Symptomatology of Urogenital Atrophy

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Typical symptoms of vaginal atrophy include vaginal dryness, vaginal irritation, as well as loss of vaginal caliber and depth in more advanced degrees of atrophy. The initial symptoms of vaginal atrophy can be promptly reversed with local estrogen therapy. However, the more long-term effects of urogenital atrophy such as loss of vaginal caliber and depth are less likely to be readily reversible. This has recently become a clinically important issue, because male erectile dysfunction can be treated pharmacologically, whereas the female partners' advanced urogenital atrophy has not been taken into account. Any attempt at sexual intercourse after a long hiatus of inactivity in a post-menopausal woman can result in sexual dysfunction and even vaginal trauma including lacerations upon attempted penetration. It is thus critical that both partners be considered when initiating erectile dysfunction therapy in the male.

Vaginal atrophy is also associated with vulvar atrophic changes. These may include lichen sclerosis as well as hypertrophic dystrophies. As a consequence, external atrophic changes may also be seen, including reduction in pubic hair volume, labial fusion, loss of labial volume, irritative vulvar symptoms, and eventual reduction in introital diameter (Figure 11-1.1).

Symptoms of urethral atrophy are typically attributed to the loss of urethral tone associated with urethral devascu-

Figure 11-1.1. Advanced urogenital atrophy with marked mucosal paleness, vulvar atrophy, and labial fusion.

larization. It is estimated that the urethral submucosal vascular plexus is responsible for up to 30% of urethral closure pressure. As a consequence, devascularization will lead to decreased urethral tone. This frequently presents with urinary urgency and frequency, presumably because of wetting of the proximal urethra during bladder filling. Nocturia is an exceedingly common symptom of urethral atrophy, and one that is promptly reversible with local estrogen in a more efficient manner than with an anti-cholinergic medication. Although hypoestrogenism leads to devascularization of the urethral submucosa, stress incontinence typically does not develop in an isolated manner secondary to menopausal urethral atrophy. Local estrogen is thus an important cofactor in the treatment of overactive bladder and stress incontinence symptoms. When used in combination with alpha-agonist medications, stress urinary incontinence symptoms may be reduced (Chapter 6-2).

We require a greater understanding of the natural history and symptomatology of urogenital atrophy. Although the occurrence of urogenital atrophy is universal after menopause, most women are asymptomatic. In a recent trial,we attempted to correlate the symptoms of urogenital atrophy with objective assessment of urogenital atrophy severity.1 We found no significant correlation between atrophy symptomatology and objective assessment tools such as maturation index, vaginal pH, or visual examination. It is thus unclear why some women become highly symptomatic of their urogenital atrophy, whereas others remain completely asymptomatic.

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