1. ENDOMETRIOSIS DYSMENORRHEA & CHRONIC PELVIC PAIN

2. Endometriosis (definition)
The presence of endometrial tissue in extrauterine locations .

3. Endometriosis - pathogenesis
The exact pathogenesis is unknown
Three theories:
Theory of the implantation (Sampson´s theory) – direct implantation of endometrial cells, typically by means of retrograde menstruation.

4. Endometriosis - pathogenesis
Coelomic metaplasia of multipotential cells in the peritoneal cavity (Meyers theory) states that, under certain conditions m-p cells can develop into endometrial tissue
Vascular and lymphatic dissemination of endometrial cells (Halbans theory) – distant sites of endometriosis can be explained by this process ( lymph nodes, pleura, kidney)

5. Endometriosis division by Semm Internal endometriosis of genital organs
Adenomyosis
(endometrial tissue in uterine wall)
Adenomyoma
(endometrial tissue in uterine myomas)
Endometriosis in the wall of uterine tube

6. Endometriosis division by Semm External endometriosis of genital organs:
Ovary:
- endometrioma
(the endometrial tissue deeply in ovary tissue as a tumor)
- on the surface of ovary.
Uterosacral ligaments, round ligament of the uterus.
Uterine tubes

7. Endometriosis division by Semm External endometriosis of genital organs:
Anterior et posterior cul-de-sacs
Pelvic peritoneum over uterus
Uterine cervix
Fornix of the vagina, vagina
Perineum

8. Endometriosis division by Semm Extragenital endometriosis
Sigmoid colon, ampula of the rectum, cecum, appendix
Urinary bladder
Umbilicus
Postoperative scars
(laparotomia, cesarean section)

9. Endometriosis division by Semm Extragenital endometriosis
Omentum
Small intestine
Femoral canal
Arms, legs
Lungs, pleura
Brain
Kidney

10. Endometriosis the most common sites
Surface of the ovary –60 – 70%
Endomerioma (ovary)– 30-40%
Peritoneum over the uterus – 40-50%
Uterine tube and mesosalpinx – 20 – 30%
Posterior cul –de –sac %
Uterosacral ligaments %
Rectosigmoid %

11. Endometriosis symptoms
Pelvic pain
Dysmenorrhea
Dyspaurenia
Dysuria, hematuria
Dyschesia, rectal bleeding
Abnormal bleeding
(irregular menstrual periods, premenstrual spotting)

12. Endometriosis complications
Infertility
Abortions
Acute abdominal emergency
(rupture or torsion of an endometrioma)

13. Infertility The higher stage of endometriosis –
In the group of infertile women the endometriosis occurs in 30-50%
In the group of women with the endometriosis infertility occurs in 30-70%
The higher stage of endometriosis –
the lower chance of pregnancy.

14. Infertility reasons
Distortion of the elements of the reproductive tract and damage to the ovary (obstruction of the uterine tube, adhesions, cysts)
Functional infertility (the influence of prostaglandin, IL-5, IL-6, complement: C3,C4 macrophages, LT helper, LT supresors, NK - anovulation, luteal phase inadequacy, phagocytosis of sperm, oocytes, unproper conditions to the implantation

15. Endometriosis the risk factors
Congenital anomalies that promote retrograde menstruation
Short period, long lasting menstruation
Dysmenorrhea
Infertility
First and second degree relatives have had endometriosis

16. Endometriosis diagnosis
Anamnesis
Physical examination
Laboratory studies are not useful at making the diagnosis but helpful in the differential diagnosis
Pelvic ultrasound
Laparoscopy
Histopathological examination

17. Endometriosis diagnosis
Establishing a diagnosis requires direct visualisation at the time of the diagnostic laparoscopy or the laparotomy
Histopatological confirmation of endometriosis is „the gold standard”

18. Laparoscopy / Laparotomy description of the lesions
Peritoneum: vascular hemorrhagic areas, white - opaque plaques, spots described as „mulberry” or „raspberry”, fibrosis surrounding these lesions, adhesions
Ovary : endometriomas – filled with thick, chockolate-appearing fluid; superficial implants
Uterine tubes: tubal occlusion, adhesions, distortion
Uterus: superficial implants, retroverted and fixed

19. Endometriosis staging
Classification system by the AFS
Stage I – minimal 1-5
Stage II – mild
Stage III – moderate
Stage IV – severe >40
Evaluation of areas of endometriosis (size,localization); adhesions (types, localization), posterior cul-desac obliteration, tubal occlusion

20. Endometriosis differential diagnosis
Abdominal pain
( PID, GI dysfunction, adhesions, tumors)
Dysmenorrhea
Dyspaurenia
(PID, colpitis, uterine retroversion)
Abnormal bleeding
(hormonal dissfunction, polyps, cervical lesions)

21. Endometriosis differential diagnosis
Acute abdominal emergency
(ectopic pregnancy, adnexal torsion, rupture of corpus luteum, acute PID – peritonitis)
Dysuria, dyschesia, hematuria, rectal beeding, hemoptysis, tumor in the scar - rare symptoms

22. Endometriosis treatment
The choice of therapy depends on
Presenting symptoms and their severity
Location and severity of endometriosis
Desire for future childbearing

