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New approaches to prolapse |
It is an indication of the very considerable measure of the man that Andrew Binns, having moved on and hopefully forgiven me for my past irrational outbursts on the subject of carbohydrates, has given me a chance to speak on a subject that I actually know something about.
The understanding and management of pelvic support failure changed little until the last few years when significant developments offered new hope to our patients with these conditions. We have certainly moved on from the standard offerings of Manchester repair or vaginal hysterectomy for apical support failure, and from wide excisions of apparently redundant vaginal skin with aggressive plication of the levator muscles in front of the rectum as a means of vaginal repair.
I have had considerable involvement with these developments and enjoy a continuing association with those who do it best so that I am hopeful that these plagiarised observations will be useful.
This will be a story in two parts – initially looking at the history of prolapse management with observations on the anatomy of what actually breaks and how we can assess this clinically. In part 2 we will consider some of the newer surgical approaches.
History
The concepts of normal vaginal support anatomy must be understood in order to understand vaginal support defects and to plan logically for successful reconstructive surgery.
The pelvis encloses organs that primarily function in storage, distension and evacuation. The pelvic viscera must maintain their normal anatomic relationships within this cavity so that these physiological functions can be sustained.
The anatomical support of the pelvic organs is provided by a joint effort between pelvic muscles, endopelvic fascia and its condensations, the pelvic ligaments, in particular the uterosacral cardinal ligament complex for uterine support, and the pubo-urethral ligaments for the mid urethra.
Important contributions to the understanding of the supports came in the last century from surgeons such as Fothergill, Paramore, Sturndorf, Zaccharin and DeLancey. In 1907 Fothergill stated that the ligamentous structures were of prime importance and based his Manchester repair on this idea. In 1908 Paramore vigorously disputed Fothergill’s viewpoint believing that the pelvic floor muscles and visceral fascia were of equal importance. In 1966 Sturndorf introduced the pelvic valve concept whereby the levator muscles helped diminish the force of intra-abdominal pressure by closing the uterovaginal angle and compressing the vaginal canal.
(Insert Fig 1)
Mengert in 1936 performed a series of experiments on fresh female cadavers aged 19 to 53, parity from 0 to 7 with no evidence of uterine prolapse. A 1 kg weight was attached to a tenaculum applied to the cervix of the cadaver. The supportive ligaments of the uterus and vagina were selectively divided until prolapse of the uterus developed. The greatest descensus of the uterus occurred with the lower two-thirds of the broad ligament known as the cardinal ligament and the upper one-third of the para-vaginal tissues, the remainder of the uterosacral cardinal ligament complex were sectioned. The length of descensus was measured as much as 10.5 cm. No significant prolapse ever occurred as long as the upper two-thirds of the para-vaginal tissues or the lower two-thirds of the parametrial tissues were intact.
Swash and Parkes reaffirmed the role of childbirth, confirming that damage to the pudendal nerves that supply the pelvic floor muscles was a common but unrecognised consequence of vaginal delivery, especially if there had been a prolonged second stage or a forceps extraction. The injuries were not observed following caesarean section.
Our own Robert Zaccharin from Melbourne performed extensive cadaveric dissections. He made critical observations about the role of the pelvic floor and described the pubo-urethral ligaments and postulated their relationship to continence, as well as noting important racial differences in genital tract supports. He concluded that pelvic floor muscles that functioned as tail movers in four-footed mammals became pelvic floor supporters in man with change to the erect attitude. Pubo-coccygeus dropped some of its coccygeal attachments to join its fellow from the opposite side in a median raphe as the levator plate. The tendinous insertion between the tip of the coccyx and anus was a fibrous extension of the abbreviated tail. This strong posterior segment and the pelvic valve mechanism described above minimised hernia through the vaginal outlet.
Development of utero-vaginal prolapse
Levator muscle defect: When damage has occurred in the levator muscle, most commonly as a result of obstetric injury, the anatomical defect is noted as a tendency towards a vertical elongation of the levator plate. This downward sagging of the levator plate results in the longitudinal enlargement of the levator hiatus with secondary placement of the cervix and upper vagina upon the levator hiatus. With increased intra-abdominal pressure the defective levator plate is no longer supportive of the downward movement of the uterus, cervix and upper vagina, which are resting upon the levator hiatus, and genital prolapse develops. Over a period of time elongation of the uterosacral and cardinal ligaments will result.
