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Chronic pelvic pain in menopausal women
Agnieszka Tołwińska, Rafał Kisielewski, Piotr Laudański
Przegląd Menopauzalny 2012; 3: 187–191
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IntroductionChronic pelvic pain (CPP), frequently encountered in physicians’ practice, is a condition affecting about 14% of adult women. The CPP is most commonly caused by the diseases of the digestive system, urinary and gynecological disorders, and diseases of the musculoskeletal system. Due to hormonal changes occurring during menopause, discrepancies appear concerning the incidence, pathogenesis, clinical picture and diagnosis of these diseases. Chronic abdominal pain associated with endometriosis usually disappears during menopause, however, some patients can be affected. Pelvic inflammatory conditions occur most frequently in women of reproductive age. Only about 2% of women diagnosed with tubo-ovarian abscess were in the menopause stage. There are also differences in the course of irritable bowel syndrome in women during menopause, compared with younger women. Symptoms more commonly appearing in the older women are constipation, chest pain, and sometimes nausea. Changes in the urogenital system in postmenopausal women cause the urinary tract dysfunction, including painful bladder syndrome and urinary bladder inflammation/interstitial cystitis. Symptoms of urinary tract dysfunction occur in approximately 50% of menopausal women and worsen with age. Discomfort associated with the musculoskeletal system that evokes abdominal pain occurs more frequently in older age groups and can be the cause
of up to 75% of CPP.
Accurate assessment of all of the individual systems allows for making the correct diagnosis and leads to beginning of treatment. However, in many patients, despite consulting experts - gastroenterologists, gynecologists, and urologists, the cause of symptoms is not diagnosed. In this situation, the treatment is applied only to reduce pain.
Definition and epidemiologyChronic Pelvic Pain (CPP) is defined as a pain occurring in the pelvis, in the anterior abdominal cavity, under the navel or as a low back pain. The pain can last for a minimum of 6 months and is not related to pregnancy or menstruation .
In Great Britain, chronic pelvic pain is the leading cause of women reporting to the primary care physician. It is estimated that among patients aged 15 to 73 years, at least 3.8% suffer from CPP. In comparison, 3.7% suffer from asthma and 2% from migraine headache . In the United States of America, 12-20% of hysterectomies and about 20-40% of laparoscopies are performed as
a part of the diagnosis and treatment of CPP.
Causes of CPP
Potential visceral sources of chronic pain include symptoms in the reproductive system as well as in the urinary and digestive tract. The potential somatic sources include the pelvic bones, ligaments, muscles and fasciae . The most frequent causes of CPP are the disorders of the digestive system (about 38%), the second in frequency are anomalies of the urinary tract (about 31%) and, finally, gynecological problems (about 20%) [2, 4]. About 20-30% of patients with CPP, reporting to primary care physician, have more than one disorder which might cause pelvic pain [5, 6].
The present paper focuses on the most common diseases encountered in the practice of family practitioners and gynecologists. Various causes of the CPP are presented in Table I.
Prevalent pathologies causing or worsening CPP are endometriosis, pelvic inflammatory disease (PID), irritable bowel syndrome (IBS), painful bladder syndrome (PBS), interstitial cystitis (IC), and myofascial pain syndromes (Table I). All of the disorders occur in peri- and postmenopausal women. The majority of studies concerning the use of laparoscopy and hysteroscopy in
the diagnosis and treatment of CPP show that, with age, there is a decrease in the detection of endometriosis simultaneous with the increase of diagnosed intrauterine adhesions and uterine fibroids .
Endometriosis is an estrogen-dependent inflammatory disease, defined as the presence of endometrial-like tissue outside the uterine cavity, mainly in the pelvic peritoneum and ovaries . The affected eutopic endometrium, as well as a proinflammatory milieu in the peritoneal cavity of patients with endometriosis, as a consequence of retrograde menstruation, leads to the alteration in the concentration and activity of different bioactive substances e.g. cytokines, chemokines, matrix metalloproteinases and other bioactive molecules, which is a key aspect of chronic pain states [9-11].
