acroreadPdf [1023 kb]

Recto enterocele repair : past problems and new horizons

Hunter New England Health Service, NSW, Australia

Abstract: Standard operations for treatment of recto-enterocoele are based on incorrect anatomical assumptions from the past. The anatomy of prolapse and the principles of hernia repair are reviewed. A new concept of the dynamic bridging graft is proposed. Key words: Recto-enterocoele; Hernia principles; Site specific defects; Mesh repair; Dynamic bridging grafts.

Present methods for treating recto-enterocoele are based on assumptions of 100 years ago. These assumptions are now known to be flawed. However, new anatomic and surgical insights into the pathogenesis of recto-enterocoele have not flowed on to improved therapy. Standard operations for recto-enterocoele, whether done as a posterior colporrhaphy or a Delorme’s procedure, are still rooted in concepts of 20 years ago.

The true basis of pelvic organ support was a complete mystery to 19th Century surgeons. The ambient belief in Victorian times was that pelvic organ support derived mainly from the stiffness of the vaginal walls, which were in turn thought to be held up by their insertion into the levator ani muscles and perineal body. Little distinction was made between prolapse of uterus, bladder or rectum. Constricting the genital hiatus and creating an obstructive shelf in the lower third of vagina was seen as a way to strengthen upper tract support (Fig. 1a & b)

However, the impression of improved uterine support after such surgery was completely erroneous. It arose because the still unsupported cervix and uterus often remained hidden within a voluminous pocket above the rigid perineal shelf, created by levatorplasty. Nonetheless, this entirely non-anatomic operation held sway until well after World War II.1

Beginning in the 1960’s, this very deforming operation of high transverse levatorplasty began to fall into disfavour, because of its high incidence of dyspareunia 2 and because it contributed little to enterocoele repair. In a search for a less morbid technique, focus shifted to Denonvillier’s fascia. This structure was first described in males, but was later recognized as having significant supportive value in women.3

Based on the assumption that rectocoeles arose because of fascial attenuation, surgeons began plicating the central portion of the rectovaginal septum, as a potentially less morbid strategy. This surgery has been done by both the transvaginal 4 and transanal routes.5

Direct comparison of the trans-vaginal and trans-anal approaches through the medical literature is impossible, because gynaecologists operate primarily for bulge control and colorectal surgeons operate primarily for obstructive defaecation. We know from clinical experience that both methods of rectocoele repair deliver reasonable symptom control, at least for a while. However, normal anatomy cannot be restored by either transvaginal or transanal plication.6 Both techniques have also been largely ineffective at restoring normal defaecation mechanics,7 and both still carry a risk of postoperative dyspareunia.6

Gynaecologists next turned to the concept of locating and specifically correcting any specific tears in the rectovag-
inal septum, as had been pre-empted by Richardson.8 Several reports of so called “defect-specific” rectocoele repairs appeared in the American literature, citing good bulge control, better functional outcomes and much reduced dyspareunia rates.7,9,10

However, the repair of these “defects” amount to nothing more than placing a finger of the non-dominant hand in the rectum at the time of surgery, and re-enforcing any area of perceived fascial weakness with isolated sutures. As explained below, this approach has failed to grasp the true nature of the “site-specific” defects that lead to rectoenterocoele formation. Not surprisingly, later reports have shown these mechanically misguided attempts at “defectspecific” rectocoele repair to be quite inefficient.11

If we are to achieve optimal anatomic and functional results from rectocoele repair, our surgical techniques must satisfy the principles of biomechanics. First and foremost, we must set aside the erroneous belief that rectocoele arises because of fascial attenuation. In reality, endopelvic fascia is like canvas – it does not easily stretch, but will tear along lines of stress.12, 13

Second, surgeons must understand the true nature of the fascial defects that cause recto-enterocoeles. The connective tissues of the postero-apical compartment form a thick and highly collagenized leash, running from sacrum to perineum (Fig. 2a).
This fascial aggregation plays an important support role, and has been designated the ‘vaginal suspensory axis’.12
Obstetric damage to the vaginal suspensory axis almost always occurs in the mid-pelvis, because expulsive forces increase exponentially as the presenting part tries to negotiate the “plane of least dimensions”. If the endopelvic fascia is torn as the head tries to enter the mid-pelvis (“engagement”), the upper margin of the pericervical ring is likely to separate from the uterosacral ligaments – setting the stage for a ‘cervix-first’ prolapse. Conversely, if damage occurs as the presenting part is exiting the ‘plane of least dimensions’ (“rotation” and “extension”), the rectovaginal septum is likely to be shorn away from the inferior border of the pericervical ring (Fig. 2b).

