Frontiers in Gynecological Endocrinology: Volume 1: From Symptoms to Therapies

21. Menopause, Aging, Pelvic Organ Prolapse, and Dysfunction

Silvia Pisaneschi1, Giulia Palla1, Stefania Spina1, Guja Bernacchi1, Elena Cecchi1, Silvia Di Bello1, Magdalena Montt Guevara1, Adrian Campelo1 and Tommaso Simoncini 

(1)

Division of Obstetrics and Gynecology, Department of Clinical and Experimental Medicine, University of Pisa, Via Roma, 67, Pisa, 56100, Italy

Tommaso Simoncini

Email: tommaso.simoncini@med.unipi.it

21.1 Introduction

The pelvic floor is a complex of units involved in many undertakings that go further than the support of pelvic organs. Pelvic floor dysfunction affects on several functions such as micturition, defecation, and sexual activity. Urinary incontinence (UI), female pelvic organ prolapse (POP), sexual dysfunction, chronic obstructive defecation syndrome (OFD), and constipation are just a few of the many facets of pelvic floor dysfunction, and their incidence increases dramatically with age and menopause.

21.1.1 POP: Definition, Signs, and Symptoms

According to the definition of a joint report by the two leading urogynecological societies, POP [1] is defined as “any descent of one or more of the anterior vaginal wall, posterior vaginal wall, the uterus (cervix) or the apex of the vagina (vaginal vault or cuff scar after hysterectomy)”. Typical manifestations of POP are vaginal bulging, vaginal bleeding, pelvic pressure, discharge and infection, and low backache. Prolapse of organs toward the vagina (urethra, bladder, small intestine, colon, or rectum) often makes it necessary to digitally replace the prolapse or to apply manual pressure, e.g., to the perineum (splinting), the vagina, or rectally (digitation) to assist micturition or defecation.

Clinical POP can be identified in 31.8 % of postmenopausal women. Yearly incidences of cystocele, rectocele, and uterine prolapse have been estimated as 9.3, 5.7, and 1.5 cases per 100 women, respectively, 3 (Table 21.1).

Table 21.1

Prevalence and incidence of POP on the basis of different definitions of POP

Study

Definition of POP

Prevalence

Incidence

Swift [2]

Pelvic organ prolapse quantification

6.4 % stage 0

43.3 % stage 1

47.7 % stage 2

2.6 % stage 3

 

Hendrix [3]

Women’s Health Initiative grading system (grades 1, 2, or 3)

Any prolapse: 41.1 %

Cystocele: 34.3 %

Uterine: 14.2 %

Rectocele: 18.6 %

 

Handa [4]

Women’s Health Initiative grading system (grades 1, 2, or 3)

Cystocele: 24.6 %

Uterine: 3.8 %

Rectocele: 12.9 %

(Grades 1, 2, or 3)

Cystocele: 9.3/100

Women-years

Uterine: 1.5/100

Women-years

Rectocele: 5.7/100

Women-years

Nygaard [5]

Pelvic organ prolapse quantification

2.3 % stage 0

33 % stage 1

63 % stage 2

1.9 % stage 3

25.6 % based on leading edgeR0

 

Bradley [6]

Pelvic organ prolapse quantification

23.5–49.4 %

 

Rortveit [7]

Patient symptoms past 12 months (not confirmed by examination)

5.7 %

 

Nygaard [8]

Affirmative to “Do you experience bulging or something falling out you can see or feel in the vaginal area?”

2.9 %

 

21.1.2 Urinary Incontinence (UI): Definition, Signs, and Symptoms

A realistic description of UI recently provided by the International Continence Society [4] is: “the burden of any uncontrollable leakage of urine”. This annotation, although correct, needs further examination: as on the type, the frequency, the severity, and the precipitating factors. Social impact and also hygiene plays an important part on quality of life. Once we have established that the individual seeks help a clinical approach is needed to assess the severity of the leakage.

The relentless increase of UI cases goes along with aging [910] (Fig. 21.1). 31.7 % of US Women over the age of 80 have clinically significant UI, compared with women aged 40–59 years, showing a prevalence of 17.2 % [8].