Endometriosis is most often diagnosed among women in their reproductive age with the average age
of 28 years. In most cases, the symptoms of endometriosis disappear at menopause. Incidence in women of menopausal age is estimated at about 5% of all cases, most of which are recorded in women taking estrogen replacement therapy . Postmenopausal endometriosis (PE) is mainly located in the ovaries as well as outside the reproductive system: the large intestine, bladder, lungs, liver and skin. PE is more common in obese women . In women with a history of endometriosis, estrogen hormone therapy (HT) during menopause can cause a reactivation of endometriosis or even a danger of occurrence of new implants . On the other hand, patients with a history of endometriosis are at high risk of long-term consequences of estrogen deficiency such as cardiovascular disease, osteoporosis, dementia, Parkinson’s syndrome, increased risk of colorectal cancer, diabetes mellitus type 2, reduced quality of life and overall mortality . The risk of recurrence of endometriosis during menopause is lower in patients with surgically removed uterus and its appendages than in patients with natural menopause. However, oophorectomy has a much stronger negative impact on the quality of life than the pharmaceutically induced menopause . It is worth mentioning that the evidence of beneficial effects of HT on the reduction of mortality applies only to younger patients under 60 years of age (due to a decrease in coronary syndrome) .In a group of older women taking HT, there is no evidence of beneficial effects of HT on the life expectancy .In postmenopausal women, HT may increase the risk of malignant transformation of the existing endometrial implants. Using estrogens in women with a body mass index (BMI) higher
than 27 is a risk factor for cancer . Simultaneous usage of progestogen and estrogen lowers the risk of the renewal of endometriosis and cancer mutations, however, it aggravates the risk of breast neoplasm. Nevertheless, a combination of low doses of estrogen and progestogen is preferred in women during menopause with a history of endometriosis . Another option is using tibolonewhich does not increase the risk of endometriosis renewal, hyperplasia or cancer in women during menopause, and is comparable to the combined and continual estrogen and progestogen usage . Regression of endometriosis in postmenopausal women using HT is an indication to discontinue the treatment.
Pelvic Inflammatory Disease
Pelvic Inflammatory Disease is another frequent cause of CPP. It is an acute or chronic inflammation
of the uterus, ovaries, fallopian tubes, and visceral peritoneum. This is caused by sexually transmitted microorganisms or through the spread of infection to nearby organs. PID affects women of reproductive age, but may appear in any age group, even during menopause. It is estimated that in the United States, PID is the cause of 5-20% of all hospitalizations for gynecologic disorders. In many patients who experienced PID, pelvic pain syndrome may also occur. The incidence of PID in menopausal women is not exactly known. Studies have shown that less than 2% of women diagnosed with
tubo-ovarian abscess were postmenopausal . There are differences in the structure of cervical epithelium in women of reproductive age and after menopause.
The cervical epithelium of younger women is more susceptible to the adhesion of Neisseria gonnorhoeae and Chlamydia trachomatis. In older patients after cervical epithelial transformation, the adhesion potency of these bacteria decreases. The cervix also acts as
a functional barrier to ascending infection. In postmenopausal women, cervical mucus is less permeable and therefore acts as a mechanical barrier against microbes. Lack of menstrual bleeding also lowers the risk of infection in the upper genitourinary tract . The risk factors, such as being exposed to sexually transmitted infections, occur less frequently after the menopause. However, in elderly women (beyond 65 years of age), PID is most often a consequence of the spread of infection from organs adjacent to pelvis. Diseases such as diverticulitis, Crohn’s disease, appendicitis, colorectal or small intestine cancer can activate the inflammation. These infections cause most frequently one-sided or bilateral tubo-ovarian abscess .
Risk factors for PID include postmenopausal gynecological procedures performed on uterus and/or anatomical abnormalities of the genital tract such as cervical stenosis, cervical cancer, uterine fibroids and endometrial polyps.
Bacterial flora of the lower genitourinary tract in postmenopausal women consists mostly of gram-
negative aerobic bacteria, especially E. coli, which are the most common cause of PID after menopause (up to 76%) and Klebsiellapneumoniae(up to 43%). In 50-67% of postmenopausal individuals both of these pathogens caused the infection . Also, Pseudomonas (14%), Staphylococcus aureus (25%), Staphylococcus albus (25%), Enterococcus spp.  and anaerobes were found in these women. The diagnosis of PID in women of reproductive age can be made based on the typical symptoms, such as pain in the lower abdomen, abnormal vaginal discharge or cervicitis. Since the main mechanism of PID in older women is the spread of inflammation from the adjacent organs, the symptoms may not occur in women of reproductive age. As mentioned earlier, the majority of postmenopausal women with PID suffer from tubo-ovarian abscess. Therefore, the most reliable diagnostic method in that case is laparoscopic surgery during which other anomalies can also be found e.g. fibroids, diverticulitis, appendicitis or cancerous intestinal infiltration.
