eMedicine Specialties > Obstetrics and Gynecology > General Gynecology

Endometriosis

Author: Dharmesh Kapoor, MD, MBBS, MRCOG, Subspecialty Fellow, Department of Gynecology, Derriford Hospital
Coauthor(s): Willy Davila, MD, Head, Section of Urogynecology and Reconstructive Pelvic Surgery, Chairman, Department of Gynecology, Cleveland Clinic Florida
Contributor Information and Disclosures

Updated: Aug 12, 2008

Introduction

Background

Endometriosis, the presence of endometriumlike glands and stroma outside the uterus, is a common, poorly understood, and extremely debilitating benign gynecological condition. The psychological impact of the severe pain experienced by the patient is compounded by the negative impact of the disease on fertility. The etiology and pathophysiology of endometriosis is not well understood because of the lack of a suitable animal model on which to study the anatomic correlates and natural history of disease.1 No cure exists for the disease, and treatment is directed toward medical suppression, surgical excision, and symptom alleviation.

Adenomyosis is the invasion of the myometrium by endometrial tissue.

Frequency

United States

Endometriosis occurs in 7-10% of women in the general population.2 It is an estrogen-dependent disease and, thus, usually affects reproductive-aged women. Endometriosis has a prevalence rate of 20-50% in infertile women3,4,5 and as high as 80% in women with chronic pelvic pain6 . Evidence of endometriosis was found during laparoscopy in 20-50% of asymptomatic women.7 Approximately 4 per 1000 women are hospitalized with endometriosis each year. A familial association exists, with a 10-fold increased incidence in women with an affected first-degree relative.8 Monozygotic twins are markedly concordant for endometriosis.9

Clinical

History

A significant number of women with endometriosis remain asymptomatic.

  • Cyclic pain: Cyclic pain is pain that accompanies bleeding at the time of menstruation. This could involve the bladder (hematuria), bowel (hematochezia and painful defecation), or, rarely, bleeding at uncommon sites such as the umbilicus, abdominal wall, or perineum.
  • Chronic pain: The most important point to remember is that the degree of visible endometriosis has no correlation with the degree of pain or other symptomatic impairment.10 However, pain does correlate with the depth of tissue infiltration.11,12 Midline disease is generally believed to be more painful than lateral disease.
  • Acute exacerbations: These are believed to be caused by chemical peritonitis due to leakage of old blood from an endometriotic cyst. Recently, with conscious laparoscopic pain mapping, painful lesions were found to involve peripheral spinal nerves rather than autonomic nerves.10
  • Dysmenorrhea: Secondary dysmenorrhea occurs twice as often in women with endometriosis as in controls.7 Pain frequently commences prior to menses. Endometriosis should be considered in a patient presenting with significant dysmenorrhea, and the patient should be started on empiric therapy.
  • Dyspareunia: Deep dyspareunia may be due to scarring of the uterosacral ligaments, nodularity of the rectovaginal septum, cul-de-sac obliteration, and/or uterine retroversion. All of these may also lead to chronic backache. These symptoms are exaggerated during menses. Women with deep infiltration of the uterosacral ligaments were shown to have the most severe impairment of sexual function.13

Physical

Pelvic examination: Tenderness upon examination is best detected at the time of menses. Nodularity of the uterosacral ligaments and the cul-de-sac may be found. The uterus may be fixed in retroversion, owing to adhesions. Occasionally, a bluish nodule may be seen in the vagina due to infiltration from the posterior vaginal wall.

Causes

Theories of causation include the following:

