Our objective was to review the current understanding of the pathophysiology of urinary incontinence (UI) in postmenopausal women and ascertain the efficacy of estrogen therapy as the recommended treatment.

The literature included in our manuscript originates from two sources. The first is a series of selected studies on the pathophysiology of urinary incontinence associated with genitourinary syndrome of menopause (GSM). These studies were not selected based on a systematic search but cited to demonstrate underlying physiological mechanisms that occur during menopause.
The second was a review of the literature on the efficacy of estrogen therapy in urinary incontinence. A search of the PubMed and Scopus databases until January 2024 was performed by crossing keywords “urinary incontinence, genitourinary syndrome of menopause, physiology, and estrogen”. Two authors reviewed each article independently and double screened for eligibility. The third author was involved in reviewing any discrepancies.

The literature search revealed the physiological changes that occur in the lower urinary tract with age. The pelvic floor strength decreases with an increase in levator hiatus in menopausal women. There is also an associated decrease in urethral closing pressure contributed by the loss of the submucosal plexus.

Eligible studies included control trials with menopausal women with urinary incontinence being treated with different aspects of estrogen administration. The trials used varying combinations of estrogen types, routes, dosage and duration of treatment. The effect of systemic estrogen administration on urinary incontinence is conflicting based on the type of urinary incontinence described. However vaginal estrogen use demonstrates clear improvement of urinary symptoms, in particular overactive bladder symptoms.

Pelvic floor muscles support the urethral in stabilising it in its correct anatomical position. The levator ani muscles and pubocervical fascia provide a base structure in supporting the urethra during episodes of raised abdominal pressure. Therefore weakness in these structures with age leads to the loss of supporting mechanism to maintain urethral continence function. 

The urethral submucosal layer contains a rich vascular plexus that partly supplies adequate occlusive pressure. This pressure is also augmented by urethral smooth muscle and striated sphincter muscles which contributes to its ability to coapt and prevent urinary leakage. The submucosal venous plexus has been described histologically as hormone-sensitive and has been demonstrated to reduce in volume and elasticity with the onset of menopause. 

As such the current thinking is that estrogen use would be beneficial in addressing these physiological changes, but our literature review has shown conflicting evidence on the efficacy of estrogen use. Due to the limited number of robust trials comparing both oral and vaginal estrogen administration and usage length in menopausal women, it is difficult to determine a direct association on the benefit of estrogen in managing urinary incontinence.

There is sufficient evidence to confirm a strong association between increasing lower urinary tract dysfunction in postmenopausal women, particularly urinary urgency and urge incontinence. However, there is conflicting data to show that estrogen is effective in managing UI, especially with systemic estrogen where there are associations with worsening urinary incontinence in some studies. But there is clear evidence demonstrating that vaginal estrogen use improves urinary urgency and urge incontinence.