ENDOMETRIOSIS

DYSMENORRHEA &

CHRONIC PELVIC PAIN

Endometriosis (definition)

The presence of endometrial tissue in extrauterine locations .

Endometriosis - pathogenesis

The exact pathogenesis is unknown

Three theories:

1. Theory of the implantation (Sampson´s theory) – direct implantation of endometrial cells, typically by means of retrograde menstruation.

Endometriosis - pathogenesis

2. Coelomic metaplasia of multipotential cells in the peritoneal cavity (Meyers theory) states that, under certain conditions m-p cells can develop into endometrial tissue

3. Vascular and lymphatic dissemination of endometrial cells (Halbans theory) – distant sites of endometriosis can be explained by this process ( lymph nodes, pleura, kidney)

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

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

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

Endometriosis division by Semm

Extragenital endometriosis

• Sigmoid colon, ampula of the rectum, cecum, appendix

• Urinary bladder• Umbilicus• Postoperative scars

(laparotomia, cesarean section)

Endometriosis division by Semm

Extragenital endometriosis

• Omentum• Small intestine• Femoral canal• Arms, legs• Lungs, pleura• Brain• Kidney

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%

Endometriosis symptoms

• Pelvic pain• Dysmenorrhea• Dyspaurenia• Dysuria, hematuria• Dyschesia, rectal bleeding• Abnormal bleeding

(irregular menstrual periods, premenstrual spotting)

Endometriosis complications

• Infertility

• Abortions

• Acute abdominal emergency (rupture or torsion of an endometrioma)

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.

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

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

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

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”

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

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

Endometriosis differential diagnosis

• Abdominal pain ( PID, GI dysfunction, adhesions, tumors)

• Dysmenorrhea• Dyspaurenia

(PID, colpitis, uterine retroversion)

• Abnormal bleeding (hormonal dissfunction, polyps, cervical

lesions)

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

Endometriosistreatment

The choice of therapy depends on

• Presenting symptoms and their severity• Location and severity of endometriosis• Desire for future childbearing

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

Endometriosismedical therapy

3 groups of medicines:1. Danazol

2. Progestins

3. Gonadotropin-releasing hormone agonists

Progestinsendometriosis treatment

• Medroxyprogesterone acetate Provera tb 20 – 40 mg/d

• Depomedroxyprogesterone acetateDepo-Provera inj. i.m. 100 mg

/ 2 weeks – 8 weeks, than 200 mg/1 month

Progestinsendometriosis treatment

Progestins supress FSH/LH release and ovarian steroidogenesis

„pseodopregnancy”

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

Danazol endometriosis treatment

• Danazol-17α-ethinyl testosterone derivativetb 600 - 800 mg/d – 1 month, than 400 mg up to 6 months

• Supresses FSH/LH release and steroidogenesis endometrial atrophy

„pseudomenopause”

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

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

GnRh agonists endometriosis treatment

• Pituitary desensybilisation supress FSH/LH release

„a state of pseudomenopase”

GnRh agonists endometriosis treatment

• Adverse effects:

hypoestrogenic propierties without androgenic effects

• The most expensive therapy but the most effective one

DYSMENORRHEA

PAINFUL MENSTRUATION

• Primary (absence of demonstrable pelvic disease)

• Secondary (presence of pelvic pathology – endometriosis, chronic PID, uterine leiomyomas)

HOW TO DISCOVER THE CAUSE OF DYSMENORRHEA ?

• Diagnostic laparoscopy

• Empiric drug therapy

• USG, RTG, MRT, CT

• Laboratory tests

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

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.

PATHOPHYSIOLOGY

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

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

TREATMENT

• ANTIINFLAMMATORY AGENTS (inhibition of prostaglandin production and action)

IBUPROFEN (arylopropionic acid derivative)

4 x 400 mg/24 h for 3 – 4 daysNAPROXEN (mefanemic acid or it’s sodium salts)

• ORAL CONRACEPTIVES(suppress endometrial PG production by inhibiting ovulation)

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 100-200 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

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

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

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.