ENDOMETRIOSIS BY DR. MEENAKSHI VEMPALLI

1. Presenter- Dr.Meenakshi Vempalli
Postgraduate , Dept of OBGYN
Mahatma Gandhi Medical College ,
Pondicherry
ENDOMETRIOSIS

3. INTRODUCTION
First described by Carl Von Rokitansky in 1860.
• Found in Medical literature in 1800’s
• But only in 20th century- common occurrence was appreciated
It is the presence of endometrial tissue (glands and stroma)
outside the uterus.
Has Unique pathology of benign proliferative growth process
yet having propensity to invade normal surrounding tissues.

4. • Average delay between onset of pain and surgically confirmed
endometriosis was quite long (8 years)
• Over past 2 decades, in delay in diagnosis & decline in
prevalence of advanced endometriosis at first diagnosis.
• Patient’s awareness about the disease has
Quality of life affected by :
Emotional impact of subfertility
Anger about disease recurrence
Uncertainity about future regarding
repeated surgeries/long term medical therapy & its side effects

5. Epidemiology:
Prevalence:
• Women of reproductive age +adolescents + post menopausal
women receiving HRT.
• Frequency –vary widely
• Prevalence-10%
• No information on incidence but temporal trends suggests
among reproductive age group.
Women with:
Pelvic pain /infertility -20-90%
Unexplained subfertility with or without pain -50%
Asymptomatic women undergoing tubal ligation
(women of proven fertility)- 3-43%

6. RISK FACTORS:
1. Early age at menarche
2. Shorter menstrual cycle length
3. Nulliparity
4. Mullerian anomalies
5. One of multiple fetal gestation
6. DES exposure
7. Endometriosis in 1st degree relative
8. High fat diet /red meat
9. Prior surgery / medical therapy for endometriosis
10. Taller women
11. Dioxin /polychlorinated biphenyl exposure
12. Pin point cervix

7. PROTECTIVE FACTORS:
• Multiparity
• Lactation
• Tobacco exposure in utero
• BMI
• Waist to hip ratios
• Diet high in vegetables & fruits
Prior use of contraception, Intra uterine device and smoking is not
associated with increased risk od endometriosis

8. Endometriosis and Cancer
• Risk of ovarian cancers
• Confined to endometroid and clear cell histologic types
• Even melanoma and non hodgkin’s lymphoma is reported

9. SITES
Common sites of endometriosis :
(1) ovary
(2) cul-de-sac
(3) uterosacral ligaments
(4) broad ligaments
(5) fallopian tubes
(6) uterovesical fold
(7) round ligaments
(8) vermiform appendix
(9) vagina
(10) rectovaginal septum
(11) rectosigmoid colon
(12) caecum
(13) ileum
(14) inguinal canals
(15) abdominal scars
(16) ureters
(17) urinary bladder
(18) umbilicus
(19) vulva
(20) peripheral sites

10. SITES:
Ovary –Most common site.
• 30-40% of all cases
• B/L mostly
• Burnt match head spots on the surface
• Tarry cysts surrounded by dense adhesions
• Endometriotic cysts –impossible to remove it intact from its
adhesions –cyst wall has already been breached.

11. Pelvic peritoneum –Uterovesical pouch and Pouch of Douglas
• POD-Second most common site
• Associated with one in the ovaries.
• Represents secondary seeding from ovarian condition
• Tarry cysts rarely bigger than a pea
• Puckering and thickening of peritoneum & by adhesions
• Occludes uterorectal space, fixing the uterus in retroversion

12. Outer Coat of Uterus
• Endometriosis of ovary ,pelvic peritoneum & associated ligaments
when adherent to uterus invades its outer coat.
• Penetration is superficial.
• Doesn’t constitute adenomyosis.

13. Round ligament, Uterosacral ligament & Rectovaginal septum
• Round ligament-Endometriosis involves in either its pelvic or
inguinal canal portion(abdominal wall tumor)
• Uterosacral ligament- more commonly affected & lesion tends to
spread into rectovaginal connective tissue.
Can occur with or without involvement of peritoneum of POD.

