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14.1: Effect of Prolapse

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    The Aetiology of Prolapse

    The aetiology of pelvic organ prolapse (POP) and stress urinary incontinence (SUI) are inseparable. These two conditions are different sides of the same coin and share common aetiological variables. Detrusor overactivity and urinary urgency, dry or wet, may co-exist in women with SUI and POP, but is a separate condition with different aetiological factors beyond the scope of this discussion. Pelvic organ prolapse (POP) is not caused by a single event or deficiency, but is the culmination of an interplay between complex multifactorial aetiologies which vary between women. It would not be wise to reduce the end result to a specific event and the best science can offer us, until we have greater understanding of these complex interactions, is to analyze different risk factors in a population and assign relative risks or odds ratios. It is difficult to counsel women regarding the ideal mode of delivery using the currently available evidence.
    Risk factors for POP can be classified into predisposing, inciting, promoting or decompensating. Predisposing factors include congenital anomalies, race, gender and hereditary defects such as Marfan’s syndrome. Inciting factors include pregnancy and vaginal delivery, surgical procedures and certain myopathies and neuropathies. Factors outside the pelvis that could elicit POP, include obesity, smoking, pulmonary disease that leads to chronic coughing and lifestyle variables including repetitive heavy lifting during occupational duties or during recreational activities. These would be considered to be promoting causes. Decompensatory mechanisms include aging, menopause, neuropathy, myopathy, debilitating diseases and medication such as cortisone. A combination of factors each influence the development of this disease to a greater or lesser degree. Overall, the risk factors most strongly associated with prolapse include advanced age, high gravidity and parity, number of vaginal deliveries and previous hysterectomy.


    Although increasing parity is a risk factor for prolapse, nulliparity does not provide absolute protection. In the Women’s Health Initiative (WHI) study nearly 20% of nulliparous women had some degree of POP. There is, however, no doubt that both pregnancy and the delivery of a baby play a role in the aetiology of POP and SUI. Francis et al found that 40% of primigravid women had some SUI before falling pregnant, which always worsened during the pregnancy, improved after the pregnancy and recurred with later pregnancies. This would eventually become a problem even when they were not pregnant. The hormonal changes associated with pregnancy have an effect on the elasticity and distension of the pelvic contents by their effect on the muscle and collagen content as well as the changes in circulation of the pelvic floor. In addition there is the added stress of increased intra-abdominal pressures and distension by the fetal presenting part.
    There are three mechanisms whereby labour influences the integrity of the pelvic floor and the continence mechanisms. Firstly, mechanical distension and tearing of muscle and connective tissue invariably occur. Secondly, vascular compression with the potential for hypoxic damage to the same structures as well as the urinary tract, and subsequent replacement of active tissue by scar formation, has also been shown to occur. The third mechanism is compression, stretching or hypoxic damage to nerve structures including both motor and sensory. EMG studies and pudendal nerve terminal motor latency (PNTML) studies have demonstrated defects after vaginal deliveries which are not apparent following elective caesarean section. Strong associations are described for long labours, macrosomic babies, forceps deliveries, 3rd degree tears and multiparity. There are numerous studies that confirm these findings.
    Among premenopausal women, those who have delivered at least one baby, have a higher prevalence of both SUI and urgency than nulliparous women. In contrast, among postmenopausal women, pregnancy and childbirth seem to have a smaller impact on SUI. Older nulliparous females have been shown in some studies to have the same prevalence of SUI as parous women. Co-morbidities, particularly aging, outweigh the effect of previous pregnancies in these women. Goldberg and Abramov report interesting findings after looking at pelvic floor dysfunction in a group of identical twin sisters, with a mean age of 47 years (range 18 and 85 years). The sibling who had at least two vaginal births was three times more likely to report faecal incontinence and four times more likely to report urinary incontinence than her nulliparous twin sister. In the WHI study, it was concluded that a woman having a history of at least one delivery had double the risk of POP when compared to nulliparous controls.

    (i) Myogenic damage:

    We have histological confirmation and radiological evidence, using ultrasound and MRI, demonstrating that the mechanical trauma of delivery leads to rupture of the pelvic muscles. Imaging studies have also shown an inverse correlation between prolapse and the total volume of levator muscle and muscle strength.