  • Retrograde menstruation
    • Sampson described this theory in his classic paper published in 1927. Retrograde flow of endometrial tissue through the fallopian tubes into the peritoneal cavity is believed to cause endometriosis.
    • Various animal experiments and clinical observations support this theory.14,15,16,17
  • Lymphatic and vascular spread
    • These pathways may explain the occurrence of endometriosis at distant, noncontiguous sites.
    • Ovarian endometriosis is also believed to be caused by lymphatic spread18 , although superficial ovarian endometriosis may also be due to implantation via retrograde menstruation.
  • Coelomic metaplasia
    • Transformation of coelomic epithelium into endometrial-type glands in response to as yet unknown stimuli could explain endometriosis in unusual sites.19
    • Coelomic metaplasia is also believed to explain the occurrence of endometriosis in women who have undergone total hysterectomy and are not taking estrogen replacement.20
    • Endometriosis may also occur in men on high-dose estrogen therapy.21
  • Immunogenetic defects
    • These are believed to increase the susceptibility of a woman to endometriosis. Humoral antibodies to endometrial tissue have also been found in sera of women with endometriosis.22
    • Recent work has focused on studying the differences between eutopic endometrium and endometriosis. In endometriosis, an aberrantly expressed factor SF-1 activates the expression of the enzyme aromatase, which converts C19 steroids to estrogens. Consequently, estrogen increases the synthesis of prostaglandin E2, which exerts a positive feedback effect, resulting in increased aromatase activity. Additionally, endometriotic tissue is deficient in the enzyme 17-beta hydroxy steroid dehydrogenase type 2, which converts E2 in eutopic endometrium to the less potent E1 under the direction of progestins. A recent study found a higher number of endometriomas, more bilateral disease, and a higher incidence of significant pain in women with aromatase positive disease.23  However, recent studies have shown increased cyclooxygenase-2 (COX-2) expression in the stromal cells24 and aberrant aromatase expression25 in eutopic endometrium of women with endometriosis.
    • While successful treatment has been described with the aromatase inhibitor anastrozole in women with severe postmenopausal endometriosis26 , more recent studies have also shown it to be effective in cases of severe endometriosis in premenopausal women27,28 . Additional data are needed before recommending this as primary treatment. See related Medscape CME Activity Aromatase Inhibitors May Relieve Endometriosis-Associated Pain: Review.
  • Anatomic spread
    • The ovary is the most common site for endometriosis. Spread to the ovary is believed to be lymphatic18 , although superficial implants may be due to retrograde menstrual flow because the ovaries are in a dependent part of the pelvis. Lesions can vary in size from spots to large endometriomas. The classic lesion is a chocolate cyst of the ovary that contains old blood that has undergone hemolysis. Once intracystic pressure rises, the cyst perforates, spilling its contents within the peritoneal cavity. This can cause the severe abdominal pain typically associated with endometriosis exacerbations. The inflammatory response causes adhesions that further increase the morbidity of the disease.
    • Uterine serosa can be affected. Vesicular lesions may provoke an inflammatory response and scarring that cause the bladder to adhere anteriorly. Posteriorly, the disease may cause obliteration of the cul-de-sac and form dense adhesions between the posterior vaginal wall or cervix and the anterior rectum. Severe dyspareunia, dyschezia, and alteration of bowel habits are the clinical sequelae of this common spread.
    • Deep peritoneal disease is caused by infiltration of the uterosacral ligaments and rectovaginal septum by endometriotic nodules. Tethering of the uterus can lead to fixed retroversion. Dyspareunia is an important feature.
    • Through contiguous spreading, endometriosis may invade the rectovaginal septum and the anterior rectal wall. It may also involve the upper rectum and sigmoid colon, infiltrating the muscularis. Cyclical rectal bleeding (hematochezia) is pathognomonic of endometriosis. However, transmural bowel involvement by endometriosis remains a rarity. The ileum, appendix, and cecum may also be involved, leading to intestinal obstruction. Cicatrization as a consequence of endometriosis may lead to symptoms of obstruction even in postmenopausal women.
    • Although uncommon, interference in the genitourinary tract by endometriosis can affect the bladder, ureters, and kidneys by invasion, compression, or scarring. Medical therapy has less than satisfactory results, and surgical intervention is often required.
    • Uncommon sites include incisional scars, the umbilicus, and the thoracic cavity. Catamenial or cyclic pneumothorax can cause hemoptysis. Remember that ectopic endometrial tissue theoretically can undergo malignant transformation; histologic evaluation may be necessary.
    • Postmenopausal endometriosis may be encountered in women who are on estrogen replacement therapy (ERT). Occasionally, if ERT is administered after total abdominal hysterectomy, endometriosis can be stimulated in an ovarian remnant. Extrapelvic endometriosis is believed to be hormone-resistant when it occurs after surgical castration.20 Transplantation of endometrial implants during the original surgery is believed to explain this occurrence. Another possible explanation is coelomic metaplasia.

More on Endometriosis

Overview: Endometriosis
Differential Diagnoses & Workup: Endometriosis
Treatment & Medication: Endometriosis
Follow-up: Endometriosis
Multimedia: Endometriosis
References
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Further Reading

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Keywords

endometriosis, benign gynecological condition, uterine adhesions, gynecologic pain, endometrioma, endometrial implants, retrograde menstruation, lymphatic and vascular spread, coelomic metaplasia, adenomyosis, immunogenetic defects, chocolate cyst, hematochezia

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Contributor Information and Disclosures

Author

Dharmesh Kapoor, MD, MBBS, MRCOG, Subspecialty Fellow, Department of Gynecology, Derriford Hospital
Disclosure: Nothing to disclose.

Coauthor(s)

Willy Davila, MD, Head, Section of Urogynecology and Reconstructive Pelvic Surgery, Chairman, Department of Gynecology, Cleveland Clinic Florida
Willy Davila, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, Colorado Medical Society, and Florida Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Thomas Michael Price, MD, Associate Professor of Reproductive Endocrinology, Director of Reproductive Fellowship Training Program, Duke University Medical Center
Thomas Michael Price, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Obstetricians and Gynecologists, American Society for Reproductive Medicine, Endocrine Society, Phi Beta Kappa, Society for Gynecologic Investigation, and South Carolina Medical Association
Disclosure: Clinical Advisors Group Consulting fee Consulting; MEDA Corp Consulting Consulting fee Consulting; Gerson Lehrman Group Advisor  Consulting fee Consulting; Roche/GSK Spokesperson  Consulting fee Consulting

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Gail F Whitman-Elia, MD, Professor, Department of Obstetrics and Gynecology, University of South Carolina School of Medicine
Gail F Whitman-Elia, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Clinical Endocrinologists, American College of Obstetricians and Gynecologists, American Institute of Ultrasound in Medicine, American Medical Association, American Medical Women's Association, American Public Health Association, American Society for Reproductive Medicine, Endocrine Society, and South Carolina Medical Association
Disclosure: Nothing to disclose.

CME Editor

Frederick B Gaupp, MD, Consulting Staff, Department of Family Practice, Hancock Medical Center
Frederick B Gaupp, MD is a member of the following medical societies: American Academy of Family Physicians
Disclosure: Nothing to disclose.

Chief Editor

Michel E Rivlin, MD, Professor, Coordinator, Quality Assurance/Quality Improvement, Department of Obstetrics and Gynecology, University of Mississippi School of Medicine
Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Mississippi State Medical Association, and Royal College of Surgeons of Edinburgh
Disclosure: Nothing to disclose.

 
 
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