Endometriosis

Endometriosis

Dr. Ruaa Abdul jabbar Alnajmawi
Overview:
Endometriosis is the presence of endometrial-like tissue outside the uterine cavity. It is estrogen dependent & therefore mostly affects women during their reproductive years. Endometriotic tissue respond to cyclical hormonal changes & therefore undergo cyclical bleeding & local inflammatory reactions. These regularly repeated episodes of bleeding & healing lead to fibrosis & adhesion formation between pelvic organs causing pain & infertility, in extreme cases a frozen pelvis results. Location of endometriosis
Common sites
• Pelvis : peritoneal lining of the pelvic side walls (most common)
• pouch of Douglas
• uterosacral ligaments
• ovarian fossae & when implanted into the ovary, endometrioma form, referred to as chocolate cyst.
• bladder peritoneum
• Rectal mucosa
Rare sites
• Lungs
• Brain.
• Muscle
• Eye.
• Umbilicus, scars If the ectopic endometrial tissue is within the myometrium itself it is called adenomyosis
Appearance of endometriosis:
. Peritoneal endometriotic lesions: appear as powder burn to 1–2cm (red, bluish, brown, black, white; vesicular, cystic, petechial) lesions.
. Ovarian endometriotic cysts: endometriomas can be >10cm in size usually filled with old blood that has thick brown appearance & for this reason brownish fluid ‘chocolate cysts often associated with local fibrosis and adhesions.
. Deep infiltrating endometriosis: rectovaginal nodules can result in fibrosis of surrounding tissue, often have solid appearance.
Etiology: The exact etiology remains unknown, various theories exist, but none accounts for all aspects of endometriosis
1. Sampsons theory: Retrograde menstruation with adherence, invasion, & growth of the tissue most popular theory; however, >90% show menstrual blood in pelvis at time of menstruation.
2. Meyers theory: Metaplasia of coelomic epithelium into endometrial cells may be due to hormonal stimuli or inflammatory irritation.
3. Halbans theory: systemic and lymphatic spread explains the rare finding of endometriosis in sites outside the peritoneal cavity such as the lungs.
4. Dmowski s theory: genetic & immunological factors alter susceptibility of women & allow her to develop endometriosis, there appear to be increased incidence in the 1st degree relatives of patient with this disorder & racial differences, with increased incidence among Orientals & low incidence among Afrocarrebians.
Incidence of endometriosis:
General female population: 10–12%.
. Infertility investigation: 20–50%
Chronic pelvic pain investigation: 20–50%.
Dysmenorrhea: 40–60%.
Clinical presentation:
Classical clinical features are severe cyclical non-colicky pelvic pain restricted to around the time of menstruation, sometimes associated with heavy menstrual loss. Symptoms may begin a few days before menses starts until the end of menses. However, women often also complain of chronic non-cyclical pelvic pain and severe fatigue. It is well recognized that there is a lack of correlation between the extent
of the disease and the intensity of symptoms.
Symptoms of endometriosis in relation to site of lesion:
1. female reproductive tract: dysmenorrhea, lower abdominal & pelvic pain, deep dyspareunia, rupture, torsion of endometerioma, low back pain, infertility(table1).
2. urinary tract: cyclical hematuria, dysuria, loin, flank pain (ureteric obstruction)
3. gastrointestinal tract: dyschesia( pain on defecation),cyclical rectal bleeding, obstruction.
4. surgical scars & umbilicus: cyclical pain, swelling & bleeding.
5. lung: cyclical hemoptysis, haemopnemothorax.
6. In 2–50% of cases there are no symptom
Table (1) Infertility & endometriosis possible mechanisms
Luteolysis caused by PGF2
Ovarian function
Oocyte maturation defect


Lutinized unruptured follicle syndrome

Altered prolactin release

anovulation

Impaired fimbrial oocyte pick up

Tubal function
Altered tubal motility

Deep dysparuenia

Coital function
Antibodies causing inactivation
Sperm function
Macrophage phagocytosis of spermatoa

Prostaglandin induced

Early pregnancy failure
Immune induced

Luteal phase defeceincy

Diagnosis:
History:
• Menstrual history.
• Nature of the pain: site, relationship to cycle (mid cycle/dysmenorrhea), deep dyspareunia
• Hematuria or rectal bleeding during menstruation.
Examination: Accuracy of clinical examination in diagnosis is limited , the condition should be suspected even if vaginal examination is normal, bimanual pelvic examination for:
1. Bimanual pelvic examination for:
• Adnexal masses (endometriomas) or tenderness.
• Nodules/tenderness in the posterior vaginal fornix or uterosacral ligaments
• Fixed retroverted uterus: differential diagnosis for restricted mobility of the uterus include: chronic pelvic inflammatory diseases (PID), uterine, cervical, or ovarian cancer.
• Rectovaginal nodules.
2.Speculum examination of vagina and cervix (rarely, lesions may be visible).
Investigations:
1. Transvaginal ultrasound ( USS) : shows endometriomas, possibly endometriosis of urinary bladder or rectum, but its use in diagnosis of smaller lesions is limited.
2. MRI: can detect lesions > 5 mm in size, in deep tissues, for example the rectovaginal septum, can allow careful pre surgical planning in difficult cases
3. Laparoscopy with biopsy for histological verification:
It affords concurrent surgical diathermy &/or excision of endometriotic lesions & also staging of the disease. the patency of the fallopian tubes can also be checked. Indications for laparoscopy:
a. NSAID-resistant lower abdominal pain/ dysmenorrhoea
b. Pain resulting in days off work / school or hospitalization
c. pain and infertility investigation.
4. Intravenous urography (IVU), or barium enema (to assess extent of rectovaginal, bladder, ureteric, or bowel involvement).
5. Serum CA125 is sometimes elevated with severe endometriosis, but there is no evidence that it is a useful screening test for this condition.
Treatment:
The approach should be determined by:
• Reason for treatment (pain or fertility).
• Side effect profile.
• Cost-effectiveness of each drug.
All drugs are equally effective in relieving pain and are associated with up to 50% recurrence after approximately 12–24months after stopping.
It is acceptable to treat women empirically with progestagens or combined oral contraceptive pills COCP without a laparoscopic diagnosis. Combined hormonal contraceptives, ideally administered continuously, should be considered as first-line agents.
NSAIDs are effective and may be used with hormonal drugs.
Severe cases of endometriosis should be referred to a center with
expertise in advanced laparoscopic surgery.
Treatment for pain:
A. Medical treatment: table2
Side effect
effect
Applications/ duration
Drug
Headaches Nausea DVT, Stroke
Ovarian suppression
Continuous >> cyclic Long term
COC
Weight gain Bloating Acne Irregular bleeding Depression
Ovarian suppression


