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Practice review

The menopause: effects on the pelvic floor, symptoms and treatment options

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Postmenopausal women are at risk of urogynaecological dysfunction. With better understanding of the pelvic floor, much can be done to improve care

 

Author

Judith Lee, MCSP, is clinical lead women’s health physiotherapist, Nottingham University Hospitals Trust.

Abstract

Lee J (2009) The menopause: effects on the pelvic floor, symptoms and treatment options. Nursing Times; 105: 48, early online publication.

This article discusses the effects of age and the menopause on the pelvic floor and subsequent risks of urogynaecological dysfunction, symptoms of this dysfunction and treatment options.

Keywords: Menopause, Pelvic floor, Continence

  • This article has been double-blind peer reviewed

 

Introduction

The physiological effects of the decline in circulating oestrogen, combined with the ageing process, put postmenopausal women at risk of urogynaecological dysfunction.  Incontinence, prolapse and sexual dysfunction are common problems, and their symptoms can greatly affect quality of life.

The average age at which women have the menopause is 51 years, and for most it occurs between 45 and 55, so women may expect some 30 years of postmenopausal life.

Healthcare professionals have a duty of care to develop the knowledge and skills to provide or direct women towards the best possible care. To do this, they need an understanding of the anatomy of the pelvic floor, its function and consequences of dysfunction.

Anatomy of pelvic floor

The pelvic floor is a fascial and muscular sheet forming the inferior boundary of the abdominopelvic cavity.

The main muscular components are puborectalis, pubococcygeus, iliococcygeus and ischiococcygeus, collectively termed the levator ani. It is a voluntary muscle supplied by the pudendal nerve which emerges from the 2nd, 3rd and 4th sacral foramina. It is a horizontal sheet with an anterior midline cleft through which the urethra, vagina and rectum pass.

It is attached to the inner surface of one side of the lesser pelvis, and  unites in midline with the opposite side, forming the greater part of the floor of the pelvic cavity.

The fascia within and covering the levator ani is the pelvic fascia. The endopelvic fascia is the connective tissue that supports the urethra, bladder, vagina and rectum. This fascia contains dense bands of connective tissue, termed ligaments, which sling the pelvic viscera to the pelvic side walls.

A thick fascial band on either side of the pelvis spanning from the ischial spine to the pubis, the arcus tendineus fascia pelvis (ATFP), provides attachment to both the endopelvic fascia and iliococcygeus.

The fascia and ligaments are made up of collagen fibres interlaced with elastin, smooth muscle cells, fibroblasts and vascular structures.

Functions of the pelvic floor

Ashton-Miller and Delancey (2007) described the functional anatomy of the pelvic floor as a supportive hammock under the urethra and bladder neck, providing a firm backstop against which the urethra is compressed during increases in abdominal pressure to maintain urethral closure and continence.

The fascia and ligaments act like a “cat’s cradle” of support to the pelvic organs and limit their downward movement during rises in intra abdominal pressure, but alone are not able to provide continual support.

Coordinated action of the levator ani muscle, in the presence of intact fascia and neural control, maintains pelvic organ support and, with urethral and anal sphincteric control, urinary and faecal continence.

This normal function relies on these structures being intact. Damage or weakness to any part can produce symptoms.

 

Physiological changes

Epidemiological studies have shown that older women are at increased risk of pelvic floor dysfunction, stress urinary incontinence, prolapse and faecal incontinence. The most significant aetiological factors for the development of prolapse are advancing age and parity (MacLennan et al, 2000).

Evidence of damage to muscles

Generally, muscle mass is lost with ageing. On average skeletal muscle strength is at its peak at 20-30 years and deteriorates by 5% per decade. The pelvic floor muscle is not immune to this ageing process. In a study of 25 dead people aged 15-80, Perucchini et al (2002) noted a 3% reduction in urethral striated muscle thickness per year in older people, showing that the rate of deterioration may indeed accelerate.

Evidence of damage to connective tissue

Several studies have investigated tissue metabolism and properties in postmenopausal women with symptoms of prolapse and/or, stress urinary incontinence. Links have been identified between these symptoms and alterations in connective tissue and oestrogen levels.

Goepel et al (2003) took biopsies of periurethral tissue from 29 women undergoing anterior repair or sacrospinous fixation surgery for prolapse. The results showed altered metabolism in all the postmenopausal women: less of types 1, 3 and 4 collagen and absent or fragmented vitronectin.

