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DEFINITION
 Presence of endometrial tissue (both glands & stroma) outside the
uterus.
 Tissue is morphologically and functionally similar to endometrial
tissue  responds to hormones in cyclical manners.
AETIOLOGY: theories
1. Sampson’s theory of menstrual regurgitation and implantation
(Metastatic theory)
 Retrograde menstruation
↓
Endometrial fragments are transported to peritoneal cavity
through tubes
↓
Viable cells implant & grow
 Young girls with obstructive anomalies of genital tract often
develop endometriosis.
2. Coelomic metaplasia theory:
 Original Coelomic membrane transforms into endometrial tissue.
 Explains endometriosis in ectopic sites.
3. Lymphatic & vascular metastases theory:
 Lymphatic & hematogenous spread of endometrial cells
 Extensive communication of lymphatics between uterus, tubes,
ovaries, pelvic & vaginal lymph nodes, kidneys & umbilicus.
4. Genetic factors: risk is 7 times more if first degree relative has
endometriosis.
4. Immunological factors: reduced clearance of endometrial cells
due to decreased natural killer cell activity or decreased
macrophage activity.
5. Inflammation: endometriosis maybe associated with subclinical
peritoneal inflammation
SITES
TYPES OF ENDOMETRIOSIS
PELVIC ENDOMETRIOSIS EXTRA PELVIC ENDOMETRIOSIS
• Peritoneal • Gastrointestinal tract
• Ovarian • Urinary tract
• Deep infiltrating • Scar endometriosis
• Vaginal endometriosis
• Thoracic endometriosis
CLINICAL PRESENTATION
PAIN:
• Classical triad: dysmenorrhea, dyspareunia & deep seated pelvic pain.
• Commence before onset of menses & continue throughout the
menstrual period. Also has a cyclical nature.
• Deep dyspareunia due to stretching of involved tissue during
intercourse.
• Fixed retroverted uterus or involvement of uterosacrals and
rectovaginal septum.
• Dysuria & dyschezia: in extragenital endometriosis
ABNORMAL BLEEDING:
• May include premenstrual spotting, polymenorrhoea & menometrorrhagia.
INFERTILITY:
• Present in majority of the women with endometriosis.
• Advanced disease, adhesions and fixity results in structural damage to
tubes and ovaries  impairs tubo-ovarian mobility.
• Ovarian problems: anovulation, luteinized unruptured follicle, oocyte
maturation defects.
• Tubal problem: altered tubal motility or ovum pick up.
• Peritoneal factors: intraperitoneal inflammation
• Sperm problems: phagocytosis by macrophages, inactivation by antibodies.
• Endometrium: luteal phase defect, implantation defects
OTHER SYMPTOMS
• Extrapelvic endometriosis: cyclical rectal bleeding or
hematuria.
• Scar endometriosis: cyclical pain and bleeding at scar.
• Umbilical endometriosis: present as umbilical mass with cyclical
pain.
• Pulmonary endometriosis: cyclical hemoptysis and hemothorax.
SIGNS & SYMPTOMS
SYMPTOMS SIGNS
• Dysmenorrhoea • Tenderness in cul-de-sac
• Dyspareunia • Nodularity in cul-de-sac
• Deep seated pelvic pain • Fixed retroverted uterus
• Dysuria • Adnexal tenderness
• Dyschezia • Adnexal masses
• Hematuria
• Infertility
INVESTIGATIONS
TRANSVAGINAL ULTRASOUND SCAN
• Retroverted uterus with obliteration of cul-de-sac &
BL complex adnexal masses maybe suggestive.
• Helps to differentiate endometrial cysts from other complex cysts like
dermoids:
• Endometrial cyst: low level internal echoes with posterior acoustic
enhancement – Ground glass appearance.
• Dermoid: posterior acoustic shadowing d/t presence of bone &
teeth in cyst. Presence of mural nodule & “pins and needle”.
CA-125
 Increased in moderate to severe endometriosis
 Also increased in non-mucinous epithelial ovarian cancers.
LAPAROSCOPY
• Gold Standard
• During laparoscopy, entire pelvis should be examined
systematically in clockwise or counterclockwise direction.
