Definition:
• Endometriosis isthe presence of functional endometrial tissue (glands and stroma)
situated in other sites other than the endometrial mucosa.
• Endometrial tissue s most commonly found in the pelvis (the posterior uterus;
ovary; broad ligaments; the uterosacral ligaments; and fallopian tubes); but can be
found in the bowl; bladder and diaphragm .
• Endometriosis has been found as far away as the breast; lungs and brain.
• Endometriosis in the ovary commonly appears as cystic collection known as an
endometrioma.
3.
Potential sites forendometriosis. The most common sites indicated by blue dots.
Risk factors
. 1st
degreerelative (mother or sister)
. Autoimmune inflammatory disorders including lupus and thyroiditis
. Certain types of epithelial ovarian cancers-( clear cell; endometrioid and low grade
serous)
. Nulliparity > 30 years
. Early menarche
. Prolonged menses
. Mullerian anomalies
7.
PATHOGENESIS:
• There areseveral theories about the pathogenesis of endometriosis which
congregate around two main themes:
I. Endometrial implants that arise from ectopic endometrium.
II. Implants that arise from tissues separate from the endometrium.
The principal ones are:
a. Retrograde menstruation (Sampson’s theory)
This theory suggests that endometrial tissue is transported through the fallopian
tubes during retrograde menstruation ,resulting in intra-abdominal pelvic implants.
8.
There isretrograde flow of menstrual blood through the uterine tubes
during menstruation.
The endometrial fragments get implanted in the peritoneal surface of
the pelvic organs (dependent sites, e.g. ovaries, uterosacral ligaments).
Subsequently, cyclic growth and shedding of the endometrium at the
ectopic sites occur under the influence of the endogenous ovarian
hormones
9.
b. Coelomic metaplasia(Meyer’s theory)
This theory proposes that multipotent cells in the peritoneum tissue undergo
metaplastic transformation into functional endometrial tissue
Chronic irritation of the pelvic peritoneum by the menstrual blood may cause
coelomic metaplasia which results in endometriosis.
Alternatively, the Mullerian tissue remnants may be trapped within the
peritoneum and they could then undergo metaplasia and be transformed into
endometrial tissue
c.
10.
c. Direct Implantation
According to this theory, the endometrial or decidual tissues
start to grow in susceptible individual when implanted in the
new sites.
Such sites are; abdominal scar following hysterectomy,
caesarean section, tubectomy and myomectomy.
Endometriosis at the episiotomy scar, vaginal or cervical site
can also be explained with this theory.
11.
Contn.......
d.Lymphatic theory( Halbantheory )
This theory proposes that the endometrial tissue is transported via the
lymphatic system to various sites in the pelvis where it grows
ectopically.
e. Vascular Theory:
This explains endometriosis at distant sites such as lungs, arms or
thighs.
12.
F. Genetic andimmunological factors
Genetic basis of endometriosis probably accounts for less
than 10 percent of the patients.
There is 6–7 times increased incidence in first degree
relatives.
Multifactorial inheritance is thought of however, a defect of
local cellular immunity may be responsible for the ectopic
tissue to grow in abnormal sites only in susceptible women.
is and interfere with fertilization.
13.
Abnormalities inboth cellular and humoral components show
involvement in various cytokines and growth factors in the pathogenesis.
Pelvic endometriosis is associated with a subclinical peritoneal
inflammation resulting in increase in peritoneal fluid.
In patients with endometriosis, the activated macrophages secrete
several factors like cytokines, interleukin–1, α TNF, integrins and
angiogenic factors.
These factors promote the growth of endometrial cells over the ectopic
sites.
Ectopic endometrium is more resistant to apoptosis.
14.
Furthermore activatedmacrophages reduce sperm motility, increase sperm
phagocytosis and interfere with fertilization.
g. Environment theory
Suggests somatic mutations of cells due to environmental factors
(pollutants, dioxins).
Ovarian and deep infiltrating endometriotic lesions are explained with this
theory.
Thus, it is certain that, not all cases of endometriosis at different sites can
be explained by a single theory
15.
Theories to explainendometriosis
at different sites
Site Theory
Pelvic Endometriosis
Pelvic peritoneum
Retrograde menstruation
Ceolomic metaplasia
Abdominal viscera
Rectovaginal septum
Umbilicus
Ceolomic metaplasia
Abdominal scar
Episiotomy scar
Vagina, cervix
Direct implantation
Lymph nodes Lymphatic spread
Distant sites, Lungs, Pleura, Skin, Nerves,
brain.
Vascular
Genetic and Immunologic
16.
Pathology
a) General Considerations
The endometrium (glands and stroma) in the ectopic sites has got the potentiality to
undergo changes under the action of ovarian hormones
proliferative changes are constantly evidenced, the secretory changes are conspicuously
absent in many; may be due to deficiency of steroid receptors in the ectopic endometrium
Cyclic growth and shedding continue till menopause.
17.
The periodicallyshed blood may remain encysted or else,
the cyst becomes tense and ruptures
As the blood is irritant, there is dense tissue reaction
surrounding the lesion with fibrosis and if it happens to
occur on the pelvic peritoneum, it produces adhesions and
puckering of the peritoneum
If encysted, the cyst enlarges with cyclic bleeding.
The serum gets absorbed in between the periods and the
content inside becomes chocolate colored.
18.
Hence, thecyst is called chocolate cyst which is commonly located in the
ovary.
Chocolate cyst may also be due to hemorrhagic follicular or corpus luteum
cyst or bleeding into a cystadenoma.
For this reason, the term endometrial cyst or endometrioma is preferred
to chocolate cyst
In spite of dense adhesions amongst the pelvic structures, the fallopian
tubes remain patent.