The fetal head then pushes the detached rectovaginal septum downwards and outwards, much like a snow plough (Fig 3).

This injury creates a low pressure zone in the upper vagina, into which the pelvic contents can herniate, driven by sustained intra-abdominal pressure:

The key reason is that pelvic connective tissues are NOT structurally suited to chronic load bearing. Hence, Nature relies upon a complex inter-relationship between the muscles and the connective tissues (Fig. 5).

The role of the pelvic floor muscles

Skeletal muscle brings two unique advantages to the biomechanics of pelvic organ support: durability and contractility.

i) Durability: All biological fibres are susceptible to strain-induced fatigue fracture, unless continuously remodelled in response to every day forces. Hence, even strong connective tissue would have difficulty in passively suspending the pelvic viscera in a species of bipeds that lives for 85+ yrs. These inherent biomechanical difficulties are brought to the fore by the combined insult of aging and prior childbirth injury. Both events disrupt the vital process of collagen homeostasis, and hence amplify the tendency of fascia (especially very weak fascia) to fail over time. Stress-strain forces also create fibre fracture in skeletal muscle. However, in contrast to fascia, microtears in the muscle bundles induce compensatory hypertrophy, making the injured muscle stronger. However, the capacity for muscle hypertrophy is also diminished in older women by catabolism (age or illness related breakdown of the body’s proteins) 14,15 and sarcopaenia (age-related acceleration of myocytes loss via apoptosis).16 Even so, muscle is a far more robust resource than fascia.

ii) Contractility: Being contractile, the pelvic floor muscles actively oppose intra-abdominal pressure, in two different but crucial ways.

The role of the endopelvic fascia

The endopelvic fascia functions more as an investing mesentery, than as a direct visceral suspensory system (such as depicted by Fig. 5D).

In this role, it attaches the pelvic organs to the axial skeleton, and thus stabilizes them over the centre of the levator plate. The endopelvic fascia has considerable mechanical strength, and can resist short term expulsive forces. However, any fascial suspension is prone to fail under sustained load, especially if ravaged by age and childbirth damage.

The pathogenesis of prolapse

Pregnancy itself softens the pelvis connective tissue, thus potentially weakening apical supports. However, the key event in recto-enterocoele formation is vaginal delivery, which can cause several complementary patterns of support failure.

Avulsive and stretch neuropathy injuries to the pelvic diaphragm result in a sagging concave levator plate and a widened urogenital hiatus (Fig. 6a & b).

Valsalva pressures are now deflected downwards and outwards, creating a sliding stress on the pelvic viscera. If the fascial mesentery is also torn, the pelvic viscera align over this widened genital hiatus, and are thus susceptible to descensus (Fig. 6c).

Childbirth is “an essential but not sufficient factor” in the pathogenesis of prolapse. However, these myofascial injuries are generally compensated for years by the strong connective tissues of young women. Whether or not this series of adverse mechanical events ever results in overt prolapse depends upon the operation of secondary factors, such as nutritional deficiency, repeated abdominal straining, central obesity and the acquired collagen weakness that inevitably develops in a torn anterior or posterior suspensory hammock.

Weakened connective tissue adjacent to the ‘site-specific’ tears has been identified as an important failure mechanism by hernia surgeons. This same phenomenon is probably just as relevant to prolapse repair.
Gynaecologists are beginning to articulate that prolapse is a form of hernia. Let us explore the implications of that assertion in a little more detail.

Hernia is the protrusion of an internal organ (usually small bowel) through the muscular wall of the body cavity, generally occurring at a site of congenital weakness. The pathogenesis of hernia has two components.

