life.

image Raised intra-abdominal pressure: Tumours or ascites may result in raised intra-abdominal pressure, but a more common cause is a chronic cough and chronic constipation.

image Hormonal changes: The symptoms of prolapse often worsen rapidly at the time of the menopause. Cessation of oestrogen production leads to thinning of the vaginal walls and the supports of the uterus. Although the prolapse is generally present before the menopause, it is at this time that the symptoms become noticeable and the degree of descent visibly worsens. The age at first vaginal childbirth affects the incidence of prolapse and urinary incontinence in later life. It has been postulated that increased maternal age predisposes to levator trauma making these women more prone to developing pelvic floor disorders.

Management

The management of prolapse can be conservative or surgical.

Conservative treatment

Minor degrees of prolapse are common after childbirth and should be treated by pelvic floor exercises or the use of a pessary. Operative intervention is deferred for at least 6 months after delivery, as the tissues remain vascular and may undergo further spontaneous improvement.

Hormone replacement therapy may be used preoperatively to prepare the tissues, but by itself is of limited benefit in alleviating symptoms.

Where short-term support is required or the general health of the woman makes operative treatment potentially dangerous, then both vaginal wall and uterine prolapse can be treated by using vaginal pessaries. It is, however, necessary to have some pelvic floor support if a pessary is to be retained.

The most widely used pessaries (Fig. 21.10) are:

The main problem with long-term use of pessaries is ulceration of the vaginal vault and rarely a fistula may form, usually between the bladder and the vagina, if the pessary is ‘neglected’ or ‘forgotten’. Pessaries should be replaced every 4–6 months and the vagina should be examined for any signs of ulceration. In postmenopausal women it is considered good practice to prescribe vaginal oestrogen creams/tablets to prevent ulceration.

Surgical treatment

The surgical management of uterovaginal prolapse has seen many changes in recent years. There is an increasing use of graft material and tissue anchors for increasing durability of the prolapse repair. Thus prolapse repairs can be classified into fascial repairs and graft augmented repairs.

Fascial repairs

Classically surgical treatment of a cystocele is by anterior colporrhaphy (Fig. 21.11). The operation consists of dissection of the prolapsed viscus (the urinary bladder) off the vaginal flaps, buttressing the pubovesicocervical fascia with durable delayed absorbable sutures and closure of the vaginal skin. Current practice does not include excision of ‘excess vaginal skin’ as the vagina is expected to remodel and the perceived laxity all but disappears in 6–8 weeks’ time.

Rectocele is repaired by again dissecting the prolapsing viscus (in this case the rectum) off the overlying vaginal skin and effecting a robust repair by apposing the torn ends of the rectovaginal fascia together with delayed absorbable sutures. Sometimes it is possible to identify the tears in the fascia and often a reattachment of the torn ends suffices. Not uncommonly a rectocele is accompanied by a deficient perineal body where the perineal muscles are attenuated or retracted laterally with the patient complaining of ‘vaginal laxity’ or sexual dysfunction. Intravaginal perineoplasty is the operation designed to treat these symptoms and involves lateral dissection to identify the retracted ends of the perineal muscles, apposing these in the midline and suturing the apposed muscles to the apex of the incision. This procedure helps recreate the perineal body, reduces the size of the genital hiatus thus improving vaginal tone and also corrects the vaginal axis. This operation is an improvement on the perineorraphy where the perineal skin is first incised and later excised but still fails to achieve the objectives stated above.

Where there is an enterocele, the procedure of choice is a McCall’s culdoplasty. This involves the placement of delayed absorbable sutures through the cut ends of the uterosacral ligaments and the intervening peritoneum hitching these successively to the vaginal vault. The aim of this operation is not just to treat the enterocele, but also to prevent occurrence of vault prolapse.

The treatment of choice for uterine prolapse depends on the woman’s preference for retaining her reproductive potential. If her family is complete then a vaginal hysterectomy usually with repair of the prolapsed vaginal walls is the preferred approach. If preservation of reproductive function is required, then the uterus can be conserved by simply excising the elongated cervix that is fashioned to an appropriate length with suturing of the cardinal ligaments in front of the cervical stump. This procedure is known as a Manchester or Fothergill repair. The vaginal skin is then sutured into the cervical stump using circumferential sutures. Additionally the operating surgeon may elect to suspend the cervix by means of sutures taken through the sacrospinous ligament called sacrospinous cervicopexy/hysteropexy.

