1. ENDOMETRIOSIS Dr. Nayan Sarkar MD(JIPMER), DNB Assistant Professor,
Department of Obst. And Gynae

2. Learning objectives-----
Define endometriosis
Evaluate a case of endometriosis
Understand the importance of diagnosis, management of such a case
How to manage a case of endometriosis

3. Definition
Presence of endometrium-like glands and stroma outside the uterus
Adenomyosis = Invasion of the myometrium by endometrial tissue

4. Prevalence Not precisely known—2-5%
20-40% of women in infertile couple vs. 5% of fertile women.
But also found in 6-43% of women undergoing laparoscopic sterilization.
52% of teenagers with CPP Syndrome.
Up to 80% women with CPP

5. What you might see..

11. Endometriomas
May reach up to 15-20cm
“Chocolate cysts”

12. Pathogenesis
Direct implantation of endometrial cells – by means of retrograde menstruation
Vascular and lymphatic dissemination of endometrial cells
Coelomic metaplasia of multipotential cells in the peritoneal cavity
Composite

13. Immune factors
Retrograde menstruation happens in nearly everyone – so why do some women get endometriosis??
Macrophages are found in higher concentration in the peritoneal fluid of women with endometriosis
They secrete growth factors and cytokines

14. Familial association Relative Risk to siblings 2.3 overall
Relative Risk to sibs if severe endometriosis 15

15. Risk factors Single/ nulliparous Early menarche Non oral contraception
Non smoker shorter cycle/longer duration of flow
Dysplastic naevus syndrome, melanoma

16. symptoms Severe dysmenorrohoea (90%) Chronic Pelvic Pain (70%)
Deep dyspareunia (75%)
infertility (55%)

17. Presentation Pelvic pain - Most common** Dysmenorrhea
Deep thrust dyspareunia
Infertility – May be only complaint
Abnormal bleeding
Cyclical hematochezia or hematuria

18. Endometriosis pain
Psycho-physical treatments-accupuncture, massage, relaxation,
Exercise
Anti-oestrogen drugs.
Laparoscopy/open surgery

19. Infertility May be caused by distortion of the pelvic anatomy
Severe adhesions may impair egg release, block sperm entry into fallopian tube, or inhibit ovum pickup
May be other mechanisms as well – anovulation, immune dysfunction, corpus luteum insufficiency, embryo or sperm toxicity of peritoneal fluid…

20. Infertility mechanisms
Adhesions distorsion
Increased PGs
Cell mediated gamete inj
Defective folliculogenisis
Chronic salpingitis
Activated macrophag
Increased prev. ABs
LUFFS
Altered tubal motil
Cytokines
Fertilization failure
hyperprolactinaemia
Impaired oocyte pick up
Sperm phagocytosed
Early spon abortion
Luteal phase deficency

21. Where can’t it go?
Most common – Ovaries (60%), pelvic peritoneum, ant and post cul-de-sacs, uterosacral ligaments, tubes, pelvic lymph nodes
Infrequent – Recto sigmoid (10-15%), other GI sites (5%), vagina
Rare – Umbilicus, episiotomy or surgical scars, kidney, lungs, arms, legs, nasal mucosa, brain

22. Differential Diagnosis
Pain - Chronic PID, Adhesions, GI dysfunction, Interstitial cystitis
Dyspareunia – Chronic PID, Ovarian cysts, Symptomatic uterine retroversion
AUB – Anovulation, Hypothyroidism, Hyperprolactinemia
Premenstrual spotting – Luteal phase defect, Polyps, Cervical lesions
Acute pain – Ecoptic, PID, Torsion, Ruptured corpus luteum

23. Evaluation H&P Transvaginal U/S
MRI – Helpful in detecting rectal involvement
Colonoscopy and barium enema if GI bleeding present
Diagnostic laparoscopy
Conscious pain mapping

24. hpe Definitive diagnosis can only be made with tissue bx
Will see endometrial
glands, stroma, and
hemosiderin-laden
macrophages

25. American Society of Reproductive Medicine Classification
Stage 1 (min)
– 1-5
Stage II (mild)
– 6-15
Stage III (mod)
– 16-40
Stage IV (severe) – >40
Has not been prospectively validated, points are arbitrarily assigned
It serves as a partially objective means of determining the extent of disease and provides a quantifiable basis for follow-up comparisons

27. treatment Is treatment always required? Who needs treatment?
Does any treatment really work?
Does treatment in young women prevent infertility and progression?

28. Difficult to answer
Endometriosis progress in most cases of moderate and severe disease.
Spontaneous regression can occur in up to 58% of milder cases.
Natural history is still uncharted to a large extent.

29. However----
Medical treatment and surgery fail to arrest disease in up to a third.
Combinations of treatments have also failed to control disease for indefinite periods when followed up.
Pregnancy has a variable effect on endometriosis—persistence, regression and progression.