This phenomenon is particularly evident in treatment failure patterns for incisional hernia. Firstly, the unsatisfactory results of Mayo duplicative suture repair for incisional hernia have been repeatedly documented, as in a National survey of German hernia surgeons.33

Analysis has not identified any consistent technique factors that predispose to failure. Secondly, a retrospective, population-based cohort study from a Washington State hospital discharge database (1987-99) demonstrated that the 5-year re-operative rate was 23.8% after the first re-operation, 35.3% after the second, and 38.7% after the third failure. In response to these tissue weakness factors, the use of synthetic mesh in incisional hernia repairs increased from 34.2% in 1987 to 65.5% in 1999. Controlling for age, sex, co-morbidity index, year of the initial procedure, and hospital descriptors, the principal hazard in this population-based cohort study proved to be the use or non-use of a tissue augmentation material (recurrence being 24.1% higher in the ‘suture-only’ repairs).34

Thirdly, a multicenter RCT comparing suture versus mesh hernioplasty in 200 patients showed the three-year cumulative recurrence rates to be 80% higher if mesh was not used (43% vs 24%; p = 0.02). Risk factors for recurrence were suture repair, infection, prostatism (in men), and previous surgery for abdominal aortic aneurysm (another disorder known to reflect collagen weakness).34 Similar reductions in inguinal hernias have also been documented in a prospective Denmark-wide study.36

Finally, the late appearance of incisional hernias several years after laparotomy and the high recurrence rates after ‘suture-only’ repair (irrespective of surgeon or technique) point to the importance of disordered collagen metabolism in the pathogenesis of both primary and recurrent incisional hernias.37

This view is supported by the demonstration of a reduced proportion of high tensile strength (type I) collagen and an increased amount of immature (type III) collagen in hernial sacs.38 Acquired degeneration in collagen quality probably occurs because the ‘site-specific’ defects in the investing fascia disrupt continuous tissue remodelling, a process that is driven by the transmission of everyday mechanical stress. Such collagen homeostasis is affected by the balance between growth factors and tissue collagenase levels (mainly matrix metalloproteinases-1 and -13).39,40 There is a suggestion of disordered MMP-1 and MMP-13 activity in both skin and scars from hernia patients, but evidence to this point has been inconsistent.41

Likewise, prolapse is the protrusion of an organ (uterus, bladder or bowel) through the vaginal fibromuscularis, usually at a site of childbirth injury. It also has mechanical and metabolic components.

– The mechanical event is a group of ‘site-specific’ tears in the endopelvic fascia, as discussed above.
The high prolapse incidence and treatment failure rates in patients with inherited collagen disorders like Ehlers Danlos or benign joint hypermobility syndromes is well known.42, 43

However, it is also likely that biochemically normal prolapse patients acquire a metabolic collagen weakness in the endopelvic fascia when daily transmission of mechanical forces to the torn suspensory hammocks is disrupted. The argument that tissue weakness is also an important factor in the aetiology of prolapse mirrors that of herniologists. The risk of operative failure rises with each successive reparative attempt, even though subsequent procedures are usually done at tertiary referral centers.44

Moreover, in a cohort of women with pelvic floor disorders who were followed prospectively for 5 years, a history of prior pelvic prolapse and urinary incontinence surgery was actually a marker for a 42% increase in the likelihood of that patient coming to re-operation.45 Such failures do not reflect tissue thinning in prolapse women – in fact, the vaginal muscularis layer in enterocoele has been shown to be thicker than normal.46

Given that the mechanical of the vaginal wall is likely to reflect composition, thickness and tissue architecture, it is noteworthy that Boreham et al have shown a reduced proportion of physiological smooth muscle and an increased proportion of disorganized smooth muscle bundles with decreased a-actin staining.47, 48 Prolapse tissue biopsies have been shown to have a decreased collagen concentration,49 lower collagen I: III ratios, and up to four times higher levels of lytic protease enzymes (as indicated by MMP activity).50-52

General surgeons have been able to reduce the failure rate for inguinal hernia from about 35% to ›2%. The main vehicle of this success has been adherence to a group of rules called the “Hernia Principles”. Logic would suggest that the same approach may help gynaecologists to improve their prolapse repair outcomes.