A978-3-319-03494-2_21_Fig1_HTML.gif

Fig. 21.1

Prevalence of urinary incontinence by decade of life (Adapted from Melville JL, Katon W)

21.1.3 Chronic Constipation: Definition, Signs, and Symptoms

Chronic constipation is a common disorder that heavily affects quality of life [11]. Frequent causes of chronic constipation are slow transit constipation and dyssynergic defecation. Irritable bowel syndrome is also associated with pelvic floor dysfunction, and particularly with hypertonic levator ani muscle and pelvic pain syndrome. Secondary causes are: low physical activity, inappropriate diet, constipating drugs (Table 21.2) or metabolic, neurological, endocrine, psychiatric or connective diseases, which are all frequent problems in older individuals [12]. Anatomical disruption of the entire pelvic floor or limited to the bowel (e.g., intussusception, rectocele, internal or external rectal prolapse) and reduced rectal sensation are also common in aging individuals [13]. This can include the consequences or complications of surgical procedures on the pelvis and the perineum [14].

Table 21.2

Drug associated with constipation in elder people

Common

 Antacids

 Anticholinergics

 Antidepressants

 Antihistamines with antimuscarinic properties

 Antispasmodies

 Calcium channel blockers

 Calcium supplement

 Diuretics

 Neuroleptics with antimuscarinic properties

 Opiate analgesics

 Oral iron

Less common

 Anticonvulsants

 Antiparkinsonian drugs

 Nonsteroidal anti-inflammatory drugs

The most referred symptoms are infrequent defecation, straining at defecation, hard or lumpy stools, sensation of incomplete defecation or anorectal obstruction, and need for manual maneuvers to facilitate bowel movements [15]. These symptoms are the basis of the most common diagnostic criteria to define constipation, the so-called Rome III criteria for functional constipation (Table 21.3). The prevalence of chronic constipation is approximately 16 % in adults overall and 33 % in adults older than 60 years and it is more common in women (F:M = 1,5:1) and increases with age. However, about 50 % of community-dwelling elderly report constipation with an estimated prevalence up to 74 % in nursing homes [1617].

Table 21.3

Rome criteria for functional constipation

Diagnostic criteriaa

1. Must include two or more of the following:

 (a) Straining during at least 25 % of defecations

 (b) Lumpy or hard stools in at least 25 % of defecations

 (c) Sensation of incomplete evacuation for at least 25 % of defecations

 (d) Sensation of anorectal obstruction/blockage for at least 25 % of defecations

 (e) Manual maneuvers to facilitate at least 25 % of defecations (e.g., digital evacuation, support of the pelvic floor)

 (f) Fewer than three defecations per week

2. Loose stools are rarely present without the use of laxatives

3. Insufficient criteria for irritable bowel syndrome

aCriteria fulfilled for the last 3 months with symptom onset at least 6 months prior to diagnosis

21.1.4 Sexual and Pelvic Floor Dysfunction

Most of the symptoms associated to these conditions have devastating effects on sexual function, due to dyspareunia or chronic pelvic pain, to the modified self-image associated to the change in the appearance of the genitalia, or to the loss of urine or feces associated with attempted coital activity [18].

21.1.5 Function and Dysfunction of the Pelvic Floor

Pelvic floor looseness depends on injury of the muscles and on the progression of pelvic floor weakening. Connective tissue degradation [19], pelvic denervation [20], devascularization, and anatomic modifications [21] all create a decline in mechanical strength and dyssynergic pelvic floor function, predisposing to prolapse [22].

Several muscles, essential for the support and function of female pelvic structures, constitute the pelvic floor complex. The levator ani is the floor of the pelvis; it is composed of three different parts: the pubococcygeus, the puborectalis, and iliococcygeus muscles. The main part of the levator ani is the pubococcygeus, which extends from the pubis toward the coccyx. Behind the anorectal junction there are the two parts (right and left) of the puborectalis, which coordinate a muscular sling. The smallest part the levator ani is the iliococcygeus.

In women with normal pelvic statics, smooth muscle fibers in the anterior vaginal wall are organized in tight bundles orientated in circular and longitudinal order, whereas in women with POP the vaginal muscularis presents a decline of overall smooth muscle amount, fewer, smaller, and disorganized bundles [23].

