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ENDOMETRIOSIS DYSMENORRHEA & CHRONIC PELVIC PAIN

ENDOMETRIOSIS DYSMENORRHEA & CHRONIC PELVIC PAIN. Endometriosis (definition). The presence of endometrial tissue in extrauterine locations. Endometriosis - pathogenesis. The exact pathogenesis is unknown Three theories:

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ENDOMETRIOSIS DYSMENORRHEA & CHRONIC PELVIC PAIN

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  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 SemmInternal 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 SemmExternal 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 SemmExternal 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 SemmExtragenital endometriosis • Sigmoid colon, ampula of the rectum, cecum, appendix • Urinary bladder • Umbilicus • Postoperative scars (laparotomia, cesarean section)

  9. Endometriosis division by SemmExtragenital 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 - 20- 30% • Uterosacral ligaments - 20-25% • Rectosigmoid - 7-10%

  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 • 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. Infertilityreasons • 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 / Laparotomydescription 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. Endometriosisstaging Classification system by the AFS • Stage I – minimal 1-5 • Stage II – mild 6-15 • Stage III – moderate 16-40 • 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. Endometriosistreatment The choice of therapy depends on • Presenting symptoms and their severity • Location and severity of endometriosis • Desire for future childbearing

  23. Endometriosistreatment 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. Endometriosismedical therapy 3 groups of medicines: • Danazol • Progestins • Gonadotropin-releasing hormone agonists

  25. Progestinsendometriosistreatment • Medroxyprogesterone acetate Provera tb 20 – 40 mg/d • Depomedroxyprogesterone acetate Depo-Provera inj. i.m. 100 mg / 2 weeks – 8 weeks, than 200 mg/1 month

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

  27. Progestinsendometriosistreatment • 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. Danazolendometriosistreatment • Danazol-17α-ethinyl testosterone derivative tb 600 - 800 mg/d – 1 month, than 400 mg up to 6 months • Supresses FSH/LH release and steroidogenesis endometrial atrophy „pseudomenopause”

  29. Danazolendometriosistreatment • 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 agonistsendometriosistreatment • 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 agonistsendometriosistreatment • Pituitary desensybilisation supress FSH/LH release „a state of pseudomenopase”

  32. GnRh agonistsendometriosistreatment • 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

  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.

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