ENDOMETRIOSIS

Definition (ten teachers)

Presence of endometrial surface epithelium and/or the presence of endometrial glands and
stroma outside the lining of the uterine cavity.

Most common sites are peritoneum and ovaries

Epidemiology

 15% women with gynecological symptoms have the condition.

 3rd most commonest gynecological condition that requires hospital admission
 Leading cause for hysterectomy
 Peak incidence 30-45 yrs of age
 Increased incidence among oriental woman and low prevalence in woman of Afro-Caribbean
origin

Pathophysiology (ten teachers)

Exact etiology is unknown
There are 4 suggested theories

1. Menstrual regurgitation and implantation

- Retrograde menstrual regurgitation of viable endometrial glands and tissue on to
peritoneal surface and subsequent implantation.
- As endometriosis commonly found in females who has abnormalities of the
genital tract causing obstruction to the vaginal outflow of menstrual fluid.
2. Coelomic epithelium transformation
- There is common origin –cells lining the Mullarian duct/peritoneal cells/ cells of
ovary.
- This theory says that these cells undergo re differentiation in to their primitive
origin and then transform in to endometrial cells.
- This transformation may due to -
Hormonal stimuli
Unidentified chemical substances from uterine endometrium
Chemical substances produce from inflammatory irritation
3. Genetic and immunological factors
- Genetic and immunological factors may alter susceptibility of a woman to
develop endometriosis
- This is suggested as increased incidence in first degree relatives of patients with
the disorder
- And racial differences of endometriosis
4. Vascular and lymphatic spread
- Vascular and lymphatic embolization to distant sites outside the peritoneal
cavity
Ex: endometriosis in rare distant sites such as lungs, skin & kidney

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 5. Other factors
- Surgical transplantation
- Digoxin exposure (damage to the immunity
 Pathogenesis may be combination of several theories.

Classification of endometriosis
According to site
According to histological sub types

Histological sub types

Histological Components Hormonal Laparoscopic

subtypes response appearance
Free Surface epithelium Proliferative, secretory Hemorrhagic vesicle
(Polypoidal cauli glands and stroma and menstrual changes /bleb
flower like structures Highly responsive to
grow along the surface alteration of oestrogen
or cover a cystic Very sensitive to
structure) hormonal suppression
Enclosed Located within tissue Proliferative and Papule and later
(implant covered with or within part of a free variable secretory nodules
surface layer of growing lesion change
peritoneum) (glands and stroma) No menstruation
(lesions react in a
similar way to basal
endometrium)
Healed Glands only Insensitive to White nodule or
Absence of functional hormonal stimuli flattened fibrotic scar
stromal cells Yellow brown
peritoneal
discoloration

Classification according to the site

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 Ovarian endometriosis
2 types of lesions in the ovary
Superficial lesions
Enclosed hemorrhagic cyst

1. Superficial lesions
- Superficial lesions commonly present as superficial hemorrhagic lesions and red
vesicles or blue-black “powder burn” lesions
- Hemorrhagic lesions are commonly associated with adhesions formation
- When adhesions involve posterior aspect of the ovary results rapid fixation of
the ovary within ovarian fossa
2. Endometrioma
- Endometrioic cyst of the ovary (or chocolate cyst)
- Characteristic dark brown content within the cyst
- Cyst wall can be lined by free endometrial tissue (which is histologically and
functionally similar to endometrial tissue)
- Long standing cases cyst may be only covering by thickened fibrotic reactive
tissue no specific stromal or glandular component
- These are thought to be commence on the outer surface initially and then
inversion of ovarian cortex
- Leakage from cyst wall leads to adhesion formation surrounding endometrioma
(posterior aspect of broad ligament and posterior aspect of ovarian fossa)
- Can be single or multiple
- May be very large

Pelvic endometriosis

- Uterosacral ligaments- thickening, nodularity, tenderness

- Broad ligament, posterior pouch, anterior pouch (less common)

