Repair of recurrent prolapse




The pathogenesis of prolapse and the requirements for a successful surgical outcome vary from one person to another. The importance of traditional risk factors is questionable, but failed previous repair is definitely an adverse prognosticator. An ideal operation should re-attach apical support to the pelvic skeleton, restore integrity within anterior and posterior suspensory hammocks and re-distribute some of the expulsive load back onto the pelvic diaphragm. Reasons for failure are best analysed by location; recurrence within the operated compartment should also be distinguished from recurrence in a different compartment. There is no all-encompassing secret to re-operating on recurrent prolapse. Success depends on sound strategic planning and using tactics to negate the greater technical difficulty and reduced collagen strength in women with prior operative failure. If an augmented repair is to be carried out, choice of biomaterials must reflect surgical objectives, movement dynamics and functional anatomy at the intended implantation site.


Introduction


Pelvic-floor disorders arise mainly through structural damage or neuro-muscular disruption to the pelvic floor, rather than from any malfunction of the specific organs themselves. Given the mechanical nature of prolapse, it is disappointing that treatments should have remained so unreliable for so many years. Of 16,600 Kaiser Permanente North West women who had pelvic floor surgery in 1995, 29% needed at least one repeat operation. Applying the epidemiologic ‘rule of thumb’ that another 40% of failures would not have returned, overall failure rate would have most likely approached 41% in primary and 67% in recurrent repair cases ( Fig. 1 ). Women know this! Prevalence of pelvic floor disorders increases in a linear fashion with age, but consultations for pelvic floor disorders have a Gaussian distribution.




Fig. 1


Outcome data from Olsen et al., with a 40% non-return correction factor applied to the known failure count. Repairing recurrent prolapse by traditional re-suture of native tissues was associated with approximately 60% higher failure rates, compared with surgical outcome in primary cases (67% v 41%).


What has led to this unsatisfactory state of affairs? The reason is that prolapse repair is inherently problematic, and is discussed below.


Misdirected surgical strategies


Reparative efforts have been thwarted by a century of misdirected surgical strategies. Gynaecological pioneers of the 1920s viewed vaginal prolapse in mechanically simplistic terms; namely, that pelvic organs bulge outwards because the adjacent connective tissue had stretched. Operations thus evolved for strengthening what were assumed to be ‘weakened ligaments’ (i.e. culdoplasty) and for plicating ‘stretched’ suspensory hammocks (i.e. anterior and posterior colporrhaphy). Modern research, however, has shown that fascia is like canvas; it does not stretch, but will tear along lines of weakness. These insights have spurred a paradigm shift, from culdoplasty and colporrhaphy to ‘site-specific’ repair (wherein the fascial tears causing support failure in each individual woman are precisely identified and accurately corrected).


Pelvic anatomy


Pelvic anatomy is complex and not truly reparable. Normal support anatomy depends upon two complementary mechanisms, each of which plays a vital role:




  • The pelvic floor muscles act as a dynamic backstop, absorbing most of the expulsive load placed on the pelvic organs by intra-abdominal forces, a task for which they are well suited. Constant postural tone from the slow twitch fibres during low exertion activity narrows the gap through which the urethra, vagina and anus exit the abdomen and rapid reflex contractions from the fast twitch fibres neutralise any sudden increase in Valsalva forces. Skeletal muscles are also renewable, meaning that any microtears in the muscle fibres heal by hypertrophy and become stronger. It is difficult for the body to compensate the avulsive and denervation muscle damage that often follows vaginal delivery.



  • The pelvic connective tissue is also important, but in a less direct way. The endopelvic fascia is basically an embryologic mesentery, which tethers the pelvic viscera to the axial skeleton. Its main suspensory role is to stabilise the organs over the posterior levator plate, where the pelvic floor muscles work most effectively. Unlike skeletal muscle, however, endopelvic fascia is neither contractile nor renewable. Moreover, the areolar tissue architecture and high smooth muscle content make endopelvic fascia structurally unsuited to the task of chronic load-bearing.



Most prolapse is associated with failure of both components, such damage often occurring in the same delivery. In that there are no effective treatments to restore levator function, current reparative strategies depend mainly on connective tissue strength.