Over the course of a couple of centuries, surgeons developed a group of cardinal operative rules to reduce hernia recurrence.53
These principles are:

  1. Avoid wound infection,
  2. Protect repair from intra-abdominal pressure,
  3. Repair tears in investing fascia,
  4. Re-anchor the torn investing fascia back onto skeleton.

The aim is to repair all “site-specific” fascial defects, using permanent suture, and with no tension in any direction. However, mobilising the retracted vaginal hammocks back to the mid-pelvis, so many years after childbirth, does inevitably produce a degree of suture line tension.

To these traditional rules, modern surgeons have added the proviso that the most effective way to avoid tension in hernia repair is through the use of mesh. There are two main rules for the prudent use of mesh in hernia surgery:

These theoretic principles also fit recto-enterocoele repair
– but we cannot directly extrapolate the choice of materials, from hernia to prolapse. The vagina is not the abdomen. Specifically:

Rules have been devised for the tension free placement of mesh:

  1. Mesh must suit surgical site,
  2. Isolate mesh from contact with a hollow viscus,
  3. Limit bacterial colonisation of the mesh,
  4. Choice of mesh must suit surgical objectives,
  5. Mesh implant must overlap the defect on all sides,
  6. Stabilize against doubling, wrinkling & undue shrinkage,
  7. Mesh must be placed in a tension-free manner.

Rectocele, enterocele and vault inversion share a common origin namely, childbirth damage to the endopelvic fascia. Such injuries often occur concomitantly.11,12
Gynecologists have traditionally regarded these three conditions as discrete entities. However, support failure within the anterior and postero-apical compartments are highly correlated.55,56

Typically, a patient will present with overt support failure in one segment and incipient weakness in adjacent sites. Paradoxically, despite marked differences in their clinical prominence, both dominant and incipient support defects are of almost equal importance to the reconstructive gynaecologist. That is to say, the fascial supports at the secondary sites may well be strong enough to maintain the status quo, but they are often too damaged to resist the new force vectors created when an adjacent vaginal segment is re-suspended. Leaving an area of incipient weakness unrepaired in such circumstances sews the seeds of early failure – often within 6 months or so. In the words of Wayne Baden,30 the prudent surgeon will always “leave the entire tract intact”, or face an unacceptable risk of early postoperative bladder, vault or rectal prolapse.

From a pragmatic perspective, pelvic visceral mesenteries resolve into two semi-independent systems – the anterior and postero-apical compartments. These two systems intersect like a flag and flagpole (Fig. 2a). The anterior hammock is vital to urinary continence, but has no major supportive role for the vagina as a whole. Conversely, the vaginal suspensory axis both suspends the vaginal apex and partitions the vagina from the cul de sac and rectum. When intact, this vaginal suspensory axis forms a membrane that guides faeces efficiently through the pelvis and out the anus. The proximate cause of recto-enterocoele is a ‘site specific tear’ in the vaginal suspensory axis – creating suspensory failure if the injury occurs above the pericervical ring and partition failure if damage occurs more distally (Fig. 2b).

Effective repair of postero-apical compartment prolapse requires that fascial integrity be restored in two different planes.

– In the sagittal plane, fascial continuity must be restored from the sacral periosteum, through the uterosacral ligaments, into the pericervical ring, down the rectovaginal septum and into the perineal body. Historically, this has been most effectively done by threading a narrow ribbon of polypropylene from the sacral promontory to the rectovaginal space (abdominal sacrocolpopexy). However, transvaginal placement of a remodeling biomesh has the potential to deliver even better performance than abdominal sacrocolpopexy, by a cheaper and less invasive technique.

– In the coronal plane, restoration of normal anatomy requires that fascial continuity be established from the ischial spines and lower margin of sacrospinous ligament, down the two fascial white lines,57 to the distally retracted edge of the rectovaginal septum (Fig. 7).