Pelvic ligament defect: In some patients the original defect resides in weakening of the uterosacral and cardinal ligaments resulting in elongation. This allows the cervix and upper vaginal to slide over the edge of the levator plate and become situated upon the levator hiatus. The increase of intra-abdominal pressure with a downward and backward force will no longer be executed upon the levator plate but in the levator hiatus, resulting in genital prolapse. Some patients, when only the upper portion of the cardinal and/or uterosacral ligaments has been weakened, develop cervical elongation, sometimes to an extraordinary degree. In these patients the cervix may be present in the lower part of the vagina but the uterine fundus and upper portion of the cardinal and uterosacral ligaments. The ultimate result of both clinical situations is genital prolapse.
(Insert Figs 2 & 4)
The present
DeLancey in 1994 defined three levels of vaginal support, reviving the importance of the connective tissue structures and giving a working basis for the present day understanding of the anatomy and surgical treatment.
(Insert Fig 3)
LEVEL 1
The cardinal uterosacral ligament complex – a suspensory mechanism working like a plumb bob suspending the vaginal apex yet still allowing moderate vertical mobility. In the normal woman the cervix will descend to but not below the plane of the ischial spines. Damage to level 1 supports permits the uterus and upper vagina to telescope downwards, rather like inverting the toe of a sock by pulling it through the ankle aperture. Complete Level 1 failure will produce a “cervix-first” prolapse.
LEVEL 2
Mid vaginal suspensory mechanism. The pubo-cervical and recto-vaginal fascia are functionally trampolines supporting anteriorly the proximal urethra, vesical neck and bladder base and posteriorly the rectum.
It is now recognised that there are four quite distinct patterns of cystocele related to defects in the pubo-cervical fascia and that these defects can be paravaginal, superior, distal or mid line. Traditionally most cystoceles have been repaired as if all the defects were mid line. Posteriorly most rectoceles arise by detachment of the recto-vaginal septum from its normal insertion into the perineal body. High rectoceles are generally an artifact of previous incomplete posterior colporrhaphy.
LEVEL 3
Anteriorly the continence mechanism maintained by integrity of the sub-urethral hammock and the insertion of Saccharin’s pubo-urethral ligaments into the mid urethra. Posteriorly the perineal body needs to be firm and substantial in size to allow stretching and angulation of the vagina around it. Again we note that in the normal nulliparous standing female the bladder, upper two-thirds of the vagina and rectum lie in an almost horizontal axis protecting against prolapse.
How symptoms relate to the level of support failure
Pelvic floor disorders become symptomatic through either of two mechanisms:
1. Mechanical difficulties produced by the actual prolapse,
2. Bladder or bowel dysfunction, disrupting either storage or emptying.
Physical findings alone are not a reliable guide to disease severity with prolapse. We see patients with quite poor pelvic support who deny any symptoms or restriction of activities and conversely patients with little anatomical prolapse may have significant bladder, bowel or sexual dysfunction. Thus any physical examination must not be used in isolation to develop treatment strategy. Any decision for surgical intervention should take account of how prolapse is affecting lifestyle. Symptoms differ according to the level of support failure.
Level 1 symptoms
The main presentations of Level 1 prolapse are ‘pelvic heaviness’, pressure, a feeling of something falling, a bulge at the entrance or a sense of sitting on something. Basically prolapse symptoms are absent in the morning and increase during the day. Discomfort brought on by standing or physical exertion is relieved by lying down.
Application of a tenaculum to the cervix to assess descent can be undertaken if the tenaculum is slowly closed on the anterior lip to a slow count of ten. Traction on the cervix will then confirm the diagnosis if the symptoms of hypogastric pain or low backache are reproduced. Initially level 1 weakness leaves the midvaginal supports intact, however once a prolapse and cervix crosses the plane of the hymen the pubo-vaginal fascia will tear away from the normal anchor points of the pelvic sidewall and can effect bladder function in a variety of ways.
If inversion of the superior segment secondarily disrupts the midvaginal suspensory hammock, urinary incontinence can develop.
If the vesical neck remains well supported, a drooping cystocele will cause voiding dysfunction rather than stress incontinence. Typical symptoms include hesitancy, straining to void, slow stream, ‘stop and start’ flow, post-void dribbling and a need to lean forward or digitally elevate the bladder base.