Orally or IM/SC injection (depot) Long term
Medroxy- progesterone acetate or other progestagens
Loss of bone density (reversible), Hot flushes, Vaginal dryness Headaches Depression
Ovarian suppression
2nd line therapy SC/IM injection or nasal spray Short or long term Should never be used without add-back HRT
Gonadotrophin releasing hormone (GnRH) analogues
Irregular bleeding , spontaneous expulsion
Endometrial suppression ;sometimes ovarian suppression

Intrauterine Long term (change every 5yrs if age <40)

Levonorgestrel- releasing IUD

Acne

Hirsutism Irreversible voice changes
Ovarian suppression
Oral 6 months longest experience))
Danazol
Ovarian cyst
Loss of bone density reversible))
Local oestrogen
suppression in endometrial lesions
Oral
Probably 6


months
still experimental and not licensed
Aromatase inhibitors

B. Surgical treatment:

Surgical management indicated once medical treatment has failed & include:
1. Fertility sparing surgery: Most surgeries for endometriosis can be achieved laproscopically, deposits of superficial peritoneal endometriosis can be easily ablated or excised. Symptomatic chocolate cyst should not only drained but its inner lining should be excised to prevent recurrence. Specialist surgery is needed to treat extensive adhesions distorting pelvic anatomy or involve other organs such as rectum, large bowel or bladder.Recurrence following conservative surgery is as high as 30% , therefore concurrent long term medical therapy is often necessary after surgery e.g: GnRH analogue for 6 months delay recurrence at 12 & 24 months following surgery
2. Hysterectomy & oophorectomy:
Hysterectomy with removal of the ovaries & all visible endometriosis lesions should be considered only in women who have completed their family & failed to respond to conservative treatment, hormone replacement therapy (HRT) started following surgery some surgeons prefer to defer treatment for up to 6 months to prevent activation of any residual disease.
Treatments for subfertility:
A. Medical treatment:
no medical treatment can improve fertility in endometriosis patients.

B. Surgical treatment

• surgical ablation\ excision of minimal & mild endometriosis does improve fertility chance
• Unclear efficacy for moderate/severe disease as no randomized controlled trials (RCTs) exist.
• it is uncertain whether surgical treatment of endometeriomas increase spontaneous or In vetro fertilization ( IVF pregnancy rates , as the removal must be balanced against damage of ovarian tissue, the consensus from fertility specialists at present is to leave endometrioma alone prior to IVF, unless they are symptomatic or reduce access for egg collection.
Premature menopause
premature menopause defined as menopause that occurs at an age more than 2 standard deviations (SDs) below the mean estimate for the reference population. The age of 40yrs is used frequently as an arbitrary limit below which the menopause is said to be premature. It affects 1% of women younger than 40yrs and 0.1% of those under 30yrs. In most cases no cause is found
Causes of premature ovarian failure
Primary
Chromosome abnormalities, FSH receptor gene polymorphism & inhibin B mutation, Enzyme deficiencies, Autoimmune disease.
Secondary
Chemotherapy and radiotherapy, Bilateral oophorectomy or surgical menopause
Hysterectomy without oophorectomy , Infection..
Presentation and assessment
The most common presentation is amenorrhoea or oligomenorrhoea (which may not necessarily be accompanied by hot flushes)
Co-existing disease may be detected, particularly: Hypothyroidism, Addison’s disease, diabetes mellitus, chromosome abnormalities(especially those who have not achieved pregnancy.
Management issues in premature menopause
1. Fertility and contraception: they have reduced fertility& may require assisted conception , These patients still need contraception if no fertility goals.
2. Women need oestrogen replacement until average age of natural menopause, which is usually regarded as 52 years..
Consequences of premature menopause
1.Women with untreated premature menopause (no oestrogen replacement) are at increased risk of osteoporosis and cardiovascular disease, but at lower risk of breast malignancy.
2. Premature menopause can lead to reduced peak bone mass (if <25yrs old) or early bone loss thereafter
3. Mean life expectancy in women with menopause before the age of 40yrs is 2.0yrs shorter than that in women with menopause after the age of 55yrs.



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