Levator ani injury has an established role in the pathophysiology of prolapse but does not explain all pelvic organ prolapses. 30 % of women with prolapse show no sign of muscle injury on MRI: highlighting the fact that the process includes other factors as well [2425]. The failure in this chain of events of one of the structural elements of the pelvic floor complex, e.g., the levator ani, results in overloading all other mechanical components (connective tissue and smooth muscle) which will eventually fail as well. On the other side, connective tissue abnormalities and smooth muscle alterations may represent the leading event in the development of prolapse [26].

Pelvic connective tissues are structured into a fascial sheet which covers the pelvic floor muscles and forms ligaments that connect pelvic organs to the bony pelvis [27]. Female pelvis has architectural characteristics, which allows for delivery of fetuses with increasing head diameters and upright standing and walking. Parallel to this evolutionary modification, connections of fascial structures to the pelvic sidewalls have progressively grown, suggesting a central role in the stabilization of the pelvic viscera of connective tissue [28]. Qualitative and quantitative alterations in collagen content and structure and in genes related to collagen remodeling in women with genital prolapse and stress urinary incontinence have been identified, which may represent individual predisposing factors for these conditions [2930].

Vessels are important for the function of the pelvic floor, as well, particularly for urinary function [31]. Large veins are located near the urethra, forming a spongious body. Intravascular pressure in this venous web determines a mechanical pressure on the urethra, working as seal and contributing to urinary continence [32], since it contributes for at least one-third of urethral pressure [33]. Indeed, incontinent postmenopausal women have less vessels in the periurethral tissue and a reduced blood pressure in these vessels [34].

21.2 Menopause and Aging: Impact on Pop and UI

The lower urinary and female genital tracts are strictly related and both derive embryologically from the urogenital sinus. 50 % of postmenopausal women complain of urogenital symptoms [35]; these appear after the menopausal transition and worsen with time. Dyspareunia, dysuria, frequency, nocturia, incontinence, and recurrent infections [36] are all facilitated by estrogen withdrawal.

Estrogen receptors (ER) are present in the epithelial tissues of the urethra, bladder, trigone, vaginal mucosa, and in the support structures of the uterosacral ligaments, as well as in levator ani muscles and pubocervical fascia [37]. Estrogen is involved in the increase of cell maturation index of these epithelial structures. It has been demonstrated that alterations in the ratio of estrogen receptor α (ERα) to ERβ may be related to the development of stress urinary incontinence [38]. Synthesis and metabolism of collagen in the genital and urinary tract is under the control of estrogens [39], which also increase the number of muscle fibers in the detrusor muscle and in the urethral muscles [40].

A hypothesis is also that estrogens influence micturition through the neurologic control in the central nervous system, changing the density of sympathetic nerve fibers in the pelvis and the central and peripheral synthesis of neurotrophins, although this set of actions is not completely understood [41].

Progesterone receptors are also expressed in the lower urinary tract, even if with less density than estrogen receptors [42]. It has been noticed that progesterone has adverse effects on female urinary tract function [43], since it is linked to an increase in the adrenergic tone, provoking a decreased tone in the ureters, urethra, and bladder. This could be the reason why urinary symptoms worsen during the secretory phase of the menstrual cycle, and progesterone may be responsible for the increase in urgency during pregnancy, although the precise mechanism is not fully figured out.

Notwithstanding all of the above, the role of menopause on pelvic floor dysfunction is unclear. Neither menopausal status [44] nor the length of hormone deficiency [3] has been clearly associated to the risk or severity of POP.

In spite of the evidence indicating generally positive effects of estrogens on the urogenital tract, there is no evidence supporting the use of estrogen therapy for the prevention or treatment of POP or UI in climacteric women [45]. In particular, available evidence does not show a beneficial effect of the use of estrogen therapy, both local and systemic, on stress urinary incontinence. On the other hand, recent studies underline that local estrogen therapy is effective for the treatment of urge urinary incontinence, overactive bladder and it can reduce the recurrence of urinary tract infections [46]. In women with overactive bladder symptoms, neuromodulatory effects by estrogens could be beneficial, as estradiol reduces the amplitude and frequency of spontaneous detrusor muscle contractions [47].