A similar procedure may be employed to treat vault prolapse occurring after hysterectomy; the procedure is then called sacrospinous colpopexy (colpos Gk: vagina).

Graft repairs

The earliest repairs using mesh have been to treat vault prolapse (Fig 21.12). The prolapsed vaginal vault is treated by suspending the vaginal vault from the anterior longitudinal ligament of the sacrum using a synthetic mesh. This procedure is known as sacrocolpopexy – a procedure that can be performed laparoscopically or through a laparotomy. More recently ‘needle driven mesh kits’ have become available to treat vaginal prolapse. The first of these kits was called the PERIGEE™ used to suspend the prolapsed bladder from one ATFP to its opposite member thus recreating the hammock like arrangement that existed in the pelvis prior to the occurrence of the prolapse. A similar device called the APOGEE™ is available to treat large enteroceles and vault prolapses. More recently newer versions called the Anterior and Posterior Elevate™ have been developed to treat anterior, middle and posterior compartment disorders that are safer to use and employ mesh that is more bio-compatible. These new devices require specialized instruction and training prior to use.

Complications

Repairs whether fascial or otherwise can result in injury to the viscus being treated, i.e. bladder, small intestines, rectum or anal canal. The sigmoid colon or the ureters may additionally be injured when a McCalls’ culdoplasty is performed. The new needle driven devices are known to be rarely associated with damage to the deeper vessels in the pelvis and with more common occurrence of vaginal mesh exposure. Primary, reactionary and secondary hemorrhage may all occur with all of these procedures as may infection. The immediate complications of vaginal hysterectomy includes haemorrhage, haematoma formation, infection and less commonly, urinary retention. The long-term complications are dyspareunia and reduced vaginal capacity especially if vaginal skin is inappropriately excised. Fascial repairs especially of the anterior compartment may recur in about a third of cases. Posterior compartment fascial repairs perform better with only 20% recurrence. Inadequate support to the vaginal apex may result in recurrence of the prolapse of the vaginal vault. Mesh repairs are more robust with lower rates of recurrence.

Urinary tract disorders

Structure and physiology of the urinary tract

The urinary bladder is a hollow muscular organ with an outer adventitial layer, a smooth muscle layer known as the detrusor muscle and an inner layer of transitional epithelium.

The innervation of the bladder contains both sympathetic and parasympathetic components. The sympathetic fibres arise from the lower two thoracic and upper two lumbar segments of the spinal cord, and the parasympathetic fibres from the second, third and fourth sacral segments.

The urethra itself begins outside the bladder wall. In its distal two thirds it is fused with the vagina, with which it shares a common embryologic derivation. From the vesical neck to the perineal membrane, which starts at the junction of the middle and distal thirds of the bladder, the urethra has several layers. An outer, circularly oriented skeletal muscle layer (urogenital sphincter) mingles with some circularly oriented smooth muscle fibres. Inside this layer is a longitudinal layer of smooth muscle that surrounds a very vascular submucosal venous plexus and non-keratinized squamous epithelium that responds to estrogenic stimulation. The continence mechanism is maintained by the urogenital sphincter, aided by the mucosal co-aptation of urethral epithelium and the ‘bulking up’ effect provided by the submucosal venous plexus.

During micturition, the pressure in the bladder rises to exceed the pressure within the urethral lumen and there is a fall in urethral resistance. The tone of muscle fibres around the bladder neck is reduced by central inhibition of the motor neurons in the sacral plexus. The bladder fills at 1–6 mL/min. The intravesical pressure remains low because of compliance of the bladder wall as it stretches and reflex inhibition of the detrusor muscle. At the same time the internal urethral meatus is closed by tonic contraction of the rhabdosphincter and the tone of the urethral mucosa. During rises in intra-abdominal pressure such as coughing or sneezing, continence is maintained by transmission of the pressure rise to the proximal urethra (which lies normally within the intra-abdominal space) and an increase in the levator tone.

The ureter is 25–30 cm long. It runs along the transverse processes of the lumbar spine, anterior to the psoas muscle, is crossed by the ovarian vessels and enters the pelvis anterior to the bifurcation of the common iliac vessels. From there it runs anterior to the internal iliac vessels to the ischial spines where it turns medially to the cervix. It turns again anteriorly 1.5 cm lateral to the vaginal fornix, crossing below the uterine vessels to enter the posterior surface of the bladder.