If incomplete emptying occurs high residual volumes and urinary stasis may result in overflow incontinence, hydro-ureter and recurrent urinary infections. The effect of a significant cystocele on ureteric drainage and its subsequent effects on renal function are often unrecognised.
Level 2 symptoms
Level 2 support failure, either anterior or posterior, produces eversion of the vaginal walls rather than inversion of the vaginal apex. Although mid vaginal weakness can present because of a vaginal bulge (cystocele or rectocele), symptoms relating the visceral dysfunction, stress incontinence, voiding difficulty, faecal soiling or incomplete rectal evacuation are more typical.
Lumbo-sacral backache is not a feature of mid vaginal weakness. If a patient with a large cystocele or rectocele complains of pelvic dragging sensation, one should suspect concomitant enterocele. Total decompensation of Level 2 supports will create a cervix-last procidentia namely a cystocele or rectocele large enough to be chronically everted. If there is associated weakness of the apical supports uterine prolapse is likely. Conversely, if Level 1 supports hold, pronounced cervical elongation could occur.
Midvaginal prolapse can also cause sexual difficulties. Rotational descent of the mid anterior vaginal wall (AVW) places the trigone in the way of penile insertion often resulting in dyspareunia. Penile pressure on the posterior vaginal wall (PVW) can be equally uncomfortable. Apart from dyspareunia women with cystocele and rectocele are at risk of urinary and faecal incontinence during coitus and finally there may be decreased libido secondary to a perceived loss of sexual desirability.
Level 3 symptoms
Distal vaginal defects create introital gaping and rolling out of the lower vagina. Concomitant flaccidity of levator muscles will further widen the uro-genital hiatus thereby accentuating any anterior or posterior wall eversion. Such patients often complain of dryness or chronic vaginitis secondary to passage of air into the vaginal lumen. Loss of vaginal tightness can also compromise sexual enjoyment.
Anterior Level 3 injuries can injure the continence mechanism and are frequently associated with severe leakage associated with detachment of the pubo-urethral ligaments and laxity of the sub-urethral hammock. Low urethral closure pressures attending mixed Level 2 and 3 weakness are a major risk factor for failure of Burch colposuspensions, but very amenable to cure by tension free vaginal tapes.
Correlation of physical examination findings with symptoms and anatomy
Examination is generally performed with the patient recumbent on the examination table with a single speculum blade to retract the vaginal walls, initially at rest and subsequently during Valsalva straining.
‘Virtual operations’ can be undertaken by gently reducing the various defects with sponge-holding forceps to ascertain the effect on symptoms. Minimal mid-urethral elevation of the urethra will usually control demonstrable stress incontinence and is a good predictor of success with nontension tape.
Bladder emptying problems can be related to either anterior compartment or posterior defects. Excess tightness or tethered vagina following colposuspension may be evident with stretching of the anterior wall by upwards and/or backwards displacement of the vault and posterior wall with the blade of a Sims speculum. This may produce incontinence by opening the bladder neck akin to the situation of the pelvic floor contracting its attachments to a tethered vagina on standing.
In cases of doubt the clinician can ask the patient to look with a hand mirror to confirm the findings and on occasion examination in the standing position may be necessary.
In asking the patient to contract her pelvic floor we are assessing two things. First, the ability to isolate. Even some nulliparous women cannot produce isolated levator contraction upon command. Education can be surprisingly difficult and may require physiotherapy with PFX evaluation. Secondly, evidence of denervation.
Partial avulsion of the upper perineal nerve fibres disrupts resting muscle tone, size and power. Power is best quantified into five grades: 0 = one movement, 1 = flicker only, 2 = short weak contractions, 3 = sustained but weak contractions, 4 = normal power, 5 = above average strength.
Integrity of the anal sphincter should be assessed for resting tone and voluntary squeeze and sensation around the vulva with the bulbo-cavernous reflex and crude sensory testing for evidence of pudental neuropathy.
Coincident an-rectal disease is common with prolapse and various degrees of prolapse of the rectal mucosa are a common finding, best viewed with straining during withdrawal of the proctoscope. The sensation of incomplete evacuation associated with obstipation and anterior pocketing is mimicked by anterior displacement of the lower rectal wall on rectal examination.
Part 2 - Prolapse - What we can do
Brendan O’Sullivan is an obstetrician and gynaecologist based in Lismore, NSW, Australia.
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