21.3 Aging and Constipation

In women aged <50 years paradoxical contraction or lack of relaxation of the pelvic floor muscles seem to be the most frequent causes of obstructed defecation. On the opposite, during aging more complex changes in the structure and function of the gastrointestinal tract, usually in the colon and in the anorectal region may develop and determine impaired bowel habits and evacuation mechanisms. Constipation is a problem that very often is related to older people, but should not be considered as a “physiological” consequence of aging. Constipation in the elderly has rarely one single cause and it is frequently secondary to emerging diseases or drugs (Table 21.2).

Aging is associated with loss of neurons (cholinergic neurons and interstitial cells of Cajal) in both the myenteric and submucosal plexus. Some studies indicate that delayed colon transit time occurs with aging. However, more recent publications underline that in healthy elder individuals, in the absence of comorbidities, there are no significant changes in the gut transit time. In any case, it is noted that in small groups of elderly patients an increased absorption of water could lead to the production of harder stools and consequently to difficulty in evacuation.

The adequate perception of rectal, anal, and perianal region is of importance in order to have a normal defecation. However, elderly people may need to have larger volumes of bowel content to stimulate rectal sensation and promote a normal defecation [48].

Changes in the anatomy of the anal canal, external anal sphincter atrophy, and internal anal sphincter degeneration have been associated with aging as much as tissue atrophy resulting in reduced distensibility. All of these could explain why aging [49] predisposes to alterations of defecatory function.

Injury of pudendal nerves can also play a role in the onset of constipation (i.e., obstructed defecation) in the elderly, particularly in women. In this condition, an abnormal perineal descent is frequently observed, causing a prolapse of the anal canal or of the anterior rectal mucosa with a consequent alteration of rectal emptying [50]. A recent study [51] seems to confirm this concept. In a group of 334 women with obstructed defecation, after eliminating the confounding effect of vaginal delivery from the risk factors, the authors find that rectocele, intussusception, rectocele associated with intussusception, rectocele associated with mucosal prolapse, and grade III enterocele/sigmoidocele increase with age.

21.4 Conclusion

Pelvic floor in women is a highly complex and vulnerable structure. Injuries, pregnancy, functional modifications, and aging of the pelvic floor structures all contribute to pelvic organ prolapse and the related symptoms. These symptoms are extremely common in aging individuals, creating a substantial discomfort and impairing a comfortable quality of life. Since POP and incontinence often develop at the time of the menopausal transition, when women already face important problems that impact on their quality of life, it is important to identify and manage appropriately these problems. Even if consensus is not available, some of the hormonal interventions that can be considered in menopausal women can also positively affect some of the symptoms that are generated by POP, such as pelvic pain, sexual dysfunction, or urinary incontinence. Pathophysiology of pelvic organ prolapse, urinary incontinence, and bowel dysfunction is different in each patient. Finding the cause is the start of a successful treatment.

References

1.

Haylen BT et al (2010) An International Urogynecological Association (IUGA)/International Continence Society (ICS) joint report on the terminology for female pelvic floor dysfunction. Neurourol Urodyn 29(1):4–20PubMed

2.

Swift SE, Tate SB, Nicholas J (2003) Correlation of symptoms with degree of pelvic organ support in a general population of women: what is pelvic organ prolapse? Am J Obstet Gynecol 189(2):372–377, discussion 377–379PubMedCrossRef

3.

Hendrix SL et al (2002) Pelvic organ prolapse in the Women’s Health Initiative: gravity and gravidity. Am J Obstet Gynecol 186(6):1160–1166PubMedCrossRef

4.

Handa VL et al (2004) Progression and remission of pelvic organ prolapse: a longitudinal study of menopausal women. Am J Obstet Gynecol 190(1):27–32PubMedCrossRef

5.

Nygaard I, Bradley C, Brandt D (2004) Pelvic organ prolapse in older women: prevalence and risk factors. Obstet Gynecol 104(3):489–497PubMedCrossRef

6.

Bradley CS et al (2007) Natural history of pelvic organ prolapse in postmenopausal women. Obstet Gynecol 109(4):848–854PubMedCrossRef

7.

Rortveit G et al (2007) Symptomatic pelvic organ prolapse: prevalence and risk factors in a population-based, racially diverse cohort. Obstet Gynecol 109(6):1396–1403PubMedCrossRef

8.

Nygaard I et al (2008) Prevalence of symptomatic pelvic floor disorders in US women. JAMA 300(11):1311–1316PubMedCentralPubMedCrossRef

9.

