Endometriosis

By
Lena Gowharji

 Ann, is a 35 year old lady,

complaining of intermittent
abdominal pain, bloating and sever
dysmenorrhoea. She has a previous
history of IBS, but recently noticed
that her symptoms are all much
worse in the week before her period.
On examination she is slim, the
abdomen was distended, non tender,
and no masses were felt. The uterus
was anteverted, mobile and no
abnormalities were found in the
adnexia.

Endometriosis
Definition: Benign condition in which
(hormone dependant) endometrial glands
and stroma are present outside the
uterine cavity and wall.
Its importance is due to its
1- Distressing symptomatology
2- Association with infertility
3- Invasive potential (adjacent organs)
4- Difficulty in being diagnosed

 Incidence:
*Its estimated that 5-15% of women have
some degree of the disease.
*1/3 of women with chronic pelvic pain have
visualized endometriosis.
*Its been noted in 5-15% of women
undergoing gynaecological laparotomies (an
unexpected finding in 50% of these cases).

 Age: It classically presents in nulliparous

infertile women in their 30s.
However, it may occur at earlier ages
(childhood and adolescents) and in such
cases its associated with obstructive genital
anomalies.
Following menopause, it regresses unless
estrogen is prescribed. 5% of new cases
develop in that age group.

 Pathogenesis: is not fully understood

However
1- genetic predisposition
2- immunological changes
have been reported to clearly play a role.
Several hypotheses have been used to
explain the various manifestations of the
disease and its various locations
1- The Retrograde menstruation theory
2- The Mullarian metaplasia theory
3- The lymphatic spread theory
4- The hematogenous spread theory

1- The retrograde menstruation

theory of Sampson: proposes that
endometrial fragments that are shed
during menstruation are transported
through the fallopian tubes, then
becoming implanted and growing in
various intra-abdominal sites. (These
endometrial fragments are viable and
capable of growing in vivo and in
vitro)

2- The mullarian metaplasia theory of Meyer:

proposes that endometriosis results from the
metaplastic transformation of peritoneal mesothelium
to endometrium under the influence of certain
unidentified stimuli.
3- The lymphatic spread theory of Halban: suggests
that the lymphatics draining the uterus transport
endometrial tissue to various pelvic site where it
grows ectopically.
*Endometrial tissue has been found in up to 20% of
patients with the disease
4- The haematogenous spread theory: explains the
presence of endometrial tissue in distant sites (lung,
axilla and forehead)

 Why dont all menstruating women develop

endometriosis?
*It has be found that the amount of exposure to
retrograde menstruation and the womans
immunological response are most critical.
*Researchers have found differences in the
chemical composition and biological pathways
of the endometrial cells in women who have
endometriosis in comparison to those who
dont.
They have also found a difference in the
inflammatory mediators and growth factors in
the peritoneal fluid of those with endometriosis
in comparison to those without.

 Sites of occurrence:
* Most commonly found in the dependant portions of
the pelvis
1- Ovaries (2 out of 3 women with endometriosis)
2- Broad ligament
3- Peritoneal surfaces of the cul-de-sac
(uterosacral ligaments and post. Cervix)
4- Rectovaginal septum
* Quite frequently is the recto-sigmoid colon, appendix,
and vesicouterine fold of the peritoneum involved.
* Laparotomy scars esp. after c section or
myomectomy or after the uterine cavity has been
entered.

 Pathology:
* The islands of endometriosis are sensitive to
ovarian hormones.
*Estrogen

proliferation

*Regression of corpus luteum and removal of

estrogen and progesterone causes them to
slough.
*These sloughed debris induce a profound
inflammatory response that causes significant
pain and long term fibrosis.

 Macroscopical appearance:
Depends on: site, size, time since
implantation and day of the menstrual cycle.
Colour is a good indicator and is determined
by the vascularity of the lesion, the presence
of fibrosis, the size of the lesion and the
presence of residual sloughed material.
It varies from red, brown, black, white-yellow.
*Newer implants: red, blood filled active
lesions
*Older lesions: scarred with a puckered
appearance.