Time and tissue weakness


Reparative difficulty increases with time and tissue weakness. The endopelvic fascia is inherently fragile, and any associated connective tissue weakness will exacerbate this flaw. This situation is not dissimilar to the problems that general surgeons face with hernia repair, where best outcome requires correction of both mechanical and metabolic failure mechanisms.


An ideal operation should re-attach the sagging pelvic organs to the pelvic skeleton, restore integrity within the anterior and posterior suspensory hammocks, and re-distribute some of the expulsive load back onto the pelvic diaphragm. Surgery should not compromise pelvic organ function or create iatrogenic morbidity. Success or failure is best analysed by location. However, recurrence within the operated compartment should be distinguished from recurrence in another compartment, as these two failure patterns reflect different phenomena. It is also appropriate to distinguish primary from recurrent prolapse operations. Success after a prior operative failure depends on sound strategic planning and the use of tactics to negate the technical difficulties and reduced collagen strength seen in recurrent cases.




Apical compartment


Support anatomy


Connective tissue filling the space between the peritoneum above and the pelvic muscles below is a loose mixture of smooth muscle and collagen fibres. This ‘endopelvic fascia’ differs from the rest of the abdominal retroperitoneum in being more condensed around certain pelvic structures, as with hypogastric vessels, pelvic nerves and the ureter. These condensations are sufficiently dense that a central septum (the cardinal ligament), and two secondary lamellae (the uterosacral and vesico-uterine ligaments) can be dissected out as seemingly discrete structures. Between these embryologically defined condensations lie eight surgically useful ‘spaces’, filled with areolar tissue and devoid of major vessels ( Fig. 2 ). These spaces provide a safe ‘surgical highway’ to the pelvic cavity, especially when one is faced with the need to dissect an operative field with distorted anatomy.




Fig. 2


Pelvic connective tissue in women: the otherwise areolar pelvic connective tissues condense around the hypogastric leash, pelvic nerves and ureter, to form the cardinal, uterosacral and vesico-uterine ‘ligaments’. Between these three condensations lie eight relatively avascular zones of enormous surgical importance. These four central spaces (pre-vesical, vesicovaginal, rectovaginal and retro-rectal) and two paired lateral pelvic spaces (paravesical and pararectal) provide safe dissection routes throughout the pelvis. Modified from Tandler J. Lehrbuch der systematischen Anatomie. Die Eingeweide. Leipzig, Vogel ). Published with permission.


Important differences are found in fibre size and direction, such that the functional anatomy of endopelvic fascia varies from site to site.




  • DeLancey level I: The uterosacral and cardinal ligaments consist of long vertically oriented fibres that suspend the cervix and upper third of the vagina to the pelvic brim. Mechanically speaking, these level I fibres are like the ropes of a ‘trapeze’. They allow physiological mobility in an upward or lateral direction, but resist downward forces. Uterosacral ligaments, however, have a high collagen content and evolve in fetal life as an important part of pelvic organ support. In contrast, the cardinal ligaments are simply a visually prominent residue of the central septum mesenchyme. The term cardinal ligament’ is misleading, as this portion of the pelvic connective tissues contains no ligamentous component and plays no major role in pelvic organ suspension.



  • DeLancey level II: The two mid-vaginal suspensory hammocks comprise short horizontally oriented fibres that attach strongly to the pelvic sidewalls. Mechanically speaking, these level II fibres are like the springs of a ‘trampoline’. They allow minimal movement of the hammocks on the pelvic bones, but provide excellent bounce-back when impacted by an abdominal pressure wave.



  • DeLancey level III: At the pelvic outlet, the billowing vaginal suspensory hammocks are fused to the pelvic floor by a group of dense interwoven fibres. Mechanically speaking, these level III fibres are like ‘tent pegs’, which tether the reproductive organs to the pelvic muscles upon which they sit. Transperineal ultrasound in women with prolapse shows that the rotatory descent of cystocoele and rectocoele primarily reflects failed apical support, with the descending mass ‘hinging’ at the level II/III junction.