Common disorders of bladder function

The common symptoms of bladder dysfunction include:

Incontinence of urine

The involuntary loss of urine may be associated with bladder or urethral dysfunction or fistula formation. Types of incontinence are listed below:

• True incontinence is continuous loss of urine through the vagina; it is commonly associated with fistula formation but may occasionally be a manifestation of urinary retention with overflow.

• Stress incontinence is the involuntary loss of urine that occurs during a brief period of raised intra-abdominal pressure. It is usually related to injury to the continence mechanism described above and lack of estrogenic stimulation and usually manifests around menopause. Examination reveals the involuntary loss of urine during coughing usually accompanied by a hypermobility of the urethra and a descent of the anterior vaginal wall.

• Urge incontinence is the problem of sudden detrusor contraction, with uncontrolled loss of urine. The condition may be due to idiopathic detrusor instability or associated with urinary infection, obstructive uropathy, diabetes or neurological disease. It is particularly important to exclude urinary tract infection.

• Mixed urge and stress incontinence occurs in a substantial number of women. Women with urge incontinence also have true stress incontinence and it is particularly important to treat the detrusor instability prior to correcting stress incontinence. Failure to do so may lead to a worsening of the condition.

• Overflow incontinence occurs when the bladder becomes dilated or flaccid with minimal or no tone/function. It is not uncommon after vaginal delivery or when the bladder is ‘neglected’ after a spinal anaesthetic. A bladder scan usually reveals the presence of a residual of more than half the bladder capacity. The bladder then becomes ‘lazy’ and empties when it becomes full.

• Miscellaneous types of incontinence include infections, medications, prolonged immobilization, cognitive impairment and in certain situations may precipitate incontinence.

Diagnosis

The diagnosis is initially indicated by the history. Continuous loss of urine indicates a fistula, but not all fistulas leak urine continuously. The fistulous communication usually occurs between the bladder and vagina, vesicovaginal fistula, and the ureter and vagina, ureterovaginal fistula. Fistula formation results from:

There are other types of fistula with communications between bowel and urinary tract and between bowel and vagina, but these are less common.

Rectovaginal fistulas have a similar pathogenesis, with the additional factor of perineal breakdown after a third-degree tear.

Urinary fistulas are localized by:

The differential diagnosis between stress and urge incontinence is more difficult and is often unsatisfactory. Adequate preoperative assessment is important if the correct operation is to be employed or if surgery is to be avoided. It is important to assess patients with a validated patient questionnaire (the Modified Bristol Female Lower Urinary Tract Symptoms Questionnaire is a good example) with a 3-day urinary diary and a pad test. These help the clinician gain an insight into how the symptoms of urinary incontinence affect the patient on a day-to-day basis. The bladder and urethra are assessed in the laboratory by urodynamics. This procedure usually involves three basic steps:

1. Uroflowmetry: The patient is asked to pass urine into a specially designed toilet that measures voided volume, maximal and average urinary flow rates. Flow rates of >15 mL/sec are considered acceptable and it is expected that a normal bladder will completely empty itself. Flow rates of <15 mL/sec are indicative of voiding dysfunction and in the female often indicate a ‘functional obstruction’ rather than an anatomic one. Occasionally a powerful detrusor may cause the bladder to contract against a closed internal urethral meatus resulting in dysfunctional voiding, a condition termed ‘detrusor–sphincter dyssynergia’.

2. The cystometrogram (Fig 21.13): Pressure is measured intravesically and intravaginally or less commonly intrarectally, because intravaginal pressure represents intra-abdominal pressure and is subtracted from the intravesical pressure to give a measure of detrusor pressure. The volume of fluid in the bladder at which the first desire to void occurs is usually about 150 mL. A strong desire to void occurs at 400 mL in the normal bladder. High detrusor pressure at a lower volume reflects an abnormally sensitive bladder associated with chronic infection. There should be no detrusor contraction during filling, and any contraction that occurs under these circumstances indicates detrusor instability. An underactive detrusor shows no contraction on complete filling and indicates an abnormality of neurological control. The average bladder has a capacity of 250–550 mL, but capacity is a poor index of bladder function. Thus, cystometry is a useful method for assessing detrusor muscle function or detrusor instability, which may result in urge incontinence.