Such a repair in the coronal plane cannot be done from above, but is readily accomplished from below.58
Such a repair can be done by re-suturing native tissues. However, given that damaged endopelvic connective tissues undergo a slow but relentless deterioration in collagen quality, use of an appropriate tissue augmentation material is more in accordance with modern hernia principles. From a biomechanical perspective, mesh re-enforcement must satisfy two goals:

Effective mesh correction of the posterior defect in two planes requires a roughly diamond-shaped graft. Key points in ensuring a safe and effective operative technique were:

In electing to use primarily biological implants, there is one important point must be made about the choice of materials. In the early 1990’s, manufacturers “leatherized” various cadaveric and animal grafts, in the hope getting an equally permanent but “more natural” scaffold. Outcome proved to be paradoxical. Although first generation biomesh is strong in vitro, reports soon surfaced of an unduly high repair failure rate when Pelvicol®, etc was used in vivo.62

Re-operation often showed no residual graft material. With the wisdom of hindsight, the reason for this phenomenon is obvious. In vivo, any denatured collagen – whether of endogenous or exogenous origin– is seen by the host’s immune system as “dead tissue”, and hence subjected to an intense biodegradation reaction (ie, encapsulation and enzymatic autolysis). In addition, Pelvicol® provokes a strong foreign body reaction, meaning that the resulting wound can be just as hard and just as stiff as with synthetic mesh. Thus, first generation biologicals with crosslinked collagen are poorly suited for use as a bridging graft, as illustrated a recent rectocoele repair series showing a 41% failure rate at 3 years.63

My experience in a pilot study using SurgiSIS® as a bridging graft has been most encouraging.64-66 At one year follow-up, 46 of 49 patients had outright or qualified anatomic success. There were statistically significant reductions in all pre-operative symptoms, including bulge, drag and defaecatory difficulties. Intraoperative complications were minimal, and no graft-related morbidity or dyspareunia has been seen.66

Prolapse repair is associated with stretch dilatation of the anterior rectal wall. However, this is a secondary event. The primary cause is a combination of pelvic muscle avulsive and denervation injury, together with various ‘site-specific’ lacerations of the suspensory hammocks. To be curative, any operation for recto-enterocele must repair the sites of fascial tearing (rather than just plicating the non-specific dilatation of the rectal muscularis).

Surgical options for prolapse repair place more reliance on the endopelvic fascia than occurs in Nature. Attaining a durable repair under these circumstances is a biomechanically difficult task even in young women with strong, anabolic tissues. However, this inherently difficult task is much harder by secondary collagen degeneration within adjacent connective tissues. Hernia surgeons have faced and overcome similar obstacles, and it is likely that some of these surgical principles are relevant to gynaecology.

In using tissue augmentation materials, surgeons need to distinguish static struts (where tensile strength is the dominant issue) from dynamic bridging grafts (where tissue flexibility and low morbidity are the main considerations). SurgiSIS® is an ideal bridging graft, under almost all circumstances. If properly sized and shaped, it can also perform well as a suspensory strut. However, there are clinical circumstances where the addition of polypropylene is prudent.