Melville JL et al (2005) Urinary incontinence in US women: a population-based study. Arch Intern Med 165(5):537–542PubMedCrossRef

10.

Irwin DE et al (2006) Population-based survey of urinary incontinence, overactive bladder, and other lower urinary tract symptoms in five countries: results of the EPIC study. Eur Urol 50(6):1306–1314, discussion 1314–1315PubMedCrossRef

11.

Bove A et al (2012) Consensus statement AIGO/SICCR: diagnosis and treatment of chronic constipation and obstructed defecation (part I: diagnosis). World J Gastroenterol 18(14):1555–1564PubMedCentralPubMedCrossRef

12.

Bosshard W et al (2004) The treatment of chronic constipation in elderly people: an update. Drugs Aging 21(14):911–930PubMedCrossRef

13.

Bharucha AE et al (2013) American Gastroenterological Association medical position statement on constipation. Gastroenterology 144(1):211–217PubMedCrossRef

14.

Murad-Regadas S et al (2009) Defecographic pelvic floor abnormalities in constipated patients: does mode of delivery matter? Tech Coloproctol 13(4):279–283PubMedCrossRef

15.

McCrea GL et al (2008) Pathophysiology of constipation in the older adult. World J Gastroenterol 14(17):2631–2638PubMedCentralPubMedCrossRef

16.

Hosia-Randell H et al (2007) Use of laxatives among older nursing home residents in Helsinki, Finland. Drugs Aging 24(2):147–154PubMedCrossRef

17.

Rao SS, Go JT (2010) Update on the management of constipation in the elderly: new treatment options. Clin Interv Aging 5:163–171PubMedCentralPubMedCrossRef

18.

Basson R et al (2000) Report of the international consensus development conference on female sexual dysfunction: definitions and classifications. J Urol 163(3):888–893PubMedCrossRef

19.

Soderberg MW et al (2007) Pelvic floor sex steroid hormone receptors, distribution and expression in pre- and postmenopausal stress urinary incontinent women. Acta Obstet Gynecol Scand 86(11):1377–1384PubMedCrossRef

20.

Dietz HP, Tekle H, Williams G (2012) Pelvic floor structure and function in women with vesicovaginal fistula. J Urol 188(5):1772–1777PubMedCrossRef

21.

Goepel C (2008) Differential elastin and tenascin immunolabeling in the uterosacral ligaments in postmenopausal women with and without pelvic organ prolapse. Acta Histochem 110(3):204–209PubMedCrossRef

22.

Fitzpatrick CC, Elkins TE, DeLancey JO (1996) The surgical anatomy of needle bladder neck suspension. Obstet Gynecol 87(1):44–49PubMedCrossRef

23.

Badiou W et al (2008) Comparative histological analysis of anterior vaginal wall in women with pelvic organ prolapse or control subjects. A pilot study. Int Urogynecol J Pelvic Floor Dysfunct 19(5):723–729PubMedCrossRef

24.

Chen BH et al (2002) Collagen metabolism and turnover in women with stress urinary incontinence and pelvic prolapse. Int Urogynecol J Pelvic Floor Dysfunct 13(2):80–87, discussion 87PubMedCrossRef

25.

Boreham MK et al (2002) Morphometric analysis of smooth muscle in the anterior vaginal wall of women with pelvic organ prolapse. Am J Obstet Gynecol 187(1):56–63PubMedCrossRef

26.

DeLancey JO et al (2007) Comparison of levator ani muscle defects and function in women with and without pelvic organ prolapse. Obstet Gynecol 109(2 Pt 1):295–302PubMedCrossRef

27.

De Blok S (1982) The connective tissue of the adult female pelvic region. A dissectional analysis. Acta Morphol Neerl Scand 20(2):191–212PubMed

28.

Pinkerton JH (1973) Some aspects of the evolution and comparative anatomy of the human pelvis. J Obstet Gynaecol Br Commonw 80(2):97–102PubMedCrossRef

29.

Jackson SR et al (1996) Changes in metabolism of collagen in genitourinary prolapse. Lancet 347(9016):1658–1661PubMedCrossRef

30.

Falconer C et al (1998) Different organization of collagen fibrils in stress-incontinent women of fertile age. Acta Obstet Gynecol Scand 77(1):87–94PubMedCrossRef

31.