    In the presence of urethral incompetence, there is low resting urethral pressure, no voluntary increase in urethral pressure, inability to stop midstream, decreased pressure transmission to the abdominal urethra and large volumes in the frequency/volume measurements. There is not always a clear-cut demarcation between the two conditions, as there may be a mixture of both stress and urge incontinence. Nevertheless, it is important to differentiate between the predominant influence of bladder neck weakness and stress incontinence, and detrusor instability and urge incontinence.

3. Urethral pressure profile: This is performed at the very end of the cystometry and measures the pressure within the mid-urethra, in particular the maximum urethral closure pressure (MUCP). This is of value in predicting the likelihood of surgical success after an anti-incontinence procedure. Pressures <20 cm of H2O are predictive of poorer outcomes.

In some units an endoscopic view of the bladder called ‘cystoscopy’ and an ultrasound scan of the pelvic floor are the additional procedures performed in the evaluation of the incontinent woman.

Management

Urinary tract fistula

In the developed world, most urinary tract fistulas result from surgical trauma. The commonest fistulas are vesicovaginal or ureterovaginal and result from surgical trauma at the time of hysterectomy, or sometimes following caesarean section.

A vesicovaginal fistula will usually become apparent in the first postoperative week. If the fistula is small, closure may be achieved spontaneously.

The patient should be treated by catheterization and continuous drainage. If closure has not occurred after 2–3 months, the fistula is unlikely to close spontaneously and surgical closure is recommended. The timing of further surgery is still a subject of controversy. Until recently, a delay of 6 months was recommended but there is increasing evidence that good results can be obtained with early surgical intervention. However, the fistulous site should be free of infection.

Surgical closure may be achieved vaginally by meticulous separation of the edges of the fistula and closure in layers of the bladder and vagina. Postoperative care includes continuous catheter drainage for 1 week and antibiotic cover. An abdominal approach to the fistula can also be used and has some advantages, allowing the interposition of omentum in cases where there is a large fistula.

Ureterovaginal fistulas are usually treated by reimplantation of the damaged ureter into the bladder.

Stress incontinence

Stress incontinence should be managed initially by pelvic floor physiotherapy. Surgical treatment is indicated where there is a failure to respond to conservative management. In the presence of anterior vaginal wall prolapse, anterior repair, with the placement of buttressing sutures at the bladder neck, has the virtue of simplicity. It will certainly relieve the prolapse but the results are variable as far as the stress incontinence is concerned, with relief in about 40–50% of cases. It is of no value in the absence of evidence of prolapse.

The following procedures are commonly used:

• Mid-urethral slings (Fig. 21.14)

image Tension-free vaginal tape (TVT™): Bladder neck elevation can be achieved by the placement of a tension-free vaginal tape. A polypropylene tape is inserted through a sub-urethral vaginal incision and guided via a needle paravesically to exit from the symphysis pubis. This can be carried out under local, regional or general anaesthetic and the tape is placed mid-urethrally in a tension-free manner. A cystourethroscopy is performed intra-operatively to rule out damage to the bladder and urethra. As this procedure is minimally invasive most women are able to return to normal activity within 1–2 weeks. The long-term success rates are around 80%.

    In recent times the procedure has become even less invasive than before and now it is possible to perform the procedure by passing needles through the obturator foramina and still site the tape as before, i.e. under the mid-urethra (MONARC™). The most recent version of the sling is called the MINIARC™. It is the most minimally invasive version of the mid-urethral sling that has the added advantage of not having to be passed through blind spaces like the retropubic space and transobturator foramina.

• Miscellaneous procedures still in vogue

image Laparoscopic Burch colposuspension involves bladder neck elevation by suturing the upper lateral vaginal walls to the iliopectineal ligaments under laparoscopic control. The success rates are around 60% and the procedure results in voiding dysfunction in a significant majority of patients. This procedure has more or less been invalidated by the more popular and safer mid-urethral slings.

image Transurethral injections: Injectable bulking agents can be injected via a cystoscope into the mid-urethra. These are simple procedures with very little perioperative morbidity and have success rates of about 40–60%. These are useful adjuncts to the mid-urethral slings especially in recurrences and in women with multiple failed operations. The commonest agents employed are collagen (glutaraldehyde cross-linked bovine collagen), silicon (macroparticulate silicon particles), Durasphere® (pyrolytic carbon-coated beads), etc.