  1. Howkins J. Shaw’s Textbook of Operative Gynaecology, Third edition. E&S Livingstone Ltd. Edinburgh and London, 1968.
  2. Francis WJ, Jeffcoate TN. Dyspareunia following vaginal operations. J Obstet Gynaecol Br Commonwealth 1961; 68: 1-10.
  3. Ulenhuth E, Wolfe WM, Smith EM, Middleton EB. The rectovaginal septum. Surg Gynecol Obstet 1948; 86: 148-63.
  4. Sullivan ES, Leaverton GH, Hardwick CE. Transrectal perineal repair: an adjunct to improved function after anorectal surgery. Dis Colon Rectum 1968; 11: 196-214.
  5. Miley PS, Nichols DH. A correlative investigation of the human rectovaginal septum. Anat Rec 1969; 163: 443-52.
  6. Kahn MA, Stanton SL. Posterior colporrhaphy: its effects on bowel and sexual function. Br J Obstet Gynaecol 1997; 104: 882-86.
  7. Kenton K, Shott S, Brubaker L. Outcome after rectovaginal fascia reattachment for rectocele repair. Am J Obstet Gynecol 1999; 181: 1360-4.
  8. Richardson AC, Lyon JB, Williams NL. A new look at pelvic relaxation. Am J Obstet Gynecol 1976; 126: 565.
  9. Cundiff GW, Weidner AC, Visco AG et al. An anatomical and functional assessment of the discrete defect rectocele repair. Am J Obstet Gynecol 1998; 179: 1451-7.
  10. Porter WE, Steele A, Walsh P et al. The anatomical and functional outcomes of defect-specific rectocele repairs. Am J Obstet Gynecol 1999; 181: 1353-9.
  11. Paraiso MF, Barber MD, Muir TW, Walters MD. Rectocele repair: a randomized trial of three surgical techniques including graft augmentation. Am J Obstet Gynecol 2006; 195: 1762-71.
  12. Zimmerman CW. Surgical correction of defects in pelvic support. In Te Linde’s Operative Gynecology. Editors: Rock JA, Jones HW III, 9th edition; pages 2003, 927-48.
  13. Zimmerman CW. Posterior vaginal reconstruction with bilateral uterosacral colpopexy. In: Kovac SR and Zimmerman CW eds. Advances in reconstructive vaginal surgery. Philadelphia: Wolters Kluwer / Lipppincott Williams & Wilkins, pages 2007, 199-210.
  14. Labrie F, Belanger A, Simard J, Van Luu-The et al. DHEA and the intracrine formation of androgens and estrogens in peripheral target tissues: Its role in aging. Steroids 1998; 63: 322-328.
  15. Lamberts SW, van den Beld AW, van der Lely AJ. The endocrinology of aging. Science 1997; 278: 419-24.
  16. Marzetti E, Leeuwenburgh C. Skeletal muscle apoptosis, sarcopenia and frailty in old age. Exp Gerontol 2006; 41: 1234-8.
  17. DeLancey JO. Structural support of the urethra as it relates to stress urinary incontinence: the hammock hypothesis. Am J Obstet Gynecol 1994; 170: 1713-23.
  18. De Lancey JO. Structural anatomy of the posterior pelvic compartment as it relates to rectocele. Am J Obstet Gynecol 1999; 180: 815–823.
  19. De Lancey JO, Ashton-Miller JA. Pathophysiology of adult urinary incontinence. Gastroenterology 2004; 126: S23-32.
  20. Hsu Y, Summers A, Hussain HK, Guire KE, DeLancey JO. Levator plate angle in women with pelvic organ prolapse compared to women with normal support using dynamic MR imaging. Am J Obstet Gynecol 2006; 194: 1427-33.
  21. Margulies RU, Hsu Y, Kearney R, Stein T, Umek WH, DeLancey JO. Appearance of the levator ani muscle subdivisions in magnetic resonance images. Obstet Gynecol 2006; 107: 1064-9.
  22. De Lancey JO, Kearney R, Chou Q et al. The appearance of levator ani muscle abnormalities in magnetic resonance imaging after vaginal delivery. Obstet Gynecol 2003; 101: 46-53.
  23. Patel DA, Xu X, Thomason AD et al. Childbirth and pelvic floor dysfunction: an epidemiologic approach to the assessment of prevention opportunities at delivery. Am J Obstet Gynecol 2006; 195: 23-28.
