Vaginal Lawsuit Statement
Vaginal Lawsuit : Incontinent nulliparous women have been shown to have a quantitative and qualitative reduction in the collagen content of their tissues12where no evidence of neuromuscular damage exists. In the Nuns Study, 50% postmenopausal) nuns complained of UI; 30% of these complained of stress incontinence, 24% had urge incontinence and 35% had mixed symptoms. Therefore, in the absence of obstetric trauma, UI is more commonly seen to be of a stress rather than an urge type It is possible that neuromuscular damage and connective tissue deficiency are co-contributors in the aetiology of UI. Among primigravid women, those with excessive bladder-neck mobility have the highest risk of postpartum urinary incontinence.14 It seems likeLy that connective tissue damage is a ‘prerequisite’, and that neuromuscular damage contributes to the aetiology of USI.
Thirty-seven percent of women notice a deterioration in symptoms prior to menstruation.15 Furthermore, progestogens have been associated with an increase in irritative bladder symptoms1617 and urinary incontinence in those women taking combined hormone replacement therapy.18 The incidence of DO in the luteal phase of the menstrual cycle may be associated with raised plasma progesterone following ovulation – progesterone has been shown to antagonize the inhibitory effect of oestradiol on rat detrusor contractions.19 This may help to explain the increased prevalence of DO found in pregnancy.
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Intervention may be preventive. Elective caesarean section may prevent neuromuscular damage9 but may not prevent postnatal UI.4 Rather, antenatal pelvic-floor-muscle training is effective in reducing the incidence of postpartum UI.8Postpartum pelvic-floor-muscle training is effective in reducing the incidence of UI at one year. Follow-up of a cohort of women who delivered in 1994 showed that 31.8% of those dry prepregnancy are now incontinent.21 Women with increased bladder-neck mobility have an increased incidence of stress incontinence at 14 weeks postpartum, even if there is no preexisting symptomatology.14 However, onset of UI prior to the initial pregnancy is the best predictor of incontinence 5-7 years later.21 Caesarean section remains protective, but less so than at three months postpartum, with a relatively greater effect with increasing parity. The effect is particularly pronounced if the caesarean section is undertaken prelabour.
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‘Routine’ episiotomy was introduced in the UK in the 18th Century and has been advocated to prevent severe perineal tears and preserve sexual function. Review of five randomized controlled trials of the use of routine and selective episiotomy reveals that sexual function is poorer in the routine group, with no difference in the prevalence of UI and no difference in pelvic-floor-muscle strength.24 Ventouse delivery is less traumatic than forceps, but its use has not been shown to be associated with a reduced incidence of UI or neuromuscular damage.
Symptoms of urogenital atrophy are a manifestation of oestrogen withdrawal following the menopause, and may appear many years after the last menstrual period.1 Oestrogen deficiency following the menopause is known to cause atrophic changes within the urogenital tract2and is associated with urinary symptoms. The role of oestrogen replacement in the treatment of these symptoms of urogenital atrophy has still not been clearly defined despite several randomized trials and widespread clinical use. This chapter presents an overview of the pathogenesis and management of urogenital symptoms and the role of oestrogen replacement therapy.
In addition to oestrogen receptors, both androgen and progesterone receptors are expressed in the lower urinary tract, although their role is Less clear. Progesterone receptors are expressed inconsistently, having been reported in the bladder, trigone and vagina. Their presence may be dependent on oestrogen status. In addition, whilst androgen receptors are present in both the bladder and urethra, their role has not yet been defined.
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Vaginal Lawsuit