 Microscopically: 2 out of 4 must be

present in the biopsied specimen to
confirm Dx
1- endometrial epithelium
2- endometrial glands
3- endometrial stroma
4- hemosiderin laden macrophages

 Endometriosis of the Ovary:

These are cysts filled with thick chocolate
coloured fluid; which may have a black tarry
consistency sometimes.
* This characteristic fluid represents aged,
haemolysed blood and desquamated
epithelium.
* The glands and stroma lining the cysts wall
may be destroyed due to an increase in
pressure. This leaves behind a fibrotic wall
with infiltrating haemosiderin layden
macrophages.

Risk factors for

endometriosis:
1. Nulliparity.
2. Infertility.
3. Reproductive age (usually, late teens
to 40s).
4. A first-degree relative with
endometriosis.
5. Regular menstrual cycle <27 days.
6. Prolonged menses of 8 or more days.

 Many patients are

asymptomatic.
Others usually have no positive
signs at examination.

The characteristic triad

of symptoms:
1- dysmenorrhea.
2- dyspareunia.
3- dyschezia.

Other symptoms:
Female reproductive tract:
1- pre and postmenstrual spotting.
2- cyclic pelvic pain.
3- low sacral backpain (especially
premenstually).
4- infertility.
5- diminished amount of menstrual flow.
6- ovulatory pain and mid-cycle vaginal
bleeding.

 If the Bladder is involved:

1- cyclic hematuria/ dysuria.
2- ureteric obstruction.
If the rectosigmoid colon is involved;
1- premenstrual tensmus or diarrhea.
2- obstruction.

Signs:
Tenderness on bimanual examination.
Tenderness or nodularity on the posterior
vaginal fornix.
Uterosacral ligament tenderness or
nodularity.
Cystic ovarian enlargement.
Fixation of adnexal structures.
Retroflexed uterus.
Episiotomy or cesarean section scars.

Differential diagnosis
1. Chronic pelvic inflammatory
disease or recurrent acute
salpingitis.
2. Hemorrhagic corpus luteum.
3. Benign or malignant ovarian
neoplasm.
4. Ectopic pregnancy.

Diagnosis
History and examination
Pelvic U/S
Direct visualization of endometriotic
lesions
Pathological examination of biopsy
specimen
Endometriosis in not a clinical diagnosis!

Diagnosis
Suspected in afebrile patient with
the characteristic triad:
1. Pelvic pain
2. Firm, fixed tender adnexal
mass
3. Tender nodularity in cul-de-sac
and uterosacral ligament

Diagnosis
(CA 125)
Frequently elevated in women
with endometriosis
Sensitivity only 20% to 30%
Not used to diagnose
endometriosis

Diagnosis
Definitive diagnosis is generally
made by:
Characteristic gross
Histological findings
Obtained by:
Laproscopy or laprotomy
Endometriosis in not a clinical
diagnosis!

Diagnosis
What do endometriosis lesions look like?
Classic are red, dark brown, dark blue or black
peritoneal implants
chocolate cysts of the ovary
Clear vesicles
White or yellow spots or nodules
Normal appearing peritoneum (microscopic disease)
Later lesions appears as powder burn implants from
thickened or scarred perilesional peritoneum

Diagnosis
Unfortunately, even the most experienced
surgoen may fail to identify endometriosis
implants because:
The older implants may have a very subtle
apperance
The deeper infiltration lesions may not be
visible at the surface
Biopsy of suspecious lesions improves
diagnosis accuracy

Staging
American Society of Reproductive
Medicine (ASRM)
Employs a staging protocol in an
attempt to correlate
Fertility potential with a quantified stage
of endometriosis

Staging
Initially started to be based on:
1- Site of involvement
2- extent of visualized disease
And was modified to include:
Description of the color of the lesions
Percentage of surface involved in each
lesion type
More detailed description of any
endometriosis

If the fimbriated end of fallopian tube is completely

enclosed, change the point assignment to 16
Denote appearance of superficial implant type as
RED [(R), red, red-pink, flamelike, vesicular
blobs, clear vesicles]
WHITE [(W), opicifications, peritoneal defect,
yellow-brown]
BLACK [(B), black, hemosiderin deposits, blue]
Denote % of total described as R__%, W__%, B__
%

Treatment
1.
2.
3.
4.
5.