For the reparative surgeon, these differences in tissue density and fibre strength resolve the pelvic connective tissues into two semi-independent systems, which inter-relate like a flag at half-mast on a flagpole.




  • The posterior portions of DeLancey levels I, II and III fascia coalesce into a collagen-rich membrane separating the urogenital and alimentary tracts. This postero-superior vaginal suspensory axis runs from the sacral periosteum, through the uterosacral ligaments and pericervical ring, down the rectovaginal septum and into the perineal body. ( Fig. 3 ). When intact, this strong ligamentous ribbon stabilises upper vaginal support; it also guides faeces smoothly through the pelvis and deflects the descending stool backwards into the anal canal. Fracture of this ‘flagpole’ above the point where the uterosacral ligaments insert into peri-cervical ring creates uterine or vaginal vault descensus. Fracture of the ‘flagpole’ below the peri-cervical ring creates a fascial defect, into which either cul-de-sac contents or large bowel will herniate. Such recto-enterocoeles are typically associated with obstructed defaecation syndrome.




    Fig. 3


    Pelvic connective tissues in women: (a) a sagittal section showing how connective tissues within the apical and posterior compartments coalesce into a strong collagenous membrane that runs from the sacral periosteum, through the uterosacral ligaments, into the pericervical ring, then down through the rectovaginal septum, to insert into the perineal body. When intact, this vaginal suspensory axis both suspends the pelvic viscera and guides bowel motions through the pelvis. The vaginal suspensory axis also suspends the anterior vaginal suspensory hammock, these two structures intersecting like a flag at half mast on a flagpole. Obstetric forces tend to tear these fascial supports in the mid pelvis (i.e. where the ‘flag’ joins the ‘flagpole’). In the postero–apical compartments, avulsion of uterosacral ligaments from pericervical ring creates uterine descensus, whereas avulsion of pericervical ring from rectovaginal septum permits herniation of ileum, sigmoid or rectum into the vaginal lumen. In the anterior compartment, avulsion of uterosacral ligaments from pericervical ring or avulsion of pericervical ring from pubocervical fascia initiates cystocoele formation; (b) a typical posterior bulge, caused by ‘partition failure’ in the postero-apical compartment. Whether the rectocoele or the enterocoele component assumes greater relative prominence is largely a matter of random variation; (c) a careful dissection on the cranial side of the rectovaginal septum, using Lone Star TM retractor to aid dissection. An avulsion line separates the extraperitoneal fat of the cul de sac (above) from the dense white fascia of the rectovaginal septum (below); (d) further dissection shows the cul-de-sac projecting downwards and forwards as a large enterocoele. The futility of ‘repairing’ this bulge by plicating this pre-peritoneal should be obvious. PCF, pubocervical fascia; RVS, rectovaginal septum; USL, uterosacral ligament.



  • The anterior portion of the DeLancey level II fascia forms a trapezoid shaped septum (the pubocervical fascia) that is vital to urinary continence, but has no major supportive role for the vagina as a whole. Tearing of the ‘flag’ creates a cystocoele, often accompanied by urinary incontinence or voiding difficulty.



Although the mechanics of prolapse are easily understood using the flag and flagpole analogy, it must be remembered that the pelvic connective tissues are an ‘integrated structure’. The integrity of one compartment depends on the other parts of the system being intact. Support failure within the anterior and postero-apical compartments is thus highly correlated.


Failure mechanisms


Vault eversion was once a major therapeutic challenge for pelvic reconstructive surgeons. Re-suspension by sutured repair, with or without hysterectomy, was the stock-in-trade of gynaecologists until the last few decades, with generally disappointing results. This situation has improved with the emergence of sacrospinous fixation and abdominal sacrocolpopexy.


Same compartment recurrence


Recurrent uterine prolapse and vault eversion reflect a detachment of the uterosacral ligament insertions from the posterior aspect of pericervical ring and upper vagina. Culdoplasty does not properly correct these DeLancey levels I defects. In addition, the uterosacral ligaments insert at the junction of middle and outer thirds of vaginal vault, and are held there by strong forces. Attempts to unite these structures in the midline would thus appear futile. Although high cure rates have been reported with culdoplasty and suturing together of the uterosacral ligaments, lasting success often came at the price of severe vaginal narrowing.