  24. Snooks SJ, Badenoch DF, Tiptaft RC, Swash M. Perineal nerve damage in genuine stress urinary incontinence: An electrophysiological study. Br J Urol 1985; 57: 422-6.
  25. Snooks SJ, Swash M, Mathers SE, Henry MM. Effect of vaginal delivery on the pelvic floor: A 5-year follow-up. Br J Surg 1990; 77: 1358-60.
  26. Allen RE, Hosker GL, Smith ARB, Warrell DW. Pelvic floor damage and childbirth: A neurophysiological study. Br J Obstet Gynaecol 1990; 97: 770-9.
  27. Lien KC, Morgan DM, DeLancey JO, Ashton-Miller JA. Pudendal nerve stretch during vaginal birth: a 3D computer simulation. Am J Obstet Gynecol 2005; 192: 1669-76.
  28. Richardson AC, Edmonds PB, Williams NL. Treatment of stress urinary incontinence due to paravaginal defect. Obstet Gynecol 1981; 57: 357-362.
  29. Richardson AC. The rectovaginal septum revisited: its relationship to rectocele and its importance in rectocele repair. Clin Obstet Gynecol 1993; 36: 976 -83.
  30. Baden WF, Walker T. Surgical repair of vaginal defects. Philadelphia, JB Lippincott, 1992.
  31. Read RC. Inguinal herniation in the adult, defect or disease: a surgeon’s odyssey. Hernia 2004; 8: 296-9.
  32. Read RC. Co-morbidity and interstitial herniation in the adult: an hypothesis. Hernia 2007; 11: 5-8.
  33. Paul A, Korenkov M, Peters S, Kohler L, Fischer S, Troidl H. Unacceptable results of the Mayo procedure for repair of abdominal incisional hernias. Eur J Surg 1998; 164: 361-67.
  34. Flum DR, Horvath K, Koepsell T. Have outcomes of incisional hernia repair improved with time? A population-based analysis. Ann Surg 2003; 237: 129-35.
  35. Luijendijk RW, Hop WC, van den Tol MP et al. A comparison of suture repair with mesh repair for incisional hernia. N Engl J Med 2000; 343: 392-98.
  36. Bay Nielsen M, Kehlet H, Strand L et al. Quality assessment of 26304 herniorrhaphies in Denmark: a prospective nationwide study. Lancet 2001; 358: 1124-28.
  37. Rosch R, Junge K, Knops M. Analysis of collagen-interacting proteins in patients with incisional hernias. Langenbecks Arch Surg 2003; 387: 427-32.
  38. Klinge U, Zheng H, Si ZY et al. Synthesis of type I and III collagen, expression of fibronectin and matrix metalloproteinases-1 and -13 in hernial sac of patients with inguinal hernia. Int J Surg Investig 1999; 1: 219-27.
  39. Hodde J. Naturally occurring scaffolds for soft tissue repair and regeneration. Tissue Engineering 2002; 8: 295-308.
  40. Badylak SF. Xenogeneic extracellular matrix as a scaffold for tissue reconstruction. Transplant Imnunology 2004; 12: 367-377.
  41. Klinge U, Si ZY, Zheng H et al. Collagen I/III and matrix metalloproteinases (MMP) 1 and 13 in the fascia of patients with incisional hernias. Invest Surg J 2001; 14: 47-54.
  42. Norton PA, Baker JE, Sharp HC, Warenski JC. Genitourinary prolapse and joint hypermobility in women. Obstet Gynecol 1995; 85: 225-8.
  43. Carley ME, Schaffer J. Urinary incontinence and pelvic organ prolapse in women with Marfan or Ehlers Danlos syndrome. Am J Obstet Gynecol 2000; 182: 1021-23.
  44. Luber KM, Boero S, Choe JY. The demographics of pelvic floor disorders: current observations and future projections. Am J Obstet Gynecol 2001; 184: 1496-1503.
  45. Clark AL, Gregory T, Smith VJ, Edwards R. Epidemiologic evaluation of reoperation for surgically treated pelvic organ prolapse and urinary incontinence. Am J Obstet Gynecol 2003; 189: 1261-67.
  46. Tulikangas PK, Walters MD, Brainard JA, Weber AM. Enterocele: is there a histologic defect? Obstet Gynecol 2001; 98: 634 -7.
  47. Boreham MK, Wai CY, Miller RT, Schaffer JI, Word RA. Morphometric analysis of smooth muscle in the anterior vaginal wall of women with pelvic organ prolapse. Am J Obstet Gynecol 2002; 187: 56-73.