• Aims:
• Detection and biopsy of lesions
• Staging disease
• Concomitant laparoscopic surgical treatment
1. PERITONEAL LESION
CLASSIC LESIONS:
• Powder burn or gunshot lesion: black to dark brown nodules
consisting of old hemorrhages surrounded by fibrosis.
• Scarring
• Adhesions: b/w ovary & broad ligament and b/w posterior uterus or
vagina & sigmoid colon.
SUBTLE LESIONS:
• Red lesions: flame like lesions and glandular excrescences.
• White lesion: white opacities, yellow peritoneal patches and
circular peritoneal defects.
2. OVARIAN ENDOMETRIOSIS
ENDOMETRIOMA OE CHOCOLATE CYST:
• Cyst contains thick tarry fluid- chocolate fluid – derived from previous
ovarian hemorrhage.
• Adherent to broad ligament and pelvic side wall.
SUPERFICIAL OVARIAN ENDOMETROSIS:
• Superficial implants on ovary.
• There can be adhesions to ovarian bed: Sub-ovarian
adhesions
3. DEEP INFILTRATING ENDOMETRIOSIS
• Lesions are usually in rectovaginal space.
• May involve uterosacral ligaments, cervix, bowel or ureters.
• Lesions cause adhesion and scarring.
• Can be felt on pelvic and rectal examination as tender nodularity.
4. EXTRAPELVIC ENDOMETRIOSIS
GASTROINTESTINAL TRACT:
• Frequently involved: sigmoid, rectum, iliocaecum & appendix.
• Symptoms: abdominal pain, disturbed bowel function & cyclical rectal
bleeding.
• There maybe pain on defecation.
• Superficial implants maybe seen on serosa.
URINARY TRACT:
• Common symptoms: cyclical hematuria, dysuria and frequency.
• Pelvic ureter & bladder shows implants  obstruction and
hydronephrosis.
Extrapelvic endometriosis cont.
SCAR ENDOMETRIOSIS:
• Seen at umbilicus, port sites following laparoscopy, abdominal
incisions following cesarean section and episiotomy scars.
• Present as painful swelling more prominent at menstruation.
• Cyclical bleeding is rare.
VAGINAL ENDOMETRIOSIS: Occurs in posterior fornix as a continuation
of endometriosis from cul-de-sac.
THORACIC ENDOMETRIOSIS: Lungs & thorax maybe involved leading to
cyclical hemoptysis & hemothorax.
INVESTIGATIONS
CT & MRI: Identical picture as in USG
COLOUR DOPPLER FLOW: Increased vascularity
CYSTOSCOPY: Involvement of bladder
SIGMOIDOSCOPY: If the women develops bowel symptoms
ANTIENDOMETRIAL ANTIBODIES: In serum, peritoneal fluid &
endometriotic fluid as well as in normal endometrial tissue
TNF: Raised proportionate to the disease
HISTOLOGY
 Histologic confirmation is essential.
 On microscopy, typical endometrial implant with endometrial
glands & stroma
CLASSIFICATION OF ENDOMETRIOSIS
• Stage I: MINIMAL: Score 1-5
• Small spots of endometriosis seen at laparoscopy, but no clinical
symptoms.
• Stage II: MILD: Score 6-10
• scattered fresh superficial lesions.
• No scarring or retraction or adnexal adhesions.
• Stage III:MODERATE: Score 16-40
• Contain endometriomas <2cm in size.
• Minimal Peritubal and periovarian adhesion.
• Stage IV: SEVERE: Score >40
• Endometriomas exceed 2cm.
• Dense Peritubal & periovarian adhesions restrict motility.
• Thickened uterosacral ligaments.
• Involvement of bowel and bladder.
DIFFEERENTIAL DIAGNOSIS
 Chronic PID
 Postoperative adhesions
 Old ectopic gestation
 Pelvic congestion syndrome
 Irritable bowel syndrome
 Diverticulitis
 Ulcerative colitis
 Crohn’s disease
MANAGEMENT
Management of
Endometriosis
Asymptomatic minimal
endometriosis
Observe 6-8 months,
Investigate infertility
Symptomatic cases
Drug treatment
Minimal invasive
surgery
Surgery
DRUG TREATMENT
1. Combined oral contraceptives:
• Administered intermittently or continuously.
• High Incidence of side effects & risk of thrombus-embolism limit their
prolonged use.