14. Fallopian tube
• Outer surface of tube occurs as a part of peritoneal endometriosis
Intestine
• Rectum,Pelvic colon-Invasion from peritoneal and ovarian
deposits or by seeding.
• Ileum,Caecum,Appendix
• Lesion rarely penetrates mucosa-rectal hemorrhage & blood cysts
on sigmoidoscopy-unlikely
• Fibrotic thickening&puckering of outer coats of
bowel,stricture,adhesions-intestinal obstruction
• DD-Ca rectum ,Ca pelvic colon

15. Bladder and ureter
• Invasion from adjacent site
Vagina and vulva
Islets of endometriosis -found in surgical & obstetrical scars in the
vagina & perineum.
MC site for vaginal endometriosis- Posterior fornix (infiltrated from
POD or from rectovaginal septum)
Multiple small blue-domed cysts in indurted area of vaginal vault
Mimics Ca.

16. Abdominal wall
• Occurs spontaneously in umbilicus and inguinal canal without
intrapelvic endometriosis
• Swelling –appears blue,bigger during menstruation, n0t
encapsulated,surrounding tissue is indurated,disvharges menstrual
blood
• Scar endometriosis-similar lesions in abdminal wall scars following
operations on uterus or tubes
• Spill of mullerian epithelium into the incision

17. Lungs and Pleura
• Pleura>lungs
• Cyclical pleuritic pain,hemothorax or hemoptysis with each
menstrual cycle

18. Theories of sites of endometriosis
SITE THEORY
Pelvic endometriosis Retrograde menstruation
Pelvic peritoneum Coelomic metaplasia
Abdominal viscera
Rectovaginal septum
Umbilicus
Coelomic metaplasia
Abdominal scar
Episiotomy scar
Vagina and cervix
Direct implantation
Lymph nodes Lymphatic spread
Others(lungs,pleura,skin) Vascular
Genetic
Immunologic

19. Etiology :
Estrogen dependent disease.
No single theory can account for location of endometriosis in
all cases.

20. Ectopic transplantation of endometrial tissue:
• Sampson’s assumption –Implantation of endometrial cells by
transtubal regurgitation during menstruation
• Retrograde menstruation occurs in 70%-90% of women & more
common in women with endometriosis than in those without
the disease
• Presence of endometrial cells in peritoneal fluid reported in
59%-79% of women during menses/early follicular phase& these
cells can be cultured in vitro
• They are present in diasylate of women undergoing peritoneal
dialysis during menses
• Occurs in dependent portions of pelvis-Ovaries, Cul-de-sac,
utero sacral ligaments, posterior uterus , posterior broad
ligaments

21. • Menstrual reflux theory + clockwise peritoneal fluid current
explains why the disease is more common on the left side of pelvis
(implant more easily in rectosigmoid area)
• Diaphragmatic endometriosis found more frequently on right side
(falciform ligament)
• Endometrium obtained during mensus can grow beneath
abdominal skin or into pelvic cavity of animals
• After surgical transposition of cervix intrabdominally to allow
menstruation, endometriosis was found in 50% of Rhesus monkeys
• Obstruction of outflow of menstrual fluid from uterus causes
retrograde menstruation

22. METASTATIC THEORY:
• Proposed by Halban et al in 1924.
• Occurrence at less accessible sites
• Embolisation of menstrual fragments through vascular or
lymphatic channels occur & endometriosis at distal sites occur.
• Demonstrable in sections of lungs taken at autopsies,pelvic lymph
nodes

23. Meyer and Ivanoff ‘s theory :
• Uterus develops from coelomic cells which form mullerian
ducts.
• Embryonic cells capable of differentiating into mullerian tissue
+ in and around peritoneum of pelvis & surface epithelium of
ovary
• Adult cells in these sites retain potential to differentiate into
endometrium and myometrium
• This concept offers an explanation for common finding of
fibromuscular tissue along ectopic endometrium
COELOMIC METAPLASIA THEORY:

24. 1) Adolescent girls in the absence of mullerian anomalies & it
can be discovered a few years after menarche before many
menstrual cycles have been experienced.
2) Prepubertal girl
3) Women who never menstruated
4) Lesions in all sites except those outside abdomen & pelvis
5) Lesion in perineum – a tongue of coelom accompanies
downgrowth of mesodermal urorectal septum which forms
rectovaginal septum & perineum.
This theory supports occurrence in :

25. INDUCTION THEORY:
• Extension of coelomic metaplasia theory
• Biochemical factor transfroms undifferentiated peritoneal cells to
endometrial glands and stroma.