  48. Boreham MK, Miller RT, Schaffer JI, Word RA. Smooth muscle heavy chain and caldesmon expression in the anterior vaginal wall of women with and without pelvic organ prolapse. Am J Obstet Gynecol 2001; 185: 944-52.
  49. Soderberg MW, Falconer C, Bystrom B, Malmstrom A, Ekman G. Young women with genital prolapse have a low collagen concentration. Acta Obstet Gynecol Scand 2004; 83: 1193-8.
  50. Jackson SR, Avery NC, Tarlton JF et al. Changes in metabolism of collagen in genitourinary prolapse. Lancet 1996; 347: 1658-61.
  51. Moalli PA, Shand SH, Zyczynski HM, Gordy SC, Meyn LA. Remodeling of vaginal connective tissue in patients with prolapse. Obstet. Gynecol 2005; 106: 953-63.
  52. Phillips CH, Anthony F, Benyon C, Monga AK. Collagen metabolism in the uterosacral ligaments and vaginal skin of women with uterine prolapse. Br J Obstet Gynaecol 2006; 113: 39-46.
  53. Franklin ME, Gonzales JJ, Glass JL. Use of porcine small intestinal mucosa as a prosthetic device for laparoscopic repair of hernias in contaminated fields: 2-year follow-up. Hernia. 2004; 8: 186-9.
  54. Amid PK. Groin hernia repair: Open techniques. World J Surg. 2005; 29: 1046-51.
  55. Summers A, Winkel LA, Hussain HK, DeLancey JO. The relationship between anterior and apical compartment support. Am J Obstet Gynecol 2006; 194:1438-43.
  56. Rooney K, Kenton K, Mueller ER et al. Advanced anterior vaginal wall prolapse is highly correlated with apical prolapse. Am J Obstet Gynecol 2006; 195: 1837-40.
  57. Leffler KS, Thompson JR, Cundiff GW. Attachment of the rectovaginal septum to the pelvic sidewall. Am J Obstet Gynecol 2001; 185: 41-3.
  58. Umek WH, Morgan DM, Ashton-Miller JA, DeLancey JO. Quantitative analysis of uterosacral ligament origin and insertion points by magnetic resonance imaging. Obstet Gynecol 2004; 103: 447-451.
  59. Klinge U, Klosterhalfen B, Müller M, Schumpelick V. Foreign body reaction to meshes used for the repair of abdominal wall hernias. Eur J Surg 1999; 165: 665-73.
  60. Wiedemann A, Otto M. Small intestinal submucosa for pubourethral sling suspension for the treatment of stress incontinence: first histopathological results in humans. J Urol 2004; 172: 215-18.
  61. Reid RI, Hodde J. The histological pattern of xenograft remodeling in vaginal paravaginal repair with SurgiSIS overlay graft. Int Urogynecol J 2006; 17 (supp 2): S105-6.
  62. Fitzgerald MP, Mollenhauer J, Bitterman P, Brubaker L. Functional failure of cadaveric allografts. Am J Obstet Gynecol 1999; 181: 1339-46.
  63. Altman D, Falconer C. Perioperative morbidity in using transvaginal mesh in pelvic organ prolapse repairs. Obstet Gynecol. 2006; 107: 59-65.
  64. Reid RI. A retrospective comparison of abdominal versus vaginal paravaginal repair for severe cysto-urethrocele. Int Urogynecol J 2005; 16 (supp 2): S45.
  65. Reid RI. Vaginal paravaginal repair with SurgiSIS overlay graft for recurrent cystourethrocele. Int Urogynecol J 2006; 17 (supp 2): S159.
  66. Reid RI. A retrospective analysis of recto-enterocele repair with SurgiSIS biomesh. Int Urogynecol J 2006; 17 (supp 2): S236.

Dr. RICHARD REID Eastpoint Tower, #607
180 Ocean St Edgecliff, NSW 2027 Australia
Telephone: + 612 9327 8033 Fax: + 612 9327 3403
E-mail: Richard_reid @

Conflict of Interest Declaration: The author is supervising investigator for a global multicentre randomized clinical trial comparing ‘suture-only’ and SurgiSIS®-augmented vaginal paravaginal repair. Beyond this research funding from Cook Incorporated, I have no commercial or employment ties to any company.