In a search for anchor points above the mid-pelvis, Amreich described a tedious and impractical procedure for stitching the vault to the sacrotuberous ligament via a trans-gluteal approach. A few years later, Sederl amended the operation into a transvaginal sacrospinous fixation that was refined by Richter and popularised by Randall and Nichols. Post World War II surgeons also sewed the uterus or vagina to the anterior abdominal wall, but discontinued because of rampant enterocoele formation. After the publication of a report of effective suspension by stitching the inverted vault directly to the anterior ligament of right sacro-iliac joint, Stanley Birnbaum advocated sacrocolpopexy using a mesh bridge. However, Birnbaum attached this mesh bridge to the sacral hollow at S 3 –S 4 level, because he considered the sacral promontory too anterior a structure. Birnbaum’s practice was quickly abandoned, because of a number of life-threatening haemorrhages from the lateral sacral veins. Sutton (a gynaecologic oncologist called in to control one such a haemorrhage) suggested that the mesh ribbon be secured to the sacral promontory instead. In 1985, Addison published a series of 56 successful cases, installing abdominal sacrocolpopexy as a gold standard for complex and recurrent vault inversion. Both techniques are predictably superior to Manchester repair or McCall culdoplasty, and have well-documented apical failure rates of less than 5%.


Historically, the greatest weakness of these two vault re-suspension techniques has been the retraction of the torn rectovaginal septum into the lower vagina. As such, the vaginal fixation sutures are placed into hypertrophied vaginal epithelium that is in direct contact with the overlying peritoneal mesothelium, but without an intervening layer of vaginal suspensory fascia. This difficulty was overcome at abdominal sacrocolpopexy by passing a mesh ribbon down the rectovaginal space and attaching it to the apex of perineal body. A similar tactic can be used to improve the reliability of sacrospinous fixation (as explained below).


Recurrence in a different compartment


Endopelvic fascia at secondary sites is often incipiently weak – not to the point of overt prolapse, but sufficient to fail rapidly if loaded with strong new forces. Hence, it is essential that repair of an adjacent compartment does not materially alter axial alignment of the pelvic organs, as the resulting vector of pelvic forces may provoke rapid exteriorisation of a seemingly normal vaginal segment ( Fig. 4 ). Both sacrospinous fixation and abdominal sacrocolpopexy are associated with an anterior compartment failure rate approaching 20%.




Fig. 4


Force vectors within the female pelvis: (a) pelvic organs, aligned in the mid vaginal axis. Pressure generated by the abdominal musculature pushes the horizontally oriented bladder, upper vagina and rectum against the levator plate, thus dissipating these potentially expulsive forces; (b) the pelvic organs have been pulled too far forwards (as often occurs with Burch colposuspension), thus exposing any incipient posterior segment weakness to accelerated enterocoele formation; (c) the pelvic organs have been pulled too far backwards (as is common with traditional methods of performing sacrospinous fixation), loading the bladder and anterior segments with new expulsive forces. SSL, sacrospinous ligament.


Repair strategies


Recurrent vault prolapse is a prime indication to use a biomaterial. Although posterior intravaginal slingplasty (TYCO, Princeton, NJ) was introduced as a minimally invasive treatment for vault prolapse, trocar-driven mesh kits have struggled to stabilise the DeLancey level I supports. In a careful simulation study in six fresh cadavers, Jelovsek et al. showed that the average trocar entry point was only 4.8 cm above the hymenal ring. This accounts for just 55% of total vaginal length. Even if the theoretic maximum were achievable (which is unlikely), the ischial spines are still situated about 2 cm inferior to POP-Q point D. Hence, recurrent apical prolapse is most commonly done via open abdominal or laparoscopic sacrocolpopexy.