Recto-vaginal septum endometriosis

- Endometriotic lesions in utero sacral ligament develops fibrosis and scarring

,and infiltrate in to recto vaginal septum
- Dense adhesions to rectum
- Partial or complete obliteration of pouch of Douglas
- Associated bowel symptoms
- Cause dyspareunia
- Palpable tender nodules in vaginal examination
- Deposits may protrude through posterior fornix as bluish spots
- Difficult to dissect due to rectum
- Difficult to visualize on laparoscopy

Peritoneal endometriosis

- Powder burn type lesions

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 Deep infiltrating endometriosis

- Endometrial glands and stroma infiltrating >5cm under the peritoneal surface
- Strongly associated with pelvic pain
- Those can develop in to severe pelvic distortion and severe pain
- These are often symptomatic
– dysmenorrohea/deep dyspareunia/chronic pelvic pain
- Painful defecation

ENDOMETRIOSIS - HISTORY
Demographic data

Age- reproductive age and ovulating woman, most common in women in the age of 30-45yrs

Parity- Nulliparous (more expose to menstruation high risk of getting endometriosis)

Parus women can get adenomyosis

Presenting complaint and history of presenting complaint

1. About 1/4th with endometriosis are asymptomatic

2. Pain – most commonest symptom
 Congestive dysmenorrohea- usually commence after age of 30 yrs and then
Gradually get worse.
- Pain starts before onset of menstruation (pre menstrual build up and pelvic
congestion)
- With menstruation due to collection of blood pain increases severity and
peak at 2nd -3rd day
- With absorption of fluid back pain settle with few days after the
menstruation
 Ovulation pain - Severe pain in mid cycle.
 Deep dyspareunia - Due to endometriosis involving utero-sacral ligament
& recto vaginal septum
- Also due to fibrosis causing fixed uterus.
 Chronic pelvic pain - Due to pelvic adhesions and fibrosis
Non cyclic pain
 Lower sacral backache - Involvement of utero sacral ligament
 Acute abdominal pain - Due to rupture of chocolate cyst
- Or acute intestinal obstruction due to bowel wall fibrosis
and stricture formation
3. Sub fertility
Infertility and endometriosis – possible mechanisms
Ovarian function - luteolysis caused by prostaglandins
- Oocyte maturation defects
- Endocrinopathies
- Luteinized unruptured follicle syndrome
- Altered prolactin release
- Anovulation

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Tubal function - Impaired fimbrial Oocyte pick up
- Altered tubal motility
- Blockage of the lumen of the tubes due to kinking of tubes(due to
Adhesions) and endometriosis involving tube wall
Coital function - Deep dyspareunia – reduced coital frequency
Sperm function - Antibodies causing inactivation
- Macrophages phagocytosis
Early pregnancy - Prostaglandins induce immune reaction
Failure - Luteal phase deficiency
- affect implantation (in adenomyosis)

4. Menstrual abnormalities -Ovarian endometriosis can present with oligomenorrhoea

-Adenomyosis can present as menorrhagia

5. Symptoms related to distal sites

 Bowel- Cyclical painful defecation

Dyschezia (shooting type rectal pain)/tenesmus/constipation
Per rectal bleeding/features of intestinal obstruction
 Bladder- Dysuria, haematuria(menouria)/frequency/urgency
 Pulmonary- Haemoptysis, haemopneumothorax
 Pleura- pleuritic type chest pain, shortness of breath
 Umbilicus-cyclical bleeding

Past medical History

Previously diagnosed obstructive anomalies of genital tract

Past surgical History

LSCS

Family History
Family history of endometriosis

EXAMINATION

General examination
Ill looking due to pain
Pale
Depression due to menorrhagia
Features of iron deficiency anemia

Abdominal Examination
LSCS scar tenderness or swelling
Umbilicus tender or swollen
Abdominal mass in case of endometrioma

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Vaginal examination
Vulva tenderness/ skin infection
Pelvic tenderness/nodularity in pouch of Douglas
Uterus will be retroverted and fixed/enlarged uterus about 12-14 wk POA and tender
(adenomyosis)
Unilateral or bilateral adenexial masses

Speculum examination
Bluish colour spots in the posterior fornix

DIFERENTIAL DIAGNOSIS
1. Chronic pelvic infection
2. Endometriosis
3. Asher man syndrome