Vitronectin is a glycoprotein which promotes cell adhesion and inhibits cell membrane damage. Similarly, Moalli et al (2003) took biopsies of the ATFP from 27 postmenopausal women during repair surgery for anterior vaginal wall prolapse, which showed a decrease in type 1 collagen. It is considered that type 1 is the main determinant of tensile strength within connective tissue, that is, the amount of load that can be exerted on it before it permanently deforms or fails.

Resilience is another property of connective tissue; this is its ability to recover to its original length after stress. In Reay Jones et al’s (2003) study, the uterosacral ligament was measured for resilience in women undergoing hysterectomy and shown to be reduced in postmenopausal women. Also the ligament itself was thinner.

Both these studies demonstrated a weakness in the passive tissues, with the consequences of pelvic organ support being more reliant on the pelvic floor muscles.

Alperin and Moalli (2006) summarised the current understanding of alterations in tissues in women with prolapse and concluded thatmetabolism of collagen and elastin is altered in prolapsed tissue. However, they said further studies are needed to fully understand physiological changes.  

Evidence of damage during childbirth

A number of studies have suggested that pudendal nerve damage and/or anal sphincter injury may occur during childbirth (Sultan et al, 1994; 1993). 

Allen et al (1990) showed pudendal nerve denervation in 80% of women following their first delivery and Snooks et al (1990) that this nerve damage may persist. The risk is that the denervated muscles undergo atrophy and pelvic organ support would be more reliant on the endopelvic fascia, which over time may become stretched.

Nicholls et al (2004) also looked at the consequences of childbirth in later life. One hundred women with symptoms of prolapse and/or urinary incontinence were asked to complete a questionnaire about faecal incontinence. Symptoms of current faecal incontinence were significantly associated with anal sphincter injury sustained during childbirth.

It may be that young parous women are not troubled bysymptoms as they are able to compensate with strong muscles and intact connective tissue. However, with ageing there is muscle weakening and changes to the connective tissue which may lengthen, stiffen and/or fail at the time of menopause. It is not until after this point that neural or anal sphincter defects become clinically evident and symptoms of faecal urgency or incontinence develop.

The fascia itself may be damaged during childbirth, either stretched or detached from the pelvic side walls, as Dietz and Lanzarone (2005) demonstrated by transperineal ultrasound. It is not yet known how significant this is later in life as the tissues age. Looking to the future, it may be that ultrasound techniques postnatally may identify those women at risk of symptomatic dysfunction in later years.

The urethra

There is also evidence that the urethra itself may be hormonally sensitive; the urethral vascular mucosa forms folds which act as a watertight seal and aid continence. In Blakeman et al’s (2001) study, comparisons were made between cell proliferation rates in the lower urinary tract of postmenopausal women, some receiving HRT and others not. The findings suggested there is a mechanism by which oestrogen has an advantageous effect on vascular mucosa of the lower urinary tract. This provides an explanation for the success of oestrogen in treating some conditions of lower urinary tract dysfunction in postmenopausal women. However, it is not within the remit of this article to discuss the use of HRT or topical oestrogens in the treatment or prevention of postmenopausal symptoms.  

Symptoms

Stress urinary incontinence (SUI) is the most common type of incontinence and involves involuntary leakage on effort or exertion, or on sneezing or coughing. Incidence is difficult to measure as many women never seek help, but it is speculated that 50% of 48 year olds experience SUI (Kuh et al, 1999).

Women often report urinary incontinence that is embarrassing and that they avoid activities that cause it to happen and feel the need to wear protection for everyday activities

Pelvic organ prolapse is the term that includes prolapse of the anterior vaginal wall (urethrocele or cystocele), the posterior vaginal wall (rectocele) or uterine or vaginal vault descent.

It is estimated that 50% of parous women have prolapse (Thakar and Stanton, 2002). Not all prolapses are problematic, but 10-20% of affected women seek help because of symptoms.

Symptoms of prolapse are often described as heaviness or a dragging sensation in the vagina, an uncomfortable bulge or a lump protruding from the vagina and possibly low backache. Bladder and bowel problems often co-exist. There may be hesitancy of initiating the flow of urine, slow urinary flow rate and incomplete emptying; there may also be urinary urgency and frequency when a cystocele is present. Constipation may be a symptom of rectocele, and some women report the feeling of incomplete emptying or that they need to manually assist defecation. Dyspareunia is the term for pain during sexual intercourse and may be a symptom of uterine prolapse, which can be compounded by vaginal dryness in postmenopausal women.