In other studies it was shown that more than 40% of postmenopausal women are affected by cancer. For this reason, in the absence of a positive response to treatment within 48 hours, a surgical treatment should be performed .
Irritable Bowel Syndrome
The main gastrological cause of CPP is irritable bowel syndrome. It is a functional disorder in bowel habits where common symptoms are chronic abdominal pain with diarrhea or constipation . According to the recent Rome III Criteria of diagnosing IBS, the time needed to recognize it was shortened from 12 to 6 months (Table II) . About 50% of women reporting to gynecological clinics due to CPP are diagnosed with IBS . The disorder starts mainly in the third and fourth decade of life. Supposedly, it is connected with visceral hypersensitivity strongly pronounced in young people . Despite this, even elderly postmenopausal patients are affected by IBS.
Three main clinical symptoms associated with IBS are abdominal pain, diarrhea and constipation. Flatulence and feeling of incomplete bowel evacuation also occur. Less common symptoms include dyspareunia, nausea, back pain, thigh pain, and chest pain, increased number of voiding, as well as depression and anxiety. In postmenopausal women, in the course of IBS, nausea is less common, while hard, lumpy stool and constipation occur. Chest pain occurs more often in menopausal women .
The diagnosis of IBS can be made based on symptomatic criteria. In any case of suspecting the presence
of organic disease and/or family history record, procedures as proctoscopy, colonoscopy, abdominal ultrasound or gastrointestinal infusion are performed .
Painful Bladder Syndrome/Interstitial Cystitis
Painful Bladder Syndrome is a group of symptoms consisting of pain above pubic symphysis associated with filling of the bladder and increased frequency
of urination during the day and night with no symptoms of urinary tract infection. Interstitial Cystitis, however, occurs in patients who have symptoms of PBS and show typical features of bladder distension during cystoscopy, such as discrete, red, and bleeding areas on the wall of the bladder, called “the Hunner’s ulcer” . The average age of women suffering from PBS/IC is 40 to 60 years.
After menopause, in the urogenital system, changes known as the urogenital atrophy (UGA) emerge. It promotes the occurrence of senile atrophic urethritis, recurrent infections of the urinary bladder and urethra. The incidence of UGA in women aged 50-60 years is estimated at 50% and in women 70 years old at 72% . In menopausal women with symptoms of PBS/IC it is essential to eliminate malignancy. In any case of persistent symptoms, after urinary tract infection remission, cystoscopy and cytology should be performed. Only after the exclusion of presence of neoplastic changes, can the estrogen therapy be applied .
Neurological and musculoskeletal disorders
Another quite common cause of pelvic pain is neurological and musculoskeletal disorders. This applies to about 15% of women with CPP in whom myofascial pain syndrome occurs . In many patients the presence of the so-called trigger points was shown. These points can be found in the abdominal wall, skeletal muscles, fasciae, and soft tissues of the pelvis. Pressing on the trigger points causes local pain and tenderness in distant locations, the so-called referred pain. The diagnosis
of allesthesia, a condition in which a sensation or stimulus is perceived at a point on the body that is remote from the point that was stimulated, can be confirmed by injecting local anesthetics into the affected areas.
Diseases associated with the musculoskeletal system, such as scoliosis, osteoarthritis, fibrosing inflammation of muscles or intervertebral discs are much more prevalent in older age groups and can cause pain radiating to the abdomen. In menopausal women, osteoporosis occurs, which further increases the pain. Abnormal posture with excessive lumbar lordosis and thoracic kyphosis, called typical pelvic pain posture can make up to 75% of cases of CPP syndrome .
References1. ACOG Committee on Practice Bulletins-Gynecology. ACOG Practice Bulletin No. 51. Chronic pelvic pain. Obstet Gynecol 2004; 103: 589-605.
2. Zondervan KT, Yudkin PL, Vessey MP, et al. Prevalence and incidence of chronic pelvic pain in primary care: evidence from a national general practice database. Br J Obstet Gynaecol 1999; 106: 1149-55.
3. International Association for the Study of pain. www.iasp-pain.org.
4. Samraj GP, Kuritzky L, Curry RW. Chronic pelvic pain in women: evaluation and management in primary care. Compr Ther 2005; 31: 28-39.
5. Zondervan KT, Yudkin PL, Vessey MP, et al. Chronic pelvic pain in the community-symptoms, investigations, and diagnoses. Am J Obstet Gynecol 2001; 184: 1149-55.