30. And also
Endometriosis may occur in the early menopause, usually in association with HRT.
Laparoscopic ablation of visible endometriotic lesion in infertile women is associated with significantly increased fertility rates.
There is no data regarding early intervention wrt prevention.

31. Treatment **There is no cure** Expectant
Medical – Good for patient’s with symptoms who desire pregnancy in the future
Surgery – Conservative or extirpative
**There is no cure**

32. Medications Analgesics (NSAIDs) OCPs
Progestins – Provera, Depo Provera
Danazol (17 alpha-ethinyl testosterone derivative)
GnRH agonists (Lupron)

33. Treatment of pain
NSAIDS: all significantly better than placebo, studies vary which one is best
Naproxen >mefanemic acid>aspirin
Naproxen=ibuprofen
Naproxen only drug with significant SEs

34. treatment of menstrual pain
Treatment level of evidence
Simple analgesics
Herbal remedies
alcohol
Antidepressants/ anxiolytics
OCPs
NSAIDS

35. OCPs
OCPs cause a decidual reaction in the functioning endometriotic tissue
Usually use low-dose OCPs continuously for 6-9 months
Contraindications – Smoker >35, hx of thromboembolic disease

36. Progestins Can use oral or depot medroxyprogesterone acetate
Progestins suppress gonadotropin release and in turn ovarian steroidogenesis
There may be a prolonged interval to resumption of ovulation with Depo so it should not be used in women who desire fertility in the near future

37. Danazol
Derivative of synthetic steroid 17α-ethinyl testosterone – has progestagenic and androgenic effects
Suppresses LH and FSH mid cycle surges so the ovary no longer produces estrogen
Symptomatic relief in 80% of pts with recurrence in 5-20% after discontinuing therapy
Side effects – weight gain, acne, hirsutism, oily skin, decrease in breast size

38. GnRH agonist
Desensitizes the pituitary and impairs release of LH and FSH and therefore estrogen production
Less androgenic side effects than Danazol

39. Aromatase inhibitors
Aromatase catalyzes the conversion of testosterone to estradiol
Being evaluated for use in refractory cases of endometriosis
Letrozole for 6 months has showed promising results in studies

40. Limitations of drug therapy
Only shrinks some types of endometriosis which are oestrogen sensitive i.e. red and blister appearance not brown, black and white.
Shrinkage not complete– usually leaves micro disease.
Results for infertility treatment no better than no treatment.
Does not deal with adhesions.

41. Conservative surgery
Typically in patients who would like to retain their fertility
Goal is to destroy all visible implants and adhesions
87% of patients report improvement in pain following ablation
High recurrence rates

42. Extirpative surgery TAH, BSO, and removal of implants
If all ovarian tissue is removed, it is unlikely residual disease will be stimulated
May leave ovarian tissue in younger patients but they may require further surgery

45. Pregnancy rates after laparoscopy
Minimal/Mild
Moderate/
Severe
Without surgery
37.4%
3.1%
After surgery
51.7%
41.3%
Conflicting data on the value of surgery for mild disease

46. META-ANALYSIS MIN/MILD ENDOMETRIOSIS
PREG RATE n
FOLLOW-UP
NO TREAT
44%
235
0.5-3
DRUG THERAPY
41%
418
1- 5
SURGERY
65%
912
1 - 6
IVF 20
257

47. Assesment

48. Best method to diagnose endometriosis
MRI
USG
Laparoscopy
PAP Smear

49. Advanced endomeriosis may contribute to sub fertility by
Distorting tubal anatomy
Causing apareunia
Creating a hostile peritoneal environment
Affecting sperm transport

50. Facts about endometriosis
Disease severity is and indicator of the amount of pain experienced by the patient F
65% of the patients have ovarian involvement
Commonly presented with superficial dyspareunia
Is easily diagnosed by clinical examination in an outpatient setting

51. Concerning endometrioma
Less than 3 cm cyst may be managed effectively medically
Cyst aspiration by usg guidance is associated with high recurrence rate
Ovulation induction with follitropin requires higher doses to yield similar result
Excision of the cyst with thermal injury to its base is the treatment of choice

52. Consisting ART in woman with advanced stage endometriosis
Ovulation induction alone is a valid option
IVF-ET is a recognized first line of treatment
Success rates are similar to those women with tubal disease
Medical therapy prior to ART increases success

53. Concerning conservative surgery for advanced stage disease in woman with subfertility
Pregnancy rate following laparotomy are significantly higher than following laparoscopy
Excision of endometriotic deposits in the POD improves fecundity
Recurrence is uncommon
It has little effect on quality of life measures

54. Concerning medical treatment for advanced stage of endometriosis and infertility
GNRH agonists are the treatment of choice for the suppression of symptoms
Pregnancy rates following discontinuation of medical therapy are similar to those following surgery
Ovarian suppression following surgery improves subsequent pregnancy rates