Faecal urgency or incontinence has a devastating effect on quality of life and is probably the most difficult symptom for women to disclose to healthcare professionals.

Treatment

For women to gain access to treatment for these symptoms, practitioners must give them time and privacy to ask questions about problems of bladder, bowel and sexual function and perineal comfort.

Stress urinary incontinence

Conservative treatment for SUI centres on a specifically designed pelvic floor muscle exercise programme, which Morkved and Bo (2000) found effective, and at least 12 weeks of muscle training should be offered as a first line treatment (NICE, 2006).

In Balmforth et al’s (2009) study, 97 women with symptoms of SUI were instructed with a 14 week programme of pelvic floor muscle rehabilitation, which included specific pelvic floor exercises and behavioural modification. Actual changes in functional anatomy were quantified using transperineal ultrasonography to measure the position of the bladder neck at rest, with maximum voluntary contraction and valsalva manoeuvre, a bearing down movement. Following treatment there was significant elevation of the bladder neck position in all three positions and less downward displacement with valsalva manoeuvre, suggesting increased support from the pelvic floor. These changes were associated with significant reductions in urinary loss.

Peng et al (2007) showed by ultrasound that the pelvic floor muscle functions differently in women with SUI compared with continent women. In continent women the pelvic floor muscle has an anticipatory activity that functions like a brake to limit downward displacement, velocity and acceleration of the urogenital structures during rises in intra abdominal pressure. In women with SUI this brake is applied late.

It is also worth considering lumbopelvic stability as an important component of the continence system. Grewer and McLean (2008) advised correcting postural and movement dysfunction and treating coexisting back pain or breathing disorders as part of the management of stress incontinence.

These studies direct us in the technique of teaching pelvic floor muscle exercises, where timing and direction of contraction is as important as strength. The optimum direction is a cranial (upwards) ventral (forwards) movement to give support to the bladder neck. When this is established, women are given an individualised exercise programme of pelvic floor contractions, of maximal strength, endurance and repetitions with breathing control in positions of comfort, but to challenge against gravity if possible.

The ideal way to assess and teach exercise technique is by digital vaginal examination by practitioners.

This should be followed by practising the short contractions of “the knack” (Miller et al, 1996). This is learning the skill of performing a short, quick, pelvic muscle contraction simultaneously with an event known to trigger leakage, in order to stop that leakage, mimicking the anticipatory response in normal muscle.

Consideration should be given to the use of electromyogram (EMG) biofeedback as an assessment and motivational tool to aid the pelvic floor exercise programme. A course of electrical muscle stimulation (EMS or weighted cones are treatment options for weak muscles.

If conservative measures fail, pharmacological therapy or surgery should be considered for SUI.

Faecal incontinence

The conservative approach to treating faecal incontinence is similar, in that following rectal examination a specifically designed exercise programme is taught, aided if necessary by anal EMG or electrical muscle stimulation (EMS) with advice on healthy bowels (NICE, 2007).

A Cochrane review examined the conservative management of pelvic organ prolapse and concluded the evidence was not sufficient to guide practice (Hagen et al, 2006). However, in Hagen et al’s (2004) survey of UK physiotherapy practice, 92% of women’s health physiotherapists were generally treating pelvic organ prolapse with a combination of pelvic floor rehabilitation and tailored advice to reduce the rise in intra abdominal pressure and strain on the pelvic organs and pelvic floor. Advice may include avoiding prolonged standing, high impact exercise and constipation to reduce symptoms, and bracing pelvic floor muscles before lifting, sneezing and so on, which should protect the pelvic floor.

Following a feasibility study by Hagen et al (2005), The Pelvic Organ Prolapse Physiotherapy (POPPY) trial is currently underway. It is a randomised controlled trial of conservative treatments for women with prolapse, with the intention of producing guidance.

In the absence of evidence based guidance, practitioners should continue to give advice to educate women with prolapse and to instruct them in pelvic floor exercises to empower them in managing their symptoms.

For prolapse which is symptomatic and for which conservative treatment is not effective, consideration should be given to mechanical devices, support pessaries or repair surgery.

Conclusion

The pelvic floor is certainly influenced by ageing and the menopause, but more research is needed to fully understand the pathophysiology, treatment selection and prevention.

However, with current knowledge and understanding there is much that can be done to provide good care for women with pelvic floor dysfunction and impact positively on their quality of life.

 

 

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