2. DEFINITION:
• The presence of endometrial tissue outside the uterus.
• This tissue is not only morphologically similar to normal endometrium
,but is also functional.
• It is typically a disease of reproductive years
4. Site of endometriosis
PELVIC ENDOMETRIOSIS
• Peritoneum
• Uterovesical fold
• Posterior cul de sac
• Pelvic side wall
EXTRA PELVIC ENDOMETRIOSIS
• Gynecologic sites
Vulva, vagina,cervix
• Non gynecologic sites
Bowel, lungs, pleural cavity
surgical scars, lymph glands,
nerves, and Tubes & ovaries.
5. Etiology
• Endometriosis is an estrogen-dependent disease.
4 theories have been proposed to explain the pathogenesis of
endometriosis:
• 1. Ectopic transplantation of endometrial tissue.
• 2. Coelomic metaplasia
• 3. The induction theory
• 4. Vascular and lymphatic spread
But
• No single theory can account for the location of endometriosis in all cases.
6. The transplantation theory
Is based on the assumption that endometriosis is caused by the
seeding or implantation of endometrial cells by trans-tubal
regurgitation during menstruation.
7. Theory of coelomic metaplasia:
• Pluripotential of coelomic epithelium to develop not only into normal
tissue but also, through programming defect into in to endometriotic
tissue.
8. Induction Theory
• It proposes that an endogenous (undefined) biochemical factor can
induce undifferentiated peritoneal cells to develop into endometrial
tissue.
9. Lymphatic & vascular metastases theory
• Embolic transport of endometrial cells through blood and lymphatic
stream may contribute to occurrence of endometriosis at distant
sites, contributing to rare cases of catamenial pneumothorax,
epilepsy, epistaxis, hemoptysis
10. Risk factors
• The risk or endometriosis is 6 to 9 times greater if a first degree
relative has been affected by endometriosis.
• Age
• Increased peripheral body fat.
• Greater exposure to menstruation
11. Clinical presentation
• Endometriosis should be suspected in women with subfertility,
dysmenorrhea, dyspareunia, or chronic pelvic pain.
• Perimenstrual pain often bowel and bladder, causing dyschezia and
dysuria.
• Chronic fatigue.
• However, endometriosis may be asymptomatic.
12. Extra-pelvic Endometriosis
• Extra-pelvic endometriosis, although often asymptomatic, should be
suspected when symptoms of pain or a palpable mass occur outside
the pelvis in a cyclic pattern.
• Intestinal tract (especially colon and rectum) is the most common
site of extra-pelvic disease and may cause abdominal and back pain,
cyclic rectal bleeding, constipation, and obstruction.
13. • Ureteral -involvement can lead to obstruction and result in cyclic pain,
dysuria, and hematuria.
• Pulmonary endometriosis can manifest as pneumothorax,
hemothorax, or hemoptysis during menses.
• Umbilical endometriosis should be suspected when a patient has a
palpable mass and cyclic pain in the umbilical area.
• Scar Endometriosis may present with cyclical pain and swelling.
14. CLINICAL EXAMINATIONS
• Recommended that pelvic examination be performed at the time of
menses when tenderness is easier to detect.
• The vulva, vagina, and cervix should be inspected for any signs of
endometriosis, although the occurrence of endometriosis in these
areas is rare (e.g., episiotomy scar).
• The uterus is often in fixed retroversion, and the mobility of the
ovaries and fallopian tubes is reduced.
15. • Other possible signs of endometriosis include uterosacral or cul-de-
sac nodularity, cervical displacement due to uterosacral scarring ,
painful swelling of the rectovaginal septum, and ovarian (cystic)
enlargement.
16.
17. • History and examination:
Alone are insufficient as pelvic inflammation and pelvic congestion
syndrome mimic endometriosis.
• Imaging study
• CA 125
• Laparoscopy
18. IMAGING STUDY
• Ultrasonography and magnetic resonance imaging can be helpful in
diagnosing endometriomas.
• However, neither can diagnose small peritoneal implants or
adhesions.
• Although transvaginal ultrasonography is highly accurate in
diagnosing ovarian endometriomas, hemorrhagic cysts account for a
significant false positive rate.
19. The CA-125 Assay
• Serum CA-125 determinations may be able to differentiate
endometriotic from non endometriotic benign adnexal cysts,
especially when combined with transvaginal ultrasonography
22. Endometriosis phenotypes at laparoscopy
• Peritoneal or typical endometriosis
• Cystic ovarian endometriosis (Endometrioma)
• Deep endometriosis
• Other phenotypes
23. Peritoneal or typical endometriosis
• Characteristic findings include typical (“powder-burn,” “gunshot”)
lesions on the serosal surfaces of the peritoneum
24. Cystic ovarian endometriosis
• Endometriomas develop as cystic lesion within the ovary, forming
chocolate cyst, due to degradation of blood over time to thick
hemosiderin rich fluid,.