Differential Diagnosis of Endometriosis by Symptom

Generalized pelvic pain

- Pelvic inflammatory disease
- Endometritis
- Pelvic adhesions
- Neoplasms, benign or malignant
- Ovarian torsion
- Sexual or physical abuse
- Non gynecologic causes

Dysmenorrhea
- Primary
- Secondary (adenomyosis, PID, submucosal/cornual fibroid, cervical stenosis)

Dyspareunia
- Musculoskeletal causes (pelvic relaxation, levator spasm)
- Gastrointestinal tract (constipation, irritable bowel syndrome)
- Urinary tract (urethral syndrome, interstitial cystitis)
- Infection
- Pelvic vascular congestion
- Diminished lubrication or vaginal expansion because of insufficient arousal

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Infertility
- Male factor
- Tubal disease (infection)
- Anovulation
- Cervical factors (mucus, sperm antibodies, stenosis)
- Luteal phase deficiency

MANAGEMENT
Diagnosis
 With classical symptoms
 Investigations
 Incidental finding

INVESTIGATIONS

Hematological
CA 125 become elevated in endometriosis
-Sensitivity about 90%, specificity 30%
-Which is a glycoprotein expressed by epithelial cells with coelomic origin
-Raised significantly in ovarian CA, not that much in endometriosis
-Elevated levels reduce with treatment and rise with recurrence
-No diagnostic benefit
Anti endometrial antibodies in peritoneal fluid and serum

Imaging
1. Ultrasonography-TAS/TVS
Diagnosing endometrioma - homogenous hypoechoeic collection of echoes within an
Ovarian cyst

2. MRI
Better than USS
Can evaluate distal site involvement
Ovarian cyst or invasion to surrounding organs
Peritoneal deposits in mm diameter not well seen

Laparoscopy
Gold standard
Direct visualization (white plaque, blue black lesions, neovascularization)
Hemorrhagic dots (like gunshot powder burns)
Red polyps, yellow polyps
Adhesions and scarred regions

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 Biopsy
Most conclusive method
Typical appearance of glands and stoma seen in microscopically and surrounding tissue may
show fibrous reaction
Very important histological confirmation of the diagnosis endometrioma >4cm in diameter.
Histology confirms the diagnosis but (-ve) histological findings do not exclude the diagnosis

MANAGEMENT
Depends on,
1. Woman’s age
2. Her desire for pregnancy
3. Severity of the symptoms and extent of the lesions
4. Results of previous therapy

Expectant management
Minimal endometriosis with no other abnormal pelvic findings
Unmarried
Young married who are ready to start the family
Approaching menopause

Observations
With pain relief
Married ones encourage to conceive

Medical management

Pain relief
NSAIDS - Ibuprofen 800-1200mg/d
- Mefenemic acid 150-600mg/d
- Paracetamol
- Narcotics (codein)
Better effect with combine therapy

Other complimentary therapy for pain relief in endometriosis

 High frequency TENS (trans cutaneous electrical nerve stimulation)
 Acupuncture
 Vitamin B1 and Magnesium treatment

Hormonal treatment
Suppression ovarian function for

Aim to achieve
 Pseudo pregnancy
 Pseudo menopause
 Medical castration

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 1. Combined oral contraceptive agents
 Suppress LH and FSH and prevent ovulation and direct influence on endometrial
tissues as well, rendering it to become thin and compact and decidualization of
endometrial implants.
 Reduce severity of dysmenorrohea and menstrual blood loss
 But less use with usual regular monthly withdrawal bleeding
 2-3 packs without break is beneficial
 Educate missing 1-2 withdrawals bleeding not harmful
 Can use as long term treatment