23. Endometriosis treatment
3 stages of the treatment by Semm
I stage: laparoscopy - surgical tratment: electrocoagulation of endometriosis, removal of the cysts and adhesions
II stage: medical therapy 3 – 6 months
III stage: surgical therapy – removal of remaining endometriosis, salpingoplasty

24. Endometriosis medical therapy
3 groups of medicines:
Danazol
Progestins
Gonadotropin-releasing hormone agonists

25. Progestins endometriosis treatment
Medroxyprogesterone acetate
Provera tb 20 – 40 mg/d
Depomedroxyprogesterone acetate
Depo-Provera inj. i.m mg / 2 weeks – 8 weeks,
than 200 mg/1 month

26. Progestins endometriosis treatment
Progestins supress FSH/LH release and ovarian steroidogenesis
„pseodopregnancy”

27. Progestins endometriosis treatment
Adverse effects:
nervous system - depresion, headache, vertigo, nervosity;
skin - oily skin, itch, hirsutism;
mastalgia, nausea, weight gain;
thrombosis, alterations of lipoprotein, glucose and Ca and P metabolism

28. Danazol endometriosis treatment
Danazol-17α-ethinyl testosterone derivative
tb mg/d – 1 month, than 400 mg up to 6 months
Supresses FSH/LH release and steroidogenesis endometrial atrophy
„pseudomenopause”

29. Danazol endometriosis treatment
Adverse effects: hypoestrogenic and androgenic properties: acne , oily skin, hirsutism, spotting, bleeding, hot flushes, atrophic vaginitis nausea, depresion, nervosity, headache, vomit, alterations of lipoprotein, glucose, Ca and P metabolism

30. GnRh agonists endometriosis treatment
Triptorelin –
Decapeptyl depot a 3.75 mg inj i.m. 1x/28d,
Dipherelinum SR a 3.75 mg inj i.m. 1x/28d
Goserelin –
Zoladex a 3.6 mg inj s.c 1x/28d
Therapy 3 – 6 months

31. GnRh agonists endometriosis treatment
Pituitary desensybilisation supress FSH/LH release
„a state of pseudomenopase”

32. GnRh agonists endometriosis treatment
Adverse effects:
hypoestrogenic propierties without androgenic effects
The most expensive therapy but the most effective one

33. DYSMENORRHEA PAINFUL MENSTRUATION
Primary (absence of demonstrable pelvic disease)
Secondary (presence of pelvic pathology – endometriosis, chronic PID, uterine leiomyomas)

34. HOW TO DISCOVER THE CAUSE OF DYSMENORRHEA ?
Diagnostic laparoscopy
Empiric drug therapy
USG, RTG, MRT, CT
Laboratory tests

35. PRIMARY DYSMENORRHEA
Begins with the onset of menstruation and lasts 12 – 72 hours
Pain in lower abdomen, most intense in the midline
Pain described as crampy and intermittent, sometimes back pain and thigh pain
Accompanied by nousea, diarrhea, fatigue, headache

36. CAUSIVE AGENTS
Released from the endometrium PGE2 and PGF2 induce smooth muscle contraction in many tissues.
Contraction of the uterus can exceeds 60 mm Hg - uterine ischemia – accumulation of anaerobic metabolites (acidosis) – stimaulation of type-C pain neurons.

37. PATHOPHYSIOLOGY
High rates of endometrial prostaglandin production require the sequential stimualation by estrogen followed by progesterone – anovulatory cycles are mostly painless.

38. SECONDARY DYSMENORRHEA
Is connected with pelvic pathology
Usually begins after age of 20
Often lasts for 5 – 7 days monthly
Has increased in severity
Some women have markedly abnormal pelvic examination

39. TREATMENT
ANTIINFLAMMATORY AGENTS (inhibition of prostaglandin production and action)
IBUPROFEN (arylopropionic acid derivative)
4 x 400 mg/24 h for 3 – 4 days
NAPROXEN (mefanemic acid or it’s sodium salts)
ORAL CONRACEPTIVES
(suppress endometrial PG production by inhibiting ovulation)

40. INHIBITORS OF PG SYNTHESIS
GRUG CLASS
DRUG
STANDARD DOSE
Fenamates
Mefenamic acid
500 mg than 4 x 250 mg/24 h
Flufenamic acid
3 x mg/24 h
Tolfenamic acid
3 x 133 mg/24 h
Phenylopropionic acid
Ibuprofen
4 x 400 mg/24 h
Naproxen sodium
550 mg than 4 x 275 mg/24 h
Ketoprofen
3 x 50 mg/24 h

41. CHRONIC PELVIC PAIN
Complain presentig in 10% to 30% of all gynecologic visits
12% to 19% of all hysterectomies are performed because of unresolved chronic pain

42. Three dimensions defining chronic pelvic pain
DIURATION - any type of pelvic pain lasting longer than 6 months
ANATOMIC – defined by physical findings at laparoscopy
AFFECTIVE/BEHAVIORAL – pain accompanied by significant altered physical activity

43. Ethiology Pelvic pathology (adhesions, endometriosis, ovarian cysts)
Unidentifiable pathology
Nongynecologic causes (constipations, irritable bowel syndrome, urethral syndrome, interstitial cystitis, bladder spasms, musculosceletal problems, psychiatric comorbidity, psychopathology).
MULTIDISCIPLINARY TREATMENT IS REQUIRED.