25. Deep endometriosis
• Lesions extending deeper than 5mm under peritoneal surface or
those involving or distorting the bowel, bladder, ureter or vagina.
• It is suggested that deep endometriosis should be redefined as
adenomyosis externa on pathological grounds.
26. Others
• Peritoneal pocket lesion
• Subtle or atypical endometriosis
Including red implants (petechial, vesicular, polypoid, hemorrhagic,
red flame like), serous or clear vesicles, white plaques or scarring,
yellow-brown discoloration of the peritoneum, and sub-ovarian
adhesions.
27. Classification systems
• ARMS:
For women undergoing surgery
• Enzian classification:
For women with deep endometriosis
• EFI:
Women for whom fertility is the future concern
28. American society for reproductive medicine
revised classification of endometriosis
• Stage I (Minimal) 1-5
• Stage II (Mild) 6-15
• Stage III (Moderate) 16-40
• Stage IV (Severe) >40
• Limitation is that it does not describe deep endometriosis adequately
and has poor correlation with fertility.
29.
30.
31. Treatment
• For women with symptoms such as pain related to endometrium
Life style and dietary intervention
Empirical medical treatment
Surgical treatment
Medical management
Complementary therapies
32. • For women with endometriosis related infertility:
• Surgery
• Assisted conception
• Adjuvant therapy to assisted conception
33. Factors influencing choice of treatment
• Women age
• Fertility status
• Nature of symptoms
• Severity o disease
• Previous treatment
• Resource implication
• Risks of treatment
• Intended duration of treatment
34. Empirical medical treatment
• 1st line
• NSAIDs, other analgesics
• COCPs
• Progestins
• 2nd line
• GnRH agonist with add back HRT
• Oral GnRH antagonists
• LNG-IUS or opioids analgesics
35. Surgical treatment
• Peritoneal Endometriosis
Laparoscopic surgical removal of endometriosis (through excision or
ablation of endometriosis ).
• Recurrence rate even after expert removal varies from 10-55 %
within 12 months.
• Pre sacral neurectomy provide benefit for small number of women,
with dysmenorrhea.
• Evidence does not support the use of short term pre and post op
medical treatment.
36. OVARIAN ENDOMETRIOSIS
• Small ovarian endometrioma (<3 cm in diameter) can be
aspirated, irrigated.
• Large (>3 cm in diameter) ovarian endometrioma
Should be aspirated, followed by incision and removal of the cyst wall
from the ovarian cortex.
• To prevent recurrence, the cyst wall of the endometrioma must be
removed.
37. OTHERS
• Deep Rectovaginal and Rectosigmoidal endometriosis
The surgical excision of deep rectovaginal and rectosigmoidal
endometriosis is associated with major complications of postoperative
bowel perforations with peritonitis have been reported in 2% to 3% of
cases .
• LUNA(Laparoscopic uterosacral nerve ablation)
• Extra-pelvic endometrio-surgical excision.
• Scar endometriosis excision.
38. Medical Treatment
• Hormonal therapy of infertility associated with endometriosis is not
of proven value.
• Medical therapy for dysmenorrhea, dyspareunia, and pelvic pain
associated with endometriosis is very successful (although relief may
be short-term).
• Endometriomas rarely decreases in size with medical therapy.
39. Oral Contraceptives
• The treatment of endometriosis with continuous low-dose monophasic
combination contraceptives ( for 6 to 12months) was originally used to
induce pseudopregnancy caused by the resultant amenorrhea and
decidualization of endometrial tissue.
• Any low-dose combination oral contraceptive containing 30 to 35 mg of
ethinyl estradiol used continuously can be effective in the management of
endometriosis
• Do not provide definitive treatment.
40. Progestins
• Progestins may exert an anti endometriotic effect by causing initial
decidualization of endometrial tissue followed by atrophy.
• They can be considered as the first choice for the treatment of
endometriosis because they are as effective as danazol or GnRH
analogues and have a lower cost and a lower incidence of side effects
than these agents.
41. • Medroxyprogesterone acetate (150 mg) given intramuscularly, every 3
months is effective for the treatment of pain associated with
endometriosis.
• Megestrol acetate has been administered in a dose of 40 mg/d
with good results .
• Other treatment strategies have included dydrogesterone (20 to 30
mg/d, and lynestrenol (10 mg/d).
42. • Local progesterone treatment with a levonorgestrol releasing
intrauterine system for 12 months has resulted in a significant
reduction in dysmenorrhea, pelvic pain and dyspareunia.
43. Progesterone Antagonists
• Progesterone antagonists may suppress endometriosis based on their
anti proliferative effects on the endometrium, without the risk for
hypo-estrogenism or bone loss that occurs with GnRH treatment
44. • Mifepristone is a potent antiprogestogen with a direct inhibitory
effect on human endometrial cells.
• The recommended dose for endometriosis is 25 to 100 mg/d.