The unstable bladder: overactive bladder syndrome (OAB)

The features of the unstable bladder are those of frequency of micturition and nocturia, urgency and urge incontinence. When confronted with this history, it is important to obtain some indication of the frequency as related to fluid intake and output. A chart should therefore be kept by the patient to clarify this aspect.

The assessment of predisposing factors includes urine culture, urinary flow rates and urodynamic studies.

Treatment will obviously be directed at the cause, so the presence of urinary tract infection necessitates the administration of the appropriate antibiotic therapy. Postmenopausal women with atrophic vaginal epithelium and symptoms of urgency and frequency often respond to replacement therapy with low-dose oestrogens.

Drug treatment

The alternative approach is to use anticholinergic drugs that act at the level of the bladder wall. These act on the muscarinic receptors on the bladder wall and cause relaxation. Some of these drugs are more specific and act on M3 receptors. The more specific the drug the less likely it is to cause side-effects. The drugs listed in Table 21.3 are in increasing order of specificity and better side-effect profile.

Table 21.3

Drug therapy of overactive bladder

Drug name Drug type Dosage Available doses Side effects
Oxybutynin Antimuscarinic 2.5–5 mg PO tid 5 mg tablet, 5 mg/mL syrup Dry mouth, constipation, dizziness, palpitations, anorexia, nausea, amblyopia
Oxybutynin (transdermal) See above 3.9 mg/d; patch changed twice weekly 36 mg patch
Tolterodine (short-acting) M3-selective antimuscarinic 1–2 mg PO bid 1, 2 mg tablet
Tolterodine (long-acting) See above 2–4 mg PO once daily 2, 4 mg capsule
Trospium chloride Antimuscarinic quaternary amine 20 mg PO bid 20 mg tablet
Darifenacin M3-selective antimuscarinic 7.5–15 mg PO daily 7.5, 15 mg tablet
Solifenacin M3-selective antimuscarinic 5–10 mg PO once daily 5, 10 mg tablets
Imipramine hydrochloride Tricyclic antidepressant, anticholinergic, adrenergic, antihistamine 10–25 mg PO qd–qid 10, 25, 50 mg tablets

image

Pelvic floor physiotherapy: pelvic floor muscle training

In women who have mild to moderate symptoms of urinary incontinence, pelvic floor muscle training (PFMT) may allow improvement if not cure. Also known as Kegel exercises, PFMT entails voluntary contraction of the levator ani muscles. These need to be repeated several times a day up to 50 or 60 times to be of any clinical benefit.

The specifics are a bit variable, being very clinician specific and also dependent on the clinical setting. Most patients find isolating the levator ani muscles most challenging and often contract their abdominal muscles instead. Therefore it is imperative that these exercises be demonstrated by a physiotherapist with a special interest in pelvic floor rehabilitation. To augment efficacy of these exercises, weighted vaginal cones or obturators may be placed into the vagina during Kegel exercises. These provide resistance against which pelvic floor muscles can work.

Biofeedback therapy

Many behavioural techniques, often considered together as biofeedback therapy, measure physiological signals such as muscle tension and then display them to a patient in real time. In general, visual, auditory, and/or verbal feedback cues are directed to the patient during these therapy sessions. These cues provide immediate performance evaluation to a patient. Specifically, during biofeedback for PFMT, a sterile vaginal probe that measures pressure changes within the vagina during levator ani muscle contraction is typically used. Readings reflect an estimate of muscle contraction strength. Treatment sessions are individualized, dictated by the underlying dysfunction, and modified based on response to therapy. In many cases, reinforcing sessions at various subsequent intervals may also prove advantageous.

The neuropathic bladder

Loss of bladder function may be associated with a variety of conditions that affect the central nervous system. These conditions may also be associated with alteration in bowel function, sexual dysfunction and loss of function of the lower limbs.

Management

The management clearly depends on establishing the cause, but symptomatically it also involves non-surgical management using absorptive pads and clean intermittent self-catheterization. Anticholinergic drugs also have a place for some patients. Surgical treatment includes the use of artificial sphincters and sacral nerve stimulators.