No treatment
Non-hormonal treatment
Hormonal treatment
Surgical treatment
Radiological treatment

I. No treatment
If small symptom less lesions
Patient observed & examined
every 6 months

II. Non-hormonal
treatment
If small lesions with mild symptoms
Analgesics are given for pain
Prostaglandin inhibitors (naproxen,
ibuprofen) are given for pain and
menorrhagia

III. Hormonal
treatment
Indications:
1. Severe symptoms with small pelvis lesions
2. Recurrence of symptoms after conservative
surgery
3. May be given for a short time (6-12 weeks)
before surgery to make dissection easier
4. After conservative surgery to allow any
residual lesion to regress
5. When operation is contraindicated or
refused by the patient

1. Pseudo pregnancy
Ovulation and menstruation are inhibited
for 9 months (6-18 months) using a
combined OCP or a progestogen alone to
avoid the oestrogenic side effects
A combined contraceptive tablet is given
daily
Oral medroxyprogesterone acetate
(provera tablets) is givin in a dose of 1030 mg daily
Side effects of progestogens: headache,
weight gain, fluid retention, breakthrough
bleeding and depression

2. Pseudo menopause
Danazol:

given orally 400-800 mg/day for 6-9 months

Weak synthetic androgen

Side effects:
1.
Androgenic effects: acne, male alopecia, hirsutism, hoarseness of
voice & hypertrophy of clitoris
2.
Hypo-oestrogenic effects: hot flushes, sweating, atrophy of
breasts, atrophic vaginitis, dry vagina, dyspareunia & decreased
libido
3.
Anabolic effects: weight gain & edema
4.
Metabolic effects: impaired glucose tolerance, increased insulin
requirements in diabetic cases, hepatic dysfunction. Blood
pressure may be elevated
5.
CNS: headache, sleep disorders, anxiety, depression & visual
disturbance
6.
GIT: nausea, vomiting & constipation
7.
Muscloskeletal: muscle cramps & swelling of joints
8.
Genitourinary: hematuria

2. Pseudo menopause
GnRH (agonist):
Nafarelin (synarel): intranasally using a
nasal spray, 200 micrograms twice daily
Goserelin (zoladex): 3.6 mg injected SC
every 4 weeks
Triptorelin ( decapeptyl): 3.75 mg injected
IM every 4 weeks
Side effects: hot flushes, dryness of the
vagina, dyspareunia & reduced libido

3. Mifepristone
50 mg/day for 6 months

IV. Surgical treatment

Indications:
1. Large lesions
2. When hormonal therapy fails

Surgery is conservative or radical

1. Conservative
surgery
If young patients below 40 years
Pre-sacral neurectomy has been
used to treat severe dysmenorrhea
Minimal to mild disease can be
removed by laser or electrocautery

2. Radical surgery
Patient above 40 years
Treatment is total hysterectomy &
bilateral salpingo-oophorectomy

Endometriosis

Removal of
Endometriosis

Dissection of an Endometrioma
Ovary
Incision
Tube

Removal

Result

V. Radiological
treatment
Induction of artificial menopause by
external pelvic radiation cures the condition
by causing atrophy of endometrial tissue
It is applied only in patients above 40 in
whom operation cant be done as in case
of wide spread pelvic endometriosis (frozen
pelvis) or endometriosis of the rectovaginal
septum which is difficult to excise surgically

Thank you