20.
b) Naked EyeAppearance:
• The appearance of the lesion depends to a great extent on the organ(s) involved, extent of
the lesion and reaction of the surrounding tissues.
Pelvic endometriosis typically, there are small black dots, the so called ‘powder burns’
seen on the uterosacral ligaments and pouch of Douglas , ovaries and pelvic
peritoneum.
Other subtle appearances are: red flame shaped areas, red polypoid areas, yellow brown
patches, white peritoneal areas, circular peritoneal defects or subovarian adhesions.
22.
These lesionsare thought to be more active than the “powder burn”
areas.
The ovaries are frequently involved usually bilaterally.
The endometriomas (chocolate cysts) are of varying sizes and are
visible as bluish colorations.
The ovaries get adherent to the pelvic structures including rectum and
sigmoid colon
23.
Clinical manifestations.
Symptoms ofendometriosis vary depending on the anatomical structures involved.
pain
Cyclic pelvic pain (75%)-begins before menses, peaks 1to 2 days before menstrual onset
and subsides at the onset of menses or shortly thereafter.
-Dysmenorrhea
Lower back pain
24.
Infertility (40–60%):
Whetherendometriosis causes infertility or infertility produces endometriosis is
not clear.
Endometriosis is found in 20–40 percent of infertile women, where as in about
40–50 percent patients with endometriosis suffer from infertility.
Dyspareunia (20–40%)
It may be due to stretching of the structures of the pouch of Douglas or direct
contact tenderness.
As such, it is mostly found in endometriosis of the rectovaginal septum or pouch
of Douglas and with fixed retroverted uterus
25.
Chronic PelvicPain
The pain varies from pelvic discomfort, lower abdominal pain or backache which may
be due to multi factorial causes such as:
(i) Inflammation in the peritoneal implants and release of PGF.
ii) action of inflammatory cytokines.
iii) invasion of nerves or involvement of the bladder and bowel.
. Abdominal Pain
There may be variable degrees of abdominal pain around the periods.
Sometimes, the pain may be acute due to rupture of endometrioma or chocolate cyst
(thick dark old blood and debris).
26.
Other Symptoms
The symptoms are related to the organ involved and include;
Urinary: frequency, dysuria, back pain or even hematuria
Sigmoid colon and rectum: painful defecation (dyschezia), diarrhea, constipation, rectal
bleeding or even melena
Chronic fatigue, perimenstrual symptoms (bowel,
bladder)
Hemoptysis (rarely), catamenial chest pain
Surgical scars, cyclical pain and bleeding.
27.
• DIAGNOSIS
physicalexamination , bimanual examination and rectal examination
laboratory ; CBC , HCG assay, RFTs, urine and vaginal cultures and Serum marker CA125
Imaging ;TVS, color doppler, MRI and CT
Colonoscopy
Laparoscopy or laparotomy -direct visualisation (The Gold standard)
Definitive diagnosis through direct visualization of the implants which vary widely in terms of
size, texture, and appearance.
28.
They mayappear as red vascular lesions, dark brown to
black powder-burn lesions, white fibrotic plaques, or as
Allen Masters window(peritoneal defects)
Endometrioma or chocolate cyst (large cystic collections of
endometriosis filled with thick dark, old blood and debris)
peritoneal biopsy is recommended for histologic
confirmation of the diagnosis of endometriosis. Extent of
disease and proper classification can be recorded
Complications of endometriosis
Endocrinopathy—This may be mostly responsible for infertility.
Rupture of chocolate cyst
Infection of chocolate cyst
Obstructive features:
Intestinal obstruction
Ureteral obstruction hydroureter hydronephrosis renal
→ → →
infection
Malignancy is rare, the commonest one being
adenoacanthoma
31.
Staging
The diagnosed endometriosisshould be appropriately staged based on
laparoscopic findings.
To predict prognosis
To choose therapy
To evaluate the treatment protocol.
The scoring is (revised) by the American Fertility Society.
32.
Staging cotn....
• Itdepends on
• Location
• Extent
• Depth of endometriosis implants
• Presence and severity of adhesions
• Presence and size of ovarian endometriosis
34.
Limitations of AmericanFertility Society (AFS) staging
Laparoscopy or laparotomy has to be done.
Interobserver and intraobserver variation.
No correlation between the extent of disease and the degree of symptoms
35.
Treatment OF ENDOMETRIOSIS
Endometriosis needs to be treated as it is a progressive
disease (30–60%).
The following are the modes of treatment that can be
employed:
Medical treatment.
This is aimed at suppression and atrophy of the endometrial
tissues.
- Analgesics (NSAIDs)
- Hormonal therapy ie cyclic or continuous estrogen-
progestin contraceptives-pills; patches; rings; and menstrual
suppression with progestins- oral; injectable or intrauterine.
-
36.
• Progestines
• GnRHantagonists eg Elagolix
• Aromatase inhibitors
• Gonadotropin releasing hormone agonist- nafarelin; goserelin and leuprolide
Preventive through,
Avoiding tubal patency test immediately after curettage or around the time of
menstruation
Avoiding forcible pelvic examination during or shortly after menstruation.
Encouraging married women with family history of endometriosis not to delay the
first conception.
37.
Surgical Treatment
Conservative(Fertility sparing); Laparoscopy
Non Conservative (Non fertility sparing); Hysterectomy and
Oophorectomy.
Combined medical and surgical treatment
medical therapy before surgery s used:
- to decrease the size of the endometral mplants
- to reduce the extent of surgery
Post operative medical therapy:
When complete removal of the implant is not possible or
advisable; it is used to treat residual disease.
38.
All the abovetreatment options depend on:
Age of patient
Size and extent of lesion
Severity of symptoms
Location of disease
Desire for fertility
Results of previous therapy