Apical compartment


Support anatomy


Connective tissue filling the space between the peritoneum above and the pelvic muscles below is a loose mixture of smooth muscle and collagen fibres. This ‘endopelvic fascia’ differs from the rest of the abdominal retroperitoneum in being more condensed around certain pelvic structures, as with hypogastric vessels, pelvic nerves and the ureter. These condensations are sufficiently dense that a central septum (the cardinal ligament), and two secondary lamellae (the uterosacral and vesico-uterine ligaments) can be dissected out as seemingly discrete structures. Between these embryologically defined condensations lie eight surgically useful ‘spaces’, filled with areolar tissue and devoid of major vessels ( Fig. 2 ). These spaces provide a safe ‘surgical highway’ to the pelvic cavity, especially when one is faced with the need to dissect an operative field with distorted anatomy.




Fig. 2


Pelvic connective tissue in women: the otherwise areolar pelvic connective tissues condense around the hypogastric leash, pelvic nerves and ureter, to form the cardinal, uterosacral and vesico-uterine ‘ligaments’. Between these three condensations lie eight relatively avascular zones of enormous surgical importance. These four central spaces (pre-vesical, vesicovaginal, rectovaginal and retro-rectal) and two paired lateral pelvic spaces (paravesical and pararectal) provide safe dissection routes throughout the pelvis. Modified from Tandler J. Lehrbuch der systematischen Anatomie. Die Eingeweide. Leipzig, Vogel ). Published with permission.


Important differences are found in fibre size and direction, such that the functional anatomy of endopelvic fascia varies from site to site.




  • DeLancey level I: The uterosacral and cardinal ligaments consist of long vertically oriented fibres that suspend the cervix and upper third of the vagina to the pelvic brim. Mechanically speaking, these level I fibres are like the ropes of a ‘trapeze’. They allow physiological mobility in an upward or lateral direction, but resist downward forces. Uterosacral ligaments, however, have a high collagen content and evolve in fetal life as an important part of pelvic organ support. In contrast, the cardinal ligaments are simply a visually prominent residue of the central septum mesenchyme. The term cardinal ligament’ is misleading, as this portion of the pelvic connective tissues contains no ligamentous component and plays no major role in pelvic organ suspension.



  • DeLancey level II: The two mid-vaginal suspensory hammocks comprise short horizontally oriented fibres that attach strongly to the pelvic sidewalls. Mechanically speaking, these level II fibres are like the springs of a ‘trampoline’. They allow minimal movement of the hammocks on the pelvic bones, but provide excellent bounce-back when impacted by an abdominal pressure wave.



  • DeLancey level III: At the pelvic outlet, the billowing vaginal suspensory hammocks are fused to the pelvic floor by a group of dense interwoven fibres. Mechanically speaking, these level III fibres are like ‘tent pegs’, which tether the reproductive organs to the pelvic muscles upon which they sit. Transperineal ultrasound in women with prolapse shows that the rotatory descent of cystocoele and rectocoele primarily reflects failed apical support, with the descending mass ‘hinging’ at the level II/III junction.



For the reparative surgeon, these differences in tissue density and fibre strength resolve the pelvic connective tissues into two semi-independent systems, which inter-relate like a flag at half-mast on a flagpole.




  • The posterior portions of DeLancey levels I, II and III fascia coalesce into a collagen-rich membrane separating the urogenital and alimentary tracts. This postero-superior vaginal suspensory axis runs from the sacral periosteum, through the uterosacral ligaments and pericervical ring, down the rectovaginal septum and into the perineal body. ( Fig. 3 ). When intact, this strong ligamentous ribbon stabilises upper vaginal support; it also guides faeces smoothly through the pelvis and deflects the descending stool backwards into the anal canal. Fracture of this ‘flagpole’ above the point where the uterosacral ligaments insert into peri-cervical ring creates uterine or vaginal vault descensus. Fracture of the ‘flagpole’ below the peri-cervical ring creates a fascial defect, into which either cul-de-sac contents or large bowel will herniate. Such recto-enterocoeles are typically associated with obstructed defaecation syndrome.