    (ii) Neuromuscular damage:

    The mechanism of neurological damage during labour is unknown, but pudendal nerve compression certainly plays a significant role. Snooks et al have shown that after vaginal delivery there is prolonged PNTML and this correlates with greater perineal descent during straining. Forceps deliveries appear to make the greatest impact on PNTML whereas subjects having an elective caesarean section were no different from nulliparous controls. Most women will recover as innervation is reestablished but in some women it never returns to normal. Viktrup et al, in a study on the risk of incontinence after delivery, report that most patients who are incontinent after the birth of their babies improve but are at a greater risk of developing incontinence a few years later. Of the women who had SUI three months after the delivery, the majority of whom were dry 1 year later, 92% became incontinent 5 years later. Sultan et al have also shown that a caesarean section performed after the onset of labour is less protective than an elective section. In the Term Breech trial, 4.5% of patients who had a caesarean section were incontinent after 3 months compared to 7.3% of the women that delivered vaginally with a relative risk (RR) of 0.62 and a confidence interval of 0.41 to 0.93.
    Data from the EPINCONT study, suggest that after one baby, the RR for SUI becomes 2.4 in women aged 20-34 years but only 1.8 when they are between 35 and 64 years of age. In both age groups, however, the associations are statistically significant. Once the patients were over 65 years of age, there was no significant association between delivery and the risk of SUI. There was, however, the same trend with a larger RR for a parity of two or more.

    (iii) Damage to the endopelvic fascia:

    During labour, tears develop in the connective tissue. This might not be immediately apparent but with continuous trauma and aging it plays an important role in the development of prolapse. It would appear that some women have a more vulnerable collagen. Studies have shown that there is a decreased collagen content in nulliparous women with SUI. There is also an increase in the concentration of weak cross-linked collagen in women with prolapse compared to the strong cross-linked collagen in women without prolapse. These differences are quantitative as well as qualitative on histo-chemical level. Furthermore, there is an increase in the metalloprotease enzyme activity in patients with prolapse suggesting an increase in the breakdown of collagen of these patients.
    There is thus no question that pregnancy and the mode of delivery influences subsequent prolapse and SUI. However, most women have pregnancies and deliveries without residual longterm POP or SUI. The scientific challenge is therefore to identify a subgroup of women who are vulnerable to the consequences of pregnancy and to offer appropriate counselling and possible intervention. Currently the only available intervention is caesarean section but the influence of this on subsequent pregnancies has to be accepted.
    Epidural analgesia is possibly associated with subsequent POP or SUI. It may indeed increase the use of forceps in some institutions and this in turn might have deleterious effects on the pelvic floor but it seems unlikely that the epidural block per se has any deleterious role.
    The use of episiotomy to prevent pelvic floor damage has no support in the literature. There is no evidence that first or second degree tears are associated with later POP. Third degree tears do appear to be associated with subsequent POP and SUI. In some studies, episiotomies contributed to third and fourth degree tears.


    Virtually all studies that address the relationship between aging and POP find a positive association. There is however controversy as to the role of the menopause.


    There certainly appears to be an association between POP and constipation. Posterior compartment prolapse can lead to difficult rectal emptying, due to herniation of the rectocele into the vagina. It has been shown that chronic constipation with repetitive straining leads not only to pelvic floor muscular damage, but also to neuropathy. Constipation appears to be significantly more common in women developing POP.

    Occupational Stresses

    There are studies from Italy and the USA reporting a correlation between a patient’s income and the prevalence of POP. The lower the income, the higher the prevalence of POP. The authors postulated that this was probably due to harder manual labour. Nursing has also been shown to be a risk factor. A study looking at 28,000 Danish nurses found an odds ratio of 1.6 for developing POP or a herniated lumbar disc compared to same-aged controls.


    Obesity increases the intraabdominal pressure significantly and chronically. Most studies have found a positive correlation between obesity and POP as well as a greater risk for surgical failure in the obese.


    According to the Oxford Family Planning Study, the incidence of POP is higher in women who undergo a hysterectomy for reasons other than prolapse. If a woman undergoes surgery for POP the subsequent risk appears to be even higher. It is uncertain whether a sub-total hysterectomy carries the same risk.

    Previous Prolapse Surgery

    There is little doubt that certain surgical procedures predispose patients to prolapse in other compartments. Two examples include an increase in posterior compartment prolapse after a Burch colposuspension and a greater number of cystocoeles after sacrospinous ligament fixation. There are also reports of prolapse of the vaginal vault after transection of the uterosacral ligaments for chronic pelvic pain.

    Collagen Synthesis Abnormalities

    As already stated above there are qualitative and quantitative differences in the connective tissue of women with and without POP. These would also include differences in the muscle actin, myosin and extra-cellular matrix proteins.

    Variations In Skeletal Anatomy

    Increases in thoracic kyphosis and decreases in lumbar lordosis both increase the risk for POP. The same is true for a wider transverse pelvic inlet.


    It would seem that POP is more common in women from European descent than African women but older publications show bigger differences than more recent publications. Access to health care facilities might play a role but quantitative and qualitative histochemical differences in collagen and muscle tissue are awaited.

    This page titled 14.1: Effect of Prolapse is shared under a CC BY-NC-SA 2.5 license and was authored, remixed, and/or curated by Stephen Jeffery and Peter de Jong via source content that was edited to the style and standards of the LibreTexts platform; a detailed edit history is available upon request.