6. Royal College of Obstetricians and Gynaecologists. Guideline No 41: The initial management of chronic pelvic pain. RCOG, London 2005.
7. Markowska J, Sochaj M, Malinowski A. Laparoskopia w diagnostyce przewlekłego bólu miednicy. Przegl Menopauz 2010; 1: 38-43.
8. Giudice LC, Kao LC. Endometriosis. Lancet 2004; 364: 1789-99.
9. Laudański P, Szamatowicz J, Oniszczuk M. Profiling of peritoneal fluid of women with endometriosis by chemokine protein array. Adv Med Sci 2006; 51: 148-52.
10. Laudański P, Szamatowicz J, Ramel P. Matrix metalloproteinase-13 and membrane type-1 matrix metalloproteinase in peritoneal fluid of women with endometriosis. GynecolEndocrinol 2005; 21: 106-10.
11. Laudański P, Szamatowicz J, Kowalczuk O, et al. Expression of selected tumor suppressor and oncogenes in endometrium of women with endometriosis. Hum Reprod 2009; 24: 1880-90.
12. Oxholm D, Knudsen UB, Kryger-Baggesen N, Ravn P. Postmenopausal endometriosis. Acta Obstet Gynecol Scand 2007; 86: 1158-64.
13. Punnonen R, Klemi PJ, Nikkanen V. Postmenopausal endometriosis. Eur J Obstet Gynecol Reprod Biol 1980; 11: 195-200.
14. Moen MH, Rees M, Brincat M, et al. EMAS position statement: Managing the menopause in women with a past history of endometriosis. Maturitas 2010; 67: 94-7.
15. Bhattacharya SM. Health-related quality of life following surgical menopause and following gonadotrophin-releasing hormone analogue-induced pseudomenopause. Gynecol Endocrinol 2009; 25: 621-23.
16. Archer DF, Hendrix S, Gallagher JC, et al. Endometrial effects of tibolone. J Clin Endocrinol Metab 2007; 92: 911-8.
17. Jackson SL, Soper DE. Pelvic inflammatory disease in the postmenopausal woman. Infect Dis Obstet Gynecol 1999; 7: 248-52.
18. Vasilev SA, Roy S, Essin DJ. Pelvic abscesses in postmenopausal women. Surg Gynecol Obstet 1989; 169: 243-6.
19. Fisher M, Drugan A, Govrin J, et al. Postmenopausal tubo-ovarian abscess. Acta Obstet Gynecol Scand 1986; 65: 661-3.
20. Lipscomb GH, Ling FW. Tubo-ovarian abscess in postmenopausal patients. South Med J 1992; 85: 696-9.
21. Longstreth GF, Thompson WG, Chey WD, et al. Functionalboweldisorders. Gastroenterology 2006; 130: 1480-91.
22. Mulak A, Waszczuk E. Zespół Jelita Nadwrażliwego. W: Zaburzenia czynnościowe przewodu pokarmowego. Paradowski L (red.). Cornetis, Wrocław 2007.
23. Banerjee S, Farrell RJ, Lembo T. Gastroenterological causes of pelvic pain. World J Urol 2001; 19: 166-72.
24. Lee OY, Mayer EA, Schmulson M, et al. Gender-related differences in IBS symptoms. Am J Gastroenterol 2001; 96: 2184-93.
25. Floch MH. Zespół jelita nadwrażliwego i czynnościowe zaburzenia przewodu pokarmowego. W: Gastroenterologia Nettera. Floch MH (red.). Elsevier Urban & Partner, Wrocław 2010.
26. Fitzgerald MP. Clinical features and diagnosis of painful bladder syndrome/ interstitial cystitis. www.uptodate.com.
27. Stachowiak G, Pertyński T. Kliniczne aspekty atrofii urogenitalnej u kobiet. Przegl Menopauz 2011; 1: 1-4.
28. Turner W, Eardley I, Joyce AD, Harnden P. Postmenopausal cystitis. BMJ 1996; 313: 1079.
29. Slocumb JC. Chronic somatic, myofascial, and neurogenic abdominal pelvic pain. Clin Obstet Gynecol 1990; 33: 145-53.
30. King PM, Myers CA, Ling FW, Rosenthal RH. Musculoskeletal factors in chronic pelvic pain. J Psychosom Obstet Gynecol 1991; 12: 87-98.
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