Enhorning GE (1976) A concept of urinary continence. Urol Int 31(1–2):3–5PubMedCrossRef

32.

Sartori MG et al (2011) Sexual steroids in urogynecology. Climacteric 14(1):5–14PubMedCrossRef

33.

Rud T et al (1980) Factors maintaining the intraurethral pressure in women. Invest Urol 17(4):343–347PubMed

34.

Jarmy-Di Bella ZI et al (2000) Power Doppler of the urethra in continent or incontinent, pre- and postmenopausal women. Int Urogynecol J Pelvic Floor Dysfunct 11(3):148–154, discussion 154–155PubMedCrossRef

35.

Bruce D, Rymer J (2009) Symptoms of the menopause. Best Pract Res Clin Obstet Gynaecol 23(1):25–32PubMedCrossRef

36.

Bygdeman M, Swahn ML (1996) Replens versus dienoestrol cream in the symptomatic treatment of vaginal atrophy in postmenopausal women. Maturitas 23(3):259–263PubMedCrossRef

37.

Gebhart JB et al (2001) Expression of estrogen receptor isoforms alpha and beta messenger RNA in vaginal tissue of premenopausal and postmenopausal women. Am J Obstet Gynecol 185(6):1325–1330, discussion 1330–1331PubMedCrossRef

38.

Xie Z et al (2007) Alterations of estrogen receptor-alpha and -beta in the anterior vaginal wall of women with urinary incontinence. Eur J Obstet Gynecol Reprod Biol 134(2):254–258PubMedCrossRef

39.

Robinson D, Cardozo LD (2003) The role of estrogens in female lower urinary tract dysfunction. Urology 62(4 Suppl 1):45–51PubMedCrossRef

40.

Aikawa K et al (2003) The effect of ovariectomy and estradiol on rabbit bladder smooth muscle contraction and morphology. J Urol 170(2 Pt 1):634–637PubMedCrossRef

41.

Zoubina EV et al (2001) Acute and chronic estrogen supplementation decreases uterine sympathetic innervation in ovariectomized adult virgin rats. Histol Histopathol 16(4):989–996PubMed

42.

Blakeman PJ, Hilton P, Bulmer JN (2000) Oestrogen and progesterone receptor expression in the female lower urinary tract, with reference to oestrogen status. BJU Int 86(1):32–38PubMedCrossRef

43.

Hextall A et al (2001) The impact of the menstrual cycle on urinary symptoms and the results of urodynamic investigation. BJOG : Int J Obstet Gynaecol 108(11):1193–1196

44.

Lawrence JM et al (2008) Prevalence and co-occurrence of pelvic floor disorders in community-dwelling women. Obstet Gynecol 111(3):678–685PubMedCrossRef

45.

Ismail SI, Bain C, Hagen S (2010) Oestrogens for treatment or prevention of pelvic organ prolapse in postmenopausal women. Cochrane Database Syst Rev 9, CD007063PubMed

46.

Nappi RE, Davis SR (2012) The use of hormone therapy for the maintenance of urogynecological and sexual health post WHI. Climacteric 15(3):267–274PubMedCrossRef

47.

Shenfeld OZ et al (1999) Rapid effects of estrogen and progesterone on tone and spontaneous rhythmic contractions of the rabbit bladder. Urol Res 27(5):386–392PubMedCrossRef

48.

Gallagher P, O'Mahony D (2009) Constipation in old age. Best Pract Res Clin Gastroenterol 23(6):875–887PubMedCrossRef

49.

Rociu E et al (2000) Normal anal sphincter anatomy and age- and sex-related variations at high-spatial-resolution endoanal MR imaging. Radiology 217(2):395–401PubMedCrossRef

50.

McFarland LV, Dublin S (2008) Meta-analysis of probiotics for the treatment of irritable bowel syndrome. World J Gastroenterol 14(17):2650–2661PubMedCentralPubMedCrossRef

51.

Murad-Regadas SM et al (2012) The influence of age on posterior pelvic floor dysfunction in women with obstructed defecation syndrome. Tech Coloproctol 16(3):227–232PubMedCrossRef



If you find an error or have any questions, please email us at admin@doctorlib.info. Thank you!