26. GENETIC FACTORS:
• Partially a genetic disease
• Genetic activation of oncogenic K ras allele supports genetic basis
of this disease
• Risk is 7 times more if first degree relative is affected
• No specific medelian inheritance pattern is identified,multifactorial
inheritance is postulated
• Mutation in short arm of chromosome 7 have been found in women
of European ancestry with endometriosis

27. IMMUNOLOGIC FACTORS:
• This theory explains why all women with retrograde menstruation do not
develop endometriosis
• Alterations in the immune system - immunologic clearance of viable
endometrial cells from pelvic cavity ( NK cell & macrophage activity )
• Cell mediated cytotoxicity towards autologous endometrial cells
• Expression of aromatase cytochrome P450 protein & mRNA + in
endometriotic implants but not in normal endometrium
• It produces estrogens –causes tissue growth by interecting with
its receptors

28. • It’s a state of subclinical peritoneal inflammation
• peritoneal fluid volume
• peritoneal WBC’s (macrophages) impair fertility by sperm
motility, sperm phagocytosis.
• inflammatory Cytokines,growth factors,angiogenesis promoting
substances.
• TNF –alpha - secreted by activated macrophages.Has potent
inflammatory properties causes pelvic implantation of ectopic
endometrium
• Macrophages –promotes growth of endometrial cells by
growth factors, angiogenic factors(macrophage derived growth
factor), fibronectin, adhesion molecules-intergrins.
• Matrix metalloproteinases –causes invasion of surrounding tissues

29. Conclusion of theories :
• All these mechanism can contribute to clinical problem in an
individual patient and the degree of contribution for each
varies from patient to patient.
• Endometrial cells can be spread by mechanical means or can
arise by metaplasia ,progression of disease is influenced by
individual’s immune mechanisms-leucocyte and cytokine
responses.

30. TYPES OF ENDOMETRIOSIS:
• Superficial (peritoneal)
• Ovarian endometriomas
• Deep infiltrating endometriosis (DIE)
Superficial Endometriosis(peritoneal):
Involves the dependent portion of the pelvis.
Most common site is surface of ovaries
Pelvic peritoneum over the anterior and posterior surfaces of the uterus, POD,
uterosacral and broad ligament are the other sites.
Pelvic nodes - 30%
Cannot be palpated on clinical examination.
Difficult to visualise on imaging and diagnosis is by laparoscopy.

32. Ovarian Endometriosis:
Also called ovarian endometrioma
There is inversion and invagination of the ovarian cortex with
superficial endometriotic deposits, which causes these lesions.
Located on the ante-mesenteric surface of the ovary and cause
adhesion to the posterior peritoneum.
Cyst wall is white or yellow and is filled with chocolate coloured
fluid, hence called chocolate cysts.
Most women have associated deep infiltrating endometriosis
When large, can be detected
on pelvic examination.` `

36. Deep Infiltrating Endometriosis:
Also called posterior pelvic endometriosis.
Lesions extend >5mm beneath the peritoneum.
Located in the rectovaginal space but may involve uterosacral
ligaments, cervix, bowel or ureters.
Can be felt on pelvic and per rectal examination as tender
induration and nodularity.
Can be visualised on imaging

37. Lesion in POD obscuring the
uterosacral ligaments and
forming adhesions
Endometriotic deposits on the
right uterosacral ligament

38. CLINICAL FEATURES :
No symptoms even when endometriosis is advanced and widespread
Small lesions –maximum symptoms
5 D’s :
1. Dysmenorrhoea
2. Disorders of menstruation
3. Dyspareunia
4. Dyschezia
5. Dull ache of abdomen
Infertility –major problem
GI symptoms (nausea, vomiting, early satiety, bloating,
altered bowel habits )

40. Dysmenorrhoea
• Classical symptom
• 50% cases +
• Progressive
• Secondary, >30 years gradually
getting worse
• Site of pain
• With multiple pelvic deposits – pain is deep seated
In lower abdomen,pelvis,rectum,lower back
•
Before
menstruation
(lesion becomes
congested)Pain
comes on
gradually
During
menstruation
(bleeding into
closed space)Pain
is severe
At the end of
menstruation –
Maximum pain

41. Abnormal menstruation
Excessive bleeding + (60% cases) of pelvic endometriosis
Menorrhagia,Polymenorrhoea.
Change in cycle-Ovaries involved
Abnormal bleeding continues when disease is quiescent –
residual adhesions

42. Dyspareunia
Deep seated pain on coitus –POD,uterosacral ligaments and
rectovaginal septum,fixed retroversion with restricted mobility
Dyschezia
Rectal involvement ,lesion when larger and tender.