    Fig. 3


    Pelvic connective tissues in women: (a) a sagittal section showing how connective tissues within the apical and posterior compartments coalesce into a strong collagenous membrane that runs from the sacral periosteum, through the uterosacral ligaments, into the pericervical ring, then down through the rectovaginal septum, to insert into the perineal body. When intact, this vaginal suspensory axis both suspends the pelvic viscera and guides bowel motions through the pelvis. The vaginal suspensory axis also suspends the anterior vaginal suspensory hammock, these two structures intersecting like a flag at half mast on a flagpole. Obstetric forces tend to tear these fascial supports in the mid pelvis (i.e. where the ‘flag’ joins the ‘flagpole’). In the postero–apical compartments, avulsion of uterosacral ligaments from pericervical ring creates uterine descensus, whereas avulsion of pericervical ring from rectovaginal septum permits herniation of ileum, sigmoid or rectum into the vaginal lumen. In the anterior compartment, avulsion of uterosacral ligaments from pericervical ring or avulsion of pericervical ring from pubocervical fascia initiates cystocoele formation; (b) a typical posterior bulge, caused by ‘partition failure’ in the postero-apical compartment. Whether the rectocoele or the enterocoele component assumes greater relative prominence is largely a matter of random variation; (c) a careful dissection on the cranial side of the rectovaginal septum, using Lone Star TM retractor to aid dissection. An avulsion line separates the extraperitoneal fat of the cul de sac (above) from the dense white fascia of the rectovaginal septum (below); (d) further dissection shows the cul-de-sac projecting downwards and forwards as a large enterocoele. The futility of ‘repairing’ this bulge by plicating this pre-peritoneal should be obvious. PCF, pubocervical fascia; RVS, rectovaginal septum; USL, uterosacral ligament.



  • The anterior portion of the DeLancey level II fascia forms a trapezoid shaped septum (the pubocervical fascia) that is vital to urinary continence, but has no major supportive role for the vagina as a whole. Tearing of the ‘flag’ creates a cystocoele, often accompanied by urinary incontinence or voiding difficulty.



Although the mechanics of prolapse are easily understood using the flag and flagpole analogy, it must be remembered that the pelvic connective tissues are an ‘integrated structure’. The integrity of one compartment depends on the other parts of the system being intact. Support failure within the anterior and postero-apical compartments is thus highly correlated.


Failure mechanisms


Vault eversion was once a major therapeutic challenge for pelvic reconstructive surgeons. Re-suspension by sutured repair, with or without hysterectomy, was the stock-in-trade of gynaecologists until the last few decades, with generally disappointing results. This situation has improved with the emergence of sacrospinous fixation and abdominal sacrocolpopexy.


Same compartment recurrence


Recurrent uterine prolapse and vault eversion reflect a detachment of the uterosacral ligament insertions from the posterior aspect of pericervical ring and upper vagina. Culdoplasty does not properly correct these DeLancey levels I defects. In addition, the uterosacral ligaments insert at the junction of middle and outer thirds of vaginal vault, and are held there by strong forces. Attempts to unite these structures in the midline would thus appear futile. Although high cure rates have been reported with culdoplasty and suturing together of the uterosacral ligaments, lasting success often came at the price of severe vaginal narrowing.


In a search for anchor points above the mid-pelvis, Amreich described a tedious and impractical procedure for stitching the vault to the sacrotuberous ligament via a trans-gluteal approach. A few years later, Sederl amended the operation into a transvaginal sacrospinous fixation that was refined by Richter and popularised by Randall and Nichols. Post World War II surgeons also sewed the uterus or vagina to the anterior abdominal wall, but discontinued because of rampant enterocoele formation. After the publication of a report of effective suspension by stitching the inverted vault directly to the anterior ligament of right sacro-iliac joint, Stanley Birnbaum advocated sacrocolpopexy using a mesh bridge. However, Birnbaum attached this mesh bridge to the sacral hollow at S 3 –S 4 level, because he considered the sacral promontory too anterior a structure. Birnbaum’s practice was quickly abandoned, because of a number of life-threatening haemorrhages from the lateral sacral veins. Sutton (a gynaecologic oncologist called in to control one such a haemorrhage) suggested that the mesh ribbon be secured to the sacral promontory instead. In 1985, Addison published a series of 56 successful cases, installing abdominal sacrocolpopexy as a gold standard for complex and recurrent vault inversion. Both techniques are predictably superior to Manchester repair or McCall culdoplasty, and have well-documented apical failure rates of less than 5%.