• Seasonal OC for 84 days , with 6 days tablet free, reduce the
menstrual periods to just four cycles in a year.
2. Oral progestogens:
• Exert an anti-oestrogenic effect and their continuous administration
causes decidualization and endometrial atrophy.
• Norethisterone 5.0 – 20.0mg daily or Dydrogesterone 10 -30mg daily.
• This hormone does not prevent ovulation and is suitable for a woman
trying to conceive.
DRUG TREATMENT
3. Danazol
• A synthetic derivative of ethinyl testosterone,
• Mildly anabolic , anti-oestrogenic and anti-progestational
• 200-800mg daily for 3-6 months starting on first day of menses.
• S/E: wt. gain, hirsutism, excessive sweating, muscle cramps,
depression, atrophy of breasts & vaginal epithelium.
4. Aromatase inhibitors:
• Letrozole(2.5mg), anastrozole(1-2mg) daily for 6 months.
• Anti-oestogenic & prevent conversion of androgen to oestrogen.
• Should be given with Vitamin D and Calcium to prevent
osteoporosis.
• Nausea , vomiting and diarrhea are other side effects.
Drug treatment
5. Gonadotropin releasing hormone:
• GnRH is administered continuously to down regulate and suppress
pituitary gonadotropins .
• It causes atrophy of endometriotic tissue.
• The synthetic analogue of GnRH is given in doses of 10-20mg
intravenously twice daily.
• Prolonged GnRH therapy over 6months causes hypo-oestrogenism &
menopausal symptoms such as hot flushes, dry vagina, urethral
syndrome and osteoporosis.
6. RU-486:
• Tried at a dose of 50mg daily for 3months.
• Reduces pain and delay recurrences.
DRUG THERAPY
Failure of drug therapy is due to :
• Drug cannot penetrate fibrotic capsule.
• Ectopic endometrium responds less to hormones as compared to
normal endometrium.
• S/E: prevent conception
MINIMAL INVASIVE SURGERY
1. Aspiration of peritoneal fluid in cul-de-sac.
2. Destruction of endometriotic implants <3cm by diathermy
cauterization or vaporization by CO2 or Nd:YAG laser.
3. Larger lesions and chocolate cyst can be excised. Residual lesion can
be dealt with by hormonal therapy. Cauterization of cyst wall – young
females.
MINIMAL INVASIVE SURGERY
4. Role of surgery:
 Failed Medical therapy
 Infertility
 Recurrence
 Chocolate cyst ovary
5. Laparoscopic breaking of adhesions in pelvis relieves dysmenorrhea
and pelvic pain.
6. LUNA (Laser uterosacral nerve ablation) for midline pain.
7. Prolapse of genital tract & bladder dysfunction is noted with LUNA.
SURGERY
Indications for surgery:
 Advanced stage of disease detected
 Large lesion
 Medical therapy fails or intolerable
 Recurrence occurs
 In elderly parous women
Aim:
 Coagulation of peritoneal endometrial lesions
 Adhesiolysis
 Fenestration & drainage of small ovarian endometriomas <3cm
diameter. Cystectomy- >3cm.
SURGERY
Laparotomy:
• In advanced & larger lesions if medical therapy fails.
• Dissection and excision of a chocolate cyst.
• Salpingo-oophorectomy
• Abdominal hysterectomy and bilateral salpingo-oophorectomy.
• Premenopausal woman may need HRT after radical surgery.
• HRT following bilateral ovarian removal in young women may be
prescribed under strict monitoring, as a risk for recurrence remains.
Total hysterectomy & B/L oophorectomy- women with severe
symptoms & those with fertility is not a problem.
COMBINED THERAPY
 Preoperative GnRH:
 monthly for 3 months
 reduces size & extend of lesions,
 softens adhesions
 makes subsequent surgery more easier & complete.
 Postoperative hormonal therapy:
 When surgery is incomplete or some residual lesion is left behind.
PROPHYLAXIS
• Low-dose OCP reduce the menstrual flow & protect against
endometriosis. 3 monthly OCP’s are convenient to take &
effective.
• Tubal patency tests should be avoided in immediate
premenstrual phase to avoid spill.
• Operations on genital tract should be scheduled in postmenstrual
period.
THANK YOU