45. Danazol
• Pharmacologic properties of danazol include suppression of GnRH or
gonadotropin secretion, direct inhibition of steroidogenesis,
increased metabolic clearance of estradiol and progesterone.
• The multiple effects of danazol produce a high androgen, low-
estrogen environment that does not support the growth of
endometriosis, and the amenorrhea that is produced prevents new
seeding of implants from the uterus into the peritoneal cavity.
46. • Start treatment with 400 mg daily (200 mg twice a day) and increase
the dose, if necessary, to achieve amenorrhea and relieve symptoms .
47. Gonadotropin-releasing Hormone Agonists
• GnRH agonists bind to pituitary GnRH receptors and stimulate LH and
FSH synthesis and release.
• However, the agonists have a much longer biologic half-life (3 to 8
hours) than endogenous GnRH (3.5 minutes), resulting in the
continuous exposure of GnRH receptors to GnRH agonist activity.
• This causes a loss of pituitary receptors and downregulation of GnRH
activity, resulting in low FSH and LH levels.
• Consequently, ovarian steroid production is suppressed, providing a
medically induced and reversible state of pseudo-menopause.
48. • These agents include leuprolide(leuporide 3.75 mg IM monthly),
buserelin, nafarelin, histrelin, goserelin, deslorelin, and triptorelin.
• These drugs are inactive orally and must be administered
intramuscularly, subcutaneously, or by intranasal absorption.
• The best therapeutic effect is often effective with an estradiol dose of
20 to 40 pg/mL (75 to 150 pmol/L).
.
50. Efficacy of Medical Treatment
• Based on published studies, medroxyprogesterone acetate, danazol, and
GnRH agonists have similar efficacy in resolution of the laparoscopically
documented disease and in pain alleviation.
• Disadvantages of medical therapy:
Over surgical therapy include the high cost of hormone preparations, the
high prevalence of side effects, and the higher recurrence rate of
endometriosis.
Conception is either impossible or contraindicated during medical treatment
of endometriosis.
51. Treatment for women with endometriosis
infertility
• Surgery
Options for egg preservations prior to surgery , if bilateral ovarian cysts
are present.
• Assisted conception
52. Assisted Reproduction and Endometriosis
• The treatment of endometriosis-related infertility is dependent on the age
of the woman, the duration of infertility, the stage of endometriosis, the
involvement of ovaries, tubes, or both in the endometriosis process,
previous therapy, associated pain symptoms, and the priorities of the
patient, the cost of treatment, her financial means, and the expected
results.
• Assisted reproduction, including controlled ovarian hyperstimulation with
intrauterine insemination, IVF, and GIFT, may be options for infertility
treatment in addition to surgical reconstruction.
• IVF is the method of choice when distortion of the tuboovarian anatomy
contraindicates the use of superovulation with intrauterine insemination or
GIFT.
53. Conclusion
• Endometriosis is a chronic, costly disease requiring long-term,
multidisciplinary treatment.
• Profound personal and economic impact.
• Timely intervention and appropriate, multifactorial treatments may
restore quality of life, preserve or improve fertility, and lead to long-
term effective management in absence of permanent cure
Inflamatory disease associated with pelvic pain or infertility.
Retrograde menstruation, proposed by Sampson, viable cells, bc mullerian anomalies, short cycles, dec parity, increased duration, left side of dt sigmoid colon, bt it occurs even before mmearchea, amenorrhic, and in men
experiments in rabbits but has not been substantiated in women
haematogenous dissemination of endometrial cells
Short cycles, long duration, reduced parity, smoking, cocps and exercise are protective
In adult women, dysmenorrhea may be especially suggestive of endometriosis if it begins after years of pain-free menses, continues throughout the cycle, Very severe pain, however, is associated with deeply infiltrating endometriosis. 3d, dysm, dyspruen, deep spp, non specific,
Infertility , distrortion of ft, ovaries, ovarian damagevia endomerioma formation, minimal endo is sometimes ass e infertility,
https://www.endofound.org/endometriosis-stages
https://www.endofound.org/endometriosis-stages
Exercise and gluten free diet, CBT, psychological support,
Medroxy, dinogest, while awaiting surgery, add back HRT to alleviate hypoestrogenic side effects, and prevent bone mass loss.
Recurrence is more at luteal phase dt retrogragde implantation while surgically removed is healing
Because estrogen is known to stimulate the growth of endometriosis, hormonal therapy has been designed to suppress estrogen synthesis, thereby inducing atrophy of ectopic endometrial implants or interrupting the cycle of stimulation and bleeding. Manipulation of the endogenous hormonal milieu is the basis for the medical management of endometriosis.
In addition, the subsequent amenorrhea induced by oral contraceptives could potentially reduce the amount of retrograde menstruation (one of the many risk factors proposed in the etiology of endometriosis)
Danazole is associated with high treatment burden of androgenic side effects