43. Abdominal pain
• Production of cytokines,growth factors by activated macrophages
associated with endometriotic implants
• Peritoneal irritation,fibrosis –bleeding from ectopic implants
• Invasion of pelvic nerves
• Aromatase present in ectopic lesions –local accumulation of
estradiol & stimulates its growth
Acute: sudden,severe pain with all symptoms and signs of an acute
abdomen.Occurs when a blood cyst ruptures.
Chronic: Cysts and adhesions among pelvic organs –chronic aching
discomfort in lower abdomen reffered to groins,hips,thighs.
Undergoes menstrual excaerbations.

44. • Infertility
Still not clear which is the cause and which is the effect
Investigation of infertility –Laparoscopy-led to diagnosis of
endometriosis
Mechanisms:
1)Mechanical interference:
Pelvic adhesions
Chronic salpingitis
Altered tubal motility
Distorsion of tubo-ovarian relations
Impaired oocyte pick up

45. 2)Alterations in peritoneal fluid:
Increased concentration of prostaglandins
Increased number of activated macrophages
Increased production of cytokine
Enhanced phagocytosis of sperm
3) Abnormal systemic immune system response:
Increased cell-mediated gamete injury
Increased prevalence of autoantibodies
Anti-endometrial antibody production
4) Hormonal or ovulatory dysfunction
Defective folliculogenesis
Luteinized unruptured follicle syndrome
Hyperprolactinemia
Luteal phase deficiency
Fertilisation or implantation failure

46. Monthly Fecundity Rate:
• Measure of no.of pregnancies occuring in single menstrual
cycle for a specified group of women
• in MFR in infertile women with minimal to mild
endometriosis than in women with unexplained infertility
• in MFR after surgical removal of endometriotic lesions.

47. Examination:
In many patients with endometriosis.no abnormality is
detected
Vulva,vagina,cervix –inspected for signs of endometriosis
Presence of pin point cervix – risk factor
Other signs:Uterosacral and cul-de-sac nodularity
Lateral cervical displacement due to cervical scarring
Painful swelling of rectovaginal septum
U/L ovarian cystic enlargement
In advanced disease :
Uterus is fixed in retroversion
Mobility of ovaries&tubes is restricted

48. CLASSIFICATION

49. • Primary method of endometriosis diagnosis is visualisation
of endometriotic lesions by laparoscopy ,with or without
biopsy for histologic confirmation.
• Extent of endometriosis can vary widely between individuals
& one classification by the American Society for
Reproductive Medicine(1997) allows disease to be
quantified.
• With this, endometriosis on peritoneum, ovaries, fallopian
tubes, cul-de-sac is scored at surgery.
• At these sites, points are assigned for disease surface area,
degree of invasion, morphology and extent of associated
adhesions
• Lesions are morphologically categorised as white, red or
black

50. • In this system, endometriosis is classified
Stage 1(minimal)
Stage 2(mild)
Stage 3(moderate)
Stage 4(severe)
Advantages :
• Wide spread implementation
• Its ease of use
• Its four simple to comprehend stages

51. • Limitations:
• Correlates poorly with infertility and pain symptoms
• Disease involving ureter,bowel or other extrapelvic sites is not
scored
So ,ENZIAN Staging system which represent DIE (Deeply infiltrating
endometriosis) & EFI (Endometrial Fertility Index) was published in
2005.
This scoring system has 3 axes in compartments a,b and c & classifies
the severity of endometriosis
The prefix ‘E’ is used to indicate the presence of an endometriotic
tumor.
The number that follows it –size of the lesion
Subsequent lower case letter indicates location or affected
compartment
Two letters-bilateral disease

56. ENDOMETRIOSIS FERTILITY INDEX(EFI)
• Adamson developed the endometriosis fertility index (EFI ) in 2010,
a scoring system consist of historical factors at the time of surgery,
adnexal function after the intervention of surgery and assessment
of endometriosis that was derived from rAFS.
• Predicts ability of pregnancy after endometriosis surgery
• Contains all the components of rAFS stage score
• Combines conception related factors: Age, years of infertility,
pregnancy history
• LF score(least function score to the appendix-fallopian
tubes,fimbriae,ovaries)
• EFI - the only validated classification of endometriosis that’s
predicts clinical outcome

59. Endometriosis has significant effect on women’s physical and
emotional health
Misdiagnosis and under-diagnosis of the disease is due to limitation of
diagnostic tool as well as lack of recognition of symptoms by patient
and physician
Knowledge on risk factors, etiology and pathogenesis along with
creating awareness should be the ideal step
.
TAKE HOME MESSAGE :

60. THANK YOU