Endometriosis is a medical condition where endometrial tissue grows outside the uterus, commonly in the ovaries, fallopian tubes, and pelvic lining. It affects 6-10% of women and causes pain, irregular bleeding, and infertility. The exact cause is unknown but theories include retrograde menