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OG31.1 | Uterine Prolapse — SDL Guide

Learning Objectives

• Describe the aetiology, classification, and pathophysiology of uterine prolapse
• Classify prolapse using the POP-Q staging system and the traditional grading system
• Outline the clinical features, diagnosis, and investigations of uterine prolapse
• Describe the principles of conservative (pessary) and surgical management
• Enumerate preventive strategies for uterine prolapse

INSTRUCTIONS

Uterine prolapse is a form of pelvic organ prolapse (POP) in which the uterus descends into or beyond the vaginal canal due to failure of pelvic floor support. It predominantly affects multiparous women and is a major cause of morbidity and surgical intervention in India. This module covers the internationally standardised POP-Q classification, the full range of management from pessaries to definitive surgery, and the critically important preventive measures.

References

• DC Dutta's Textbook of Gynaecology, 7th edition, Ch 19 (textbook)
• Shaw's Textbook of Gynaecology, 17th edition, Ch 14 (textbook)
• ICS POP-Q Standardisation Committee — POP-Q System (Bump et al., 1996) (guideline)

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Version 2.0 | NMC CBUC 2024

Clinical Presentation of Uterine Prolapse

Uterine prolapse presents with a constellation of symptoms that reflect the descent of the uterus and the associated defects of the anterior and posterior vaginal walls. The hallmark complaint is a sensation of something coming down or a bulge at the vaginal introitus, which worsens on prolonged standing, straining, coughing, or lifting heavy loads, and is temporarily relieved by lying supine. Women often report a dragging or heaviness in the lower abdomen and perineum, particularly towards the end of the day.

Associated bladder symptoms arise from the cystocele (anterior wall descent): stress urinary incontinence (leakage on coughing/sneezing), frequency, urgency, incomplete bladder emptying, difficulty initiating micturition, and — in advanced prolapse — urinary retention requiring the patient to manually reduce the prolapse to void. Bowel symptoms from rectocele (posterior wall descent) include constipation, incomplete evacuation, and the need to digitally reduce the posterior wall to complete defaecation. Sexual dysfunction — dyspareunia and reduced sensation — is common. In the most advanced cases, the prolapsed uterus may ulcerate at the cervix due to chronic friction, causing discharge, bleeding, or secondary infection. Symptoms are invariably worse in multiparous, postmenopausal, and physically active women.

Types of Pelvic Organ Prolapse — Sagittal Anatomical Views with DeLancey Support Levels

Anatomy of Pelvic Floor Support and Aetiology

The uterus is maintained in its normal anteverted, anteflexed position by an integrated system of ligaments, fascial condensations, and muscles. DeLancey's three levels of support provide a useful anatomical framework: Level I support (apical) is provided by the cardinal (Mackenrodt's) ligaments and uterosacral ligaments, which suspend the cervix and upper vagina from the lateral pelvic sidewall and sacrum — damage here leads to uterine descent and vault prolapse. Level II support (lateral) consists of the paravaginal attachments of the mid-vaginal walls to the arcus tendineus fasciae pelvis — damage leads to cystocele and rectocele. Level III support (distal) is provided by the perineal body, perineal membrane, and external anal sphincter — damage leads to perineal descent and gaping introitus.

The levator ani muscle (comprising pubococcygeus, iliococcygeus, and puborectalis) forms the muscular floor of the pelvis and maintains the vaginal axis; its denervation or tearing during childbirth is a key contributor to prolapse. The pubocervical fascia (anterior) and rectovaginal fascia (Denonvilliers' fascia, posterior) are the connective tissue layers whose integrity prevents cystocele and rectocele respectively.

Pelvic Floor Support Structures and DeLancey's Three Levels of Vaginal Support

Aetiology and risk factors: The most important risk factor is vaginal childbirth — particularly prolonged second stage, instrumental delivery (forceps), delivery of a large baby, and unrepaired perineal tears. These injure the levator ani, stretch the ligamentous supports, and damage the pudendal nerve. Multiparity (especially ≥3 deliveries) is the single strongest risk factor in India. Menopause and oestrogen deficiency accelerate atrophy of collagen in the pelvic floor. Chronic raised intra-abdominal pressure from chronic cough, constipation, obesity, or heavy manual labour overloads the already compromised supports. Congenital connective tissue disorders (e.g. Marfan, Ehlers-Danlos) predispose even nulliparous women. Racial factors — White and Asian women have higher prolapse rates than Black women, attributed to differences in levator ani muscle anatomy.

Pathophysiology of Prolapse

The pathophysiology of uterine prolapse is best understood as a progressive failure of the integrated pelvic support system rather than a single-structure injury. Under normal conditions, the levator ani maintains the genital hiatus closed; the vagina lies horizontally over the levator plate, and the uterus is kept anterosuperior to the rectum by the cardinal-uterosacral complex. When this system fails at one or more DeLancey levels, the downward force of intra-abdominal pressure is no longer counteracted.

The primary pathological events are: (1) stretching and denervation of the levator ani during childbirth — the pubovisceral muscle is the most commonly injured component, widening the genital hiatus and converting the horizontal vaginal axis to a more vertical orientation; (2) tearing or attenuation of the fascial condensations — the cardinal and uterosacral ligaments lose collagen strength, particularly under the influence of oestrogen deficiency; (3) progressive descent — once the levator plate can no longer close the hiatus, the vaginal walls and uterus herniate downward with each Valsalva manoeuvre, analogous to a hernia through a defect. The process is typically slow and progressive over years, with menopause markedly accelerating the collagen degradation. The cervix descends first (descent), then appears at the introitus (procidentia first degree), and in the most advanced cases the entire uterus everts outside the vagina (procidentia or complete prolapse) — at which point the bladder base, rectum, and sometimes loops of small bowel (enterocele) are drawn down with it.

Pathophysiology of Uterine Prolapse: From Childbirth Injury to Procidentia