Aetiology
The aetiology of uterine prolapse is not totally understood. Vaginal childbirth is one of the most frequent risk factors associated with prolapse. Investigators suggest that this is because of damage to the pudendal nerve, connective tissue, and muscle structure during delivery.[7][8] Advancing age, obesity, previous surgery for prolapse, genetic factors, white ancestry, connective tissue disorders, and increased intra-abdominal pressure (e.g., chronic obstructive airway disease, chronic constipation with excessive straining, heavy lifting, and hard physical activity) are also known to be risk factors.
Genetic or familial predispositions are not yet well understood. A higher risk of prolapse has been noted in women with a mother or sister reporting prolapse.[9] In one study, the T variant of the laminin subunit gamma 1 (LAMC1) gene was 5 times more common among probands with pelvic organ prolapse (POP) than in the general population.[10] This variant affects the binding site for nuclear factor, interleukin 3-regulated (NFIL3), a transcription factor that was verified to be co-expressed in vaginal tissue. Hence, polymorphism in this area may increase the susceptibility to early onset POP.[10]
Although menopause is often cited as a risk factor for POP, researchers have failed to find an association with oestrogen status.[2][5][6][7][11] Nulliparous women can also develop the condition: after hysterectomy, for example.[12]
Pathophysiology
Uterine prolapse is predominantly a disorder of parous women, in whom there is damage to the musculature, ligaments, and nerves.
Pelvic floor muscles are contracted at rest and act to close the genital hiatus and provide a stable platform for the pelvic viscera. Levator ani tone is essential for maintaining the pelvic organs in place. Decline of normal levator ani tone by direct muscle trauma or a denervation injury may occur during vaginal delivery. This results in an open urogenital hiatus and changes to the horizontal orientation of the levator plate, which causes a prolapse.[8] In a case control study, magnetic resonance imaging demonstrated that women with prolapse were more likely to have anatomical defects in the levator ani. Consequently, in these women the levator ani generated less vaginal closure force during maximal contraction.[13][14]
The endopelvic fascia is the connective tissue network that envelops all organs of the pelvis and connects them loosely to the supportive musculature and bones of the pelvis. Pelvic floor dysfunction can cause prolapse, which specifically can involve the anterior, posterior, and apical vagina and the uterus. Disruption or stretching of these connective tissue attachments happens during vaginal delivery or hysterectomy (by any route), as a consequence of chronic straining, or as part of normal ageing.[13] Patients with prolapse may have altered collagen metabolism, and this can lead to prolapse.[13][15][16] Women with joint hypermobility and collagen-associated disorders (e.g., Ehlers-Danlos syndrome or Marfan syndrome) have a higher prevalence of pelvic organ prolapse.[15][16][17][18]
As the anterior vagina loses support, the bladder and urethral support is lost, potentially affecting the continence mechanism. Urinary incontinence may result from changes in the vaginal support.[19] Urethral hypermobility can be easily diagnosed by clinical observation when asking the patient to strain. In advanced uterovaginal prolapse stages, the urethra is mechanically kinked and may obstruct the urine flow.
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