Historically, the greatest weakness of these two vault re-suspension techniques has been the retraction of the torn rectovaginal septum into the lower vagina. As such, the vaginal fixation sutures are placed into hypertrophied vaginal epithelium that is in direct contact with the overlying peritoneal mesothelium, but without an intervening layer of vaginal suspensory fascia. This difficulty was overcome at abdominal sacrocolpopexy by passing a mesh ribbon down the rectovaginal space and attaching it to the apex of perineal body. A similar tactic can be used to improve the reliability of sacrospinous fixation (as explained below).


Recurrence in a different compartment


Endopelvic fascia at secondary sites is often incipiently weak – not to the point of overt prolapse, but sufficient to fail rapidly if loaded with strong new forces. Hence, it is essential that repair of an adjacent compartment does not materially alter axial alignment of the pelvic organs, as the resulting vector of pelvic forces may provoke rapid exteriorisation of a seemingly normal vaginal segment ( Fig. 4 ). Both sacrospinous fixation and abdominal sacrocolpopexy are associated with an anterior compartment failure rate approaching 20%.




Fig. 4


Force vectors within the female pelvis: (a) pelvic organs, aligned in the mid vaginal axis. Pressure generated by the abdominal musculature pushes the horizontally oriented bladder, upper vagina and rectum against the levator plate, thus dissipating these potentially expulsive forces; (b) the pelvic organs have been pulled too far forwards (as often occurs with Burch colposuspension), thus exposing any incipient posterior segment weakness to accelerated enterocoele formation; (c) the pelvic organs have been pulled too far backwards (as is common with traditional methods of performing sacrospinous fixation), loading the bladder and anterior segments with new expulsive forces. SSL, sacrospinous ligament.


Repair strategies


Recurrent vault prolapse is a prime indication to use a biomaterial. Although posterior intravaginal slingplasty (TYCO, Princeton, NJ) was introduced as a minimally invasive treatment for vault prolapse, trocar-driven mesh kits have struggled to stabilise the DeLancey level I supports. In a careful simulation study in six fresh cadavers, Jelovsek et al. showed that the average trocar entry point was only 4.8 cm above the hymenal ring. This accounts for just 55% of total vaginal length. Even if the theoretic maximum were achievable (which is unlikely), the ischial spines are still situated about 2 cm inferior to POP-Q point D. Hence, recurrent apical prolapse is most commonly done via open abdominal or laparoscopic sacrocolpopexy.




Anterior compartment


Support anatomy


The anterior vaginal wall is a fascial diaphragm, tautly strung between the pericervical ring above and the urogenital diaphragm below, and attached laterally to the two fascial white lines. As such, the pubocervical fascia functions like a trampoline, providing all direction support to the proximal urethra and bladder base. It was traditionally believed that the central fascia of this suspensory hammock attenuates after childbirth, thus forming the bulge of a cystocele or cysto-urethrocoele. As a matter of engineering principle, these pre-determined points of weakness lie where the lines of force concentrate; namely, along the peripheral margins, not within the central hammock. In the lower vagina, the distal attachment of the bladder hammock to the pubic ramus is strong, and extension of the fetal head focuses childbirth forces posteriorly. In contrast, the superior and lateral margins of the anterior suspensory hammock are exposed to strong avulsive and compressive forces, as the presenting part overcomes soft tissue resistance in the mid-pelvis. Fascial avulsion or ischaemic necrosis during engagement and rotation will transform this trampoline-like diaphragm into a trapdoor. Valsalva pressure will subsequently create a ‘displacement’ cystocoele, with no stretched component ( Fig 5 ). So-called ‘distension’ cystocoeles can be identified, but this probably represents long-term disruption of collagen homeostasis within a sagging anterior hammock, rather than direct obstetric trauma.


Nov 9, 2017 | Posted by in OBSTETRICS | Comments Off on Repair of recurrent prolapse

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