2. Progestrogens
Cause pseudo pregnancy state and pseudodecidualization

Oral - MPA (medroxy progesterone acetate) – 10mg tds 6-9 months

Dydrogesterone 10mg bd 6-9 months
Noethisteron 5mg tds 6-9 months

IM - DMPA - 150mg monthly for 6 months

Required dose is little high and return to fertility also delayed

SE- breakthrough bleeding, breast enlargement, weight gain, fluid retention

3. GnRH analogue
Agonists
- Initially stimulation of gonadotrophin production
Long term use down regulation of receptors
Disturbed pulsatile secretion  inhibit LH, FSH scretion
Antagonists
Short term pituitary suppression
 Hypogonadotrophic hypogonadism or pseudo menopause
 There is associated 6% bone mineral loss (mainly at lumbar spine) which is not fully
reversible and hypoestrogenic side effects
 Thus add back therapy of low dose of estrogen and progesterone or estrogen only
therapy or Tibolone (synthetic steroid which mimics activity of estrogen)
 Not continued more than 6 months
 Leuprolide (lupron)- IM every month for 6 months
 Goseraline (Zoladex)- SC in upper abdominal wall in every 28 days
 Naferalin nasal spray- 1spray to one nostril in the a.m and another one spray to
other nostril at p.m. start therapy on day 2-4 of menstrual cycle.

4. Danazole/ Gastrinone
Synthetic androgen which inhibits LH and FSH results hypo estrogenic state and endometrial
atrophy
Expensive
Dose 800mg daily 4 divided doses for 6 months
Should be commenced early follicular phase of menstrual cycle, barrier method for
contraception must be used

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 Long term use - do alternative lipid profile and liver functions
SE-* weight gain/hirsutism/acne/odema/ deepening of voice/greasy skin/ovarian cancer
association
Gastrinone similar effects as Danazole, easy to administrate twice weekly 2.5mg and less
side effects
Other indications of Danazole are- Precocious puberty
- DUB
- Symptomatic fibroid

5. New treatments
 RU486 (mifepristone)
 SPRMs (selective progesterone receptor modulators)
 TNF- inhibitors
 Angiogenesis inhibitors
 MMP inhibitors (matrix metaloproteinases)
 Immunomodulators
 Estrogen receptors beta agonists
 Aromatase inhibitors

Surgical management

Ideal practice is diagnosis endometriosis and removal of endometrial deposits surgically

Conservative surgery- laparatomy or laparoscopic

Remove entire lesion in severe and deeply infiltrating disease with preservation of reproductive
organs and it is very effective in management of pain.

- Aspiration or enucleation of cyst/ laparoscopic cystectomy for ovarian endometrioma

- Or cyst drained and opened cyst wall and lining destroyed and vaporized with laser.
- Specially cyst >4cm should confirm diagnosis histologically
- Ablation of deposits by KTP laser or diathermy or CO2
- Laparoscopic uterine nerve ablation no effective in reducing dysmenorrohea and fertility
issues
- Symptom relief and improvement in fertility

Corrective surgery
- Adhesiolysis
- Partial excision of adenomyotic tissue – adenomyomectomy
- Tubal flushing with oil soluble media- improves fertility rate

Curative surgery
- Done when woman’s family was completed or in severe progressive endometriosis
- Definitive relief for the dysmenorrohea and pain
- Generalized endometriosis- TAH and BSO followed by HRT

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 ENDOMETRIOSIS ASSOCIATED INFERTILITY

IUI improves fertility in minimal to mild endometriosis

IVF indicated especially when tubal function is compromised or there is male factor infertility
or other treatments have failed.
Rx with GnRH agonists 3-6 months before IVF this increase rate of clinical pregnancy

ADENOMYOSIS

 Adenomyosis is characterized by presence of endometrial glands deep within the

myometrium
 Aetiology is unknown
 Patients with adenomyosis are usually multiparous & diagnosed in their late 30’s or early 40’s
 Presents with severe secondary spasmodic dysmenorrohea and increased menstrual blood
loss.
 Examination- bulky tender uterus
 USS features - Alteration of the echogenicity within the myometrium, due to localized
haemorrhage filled distended endometrial glands
 Investigation of choice in adenomyosis is MRI
 Rx as endometriosis and definitive treatment is hysterectomy

Laparoscopic excision of nodular lesions Cystic implants adjacent to the right ovary bluish appearance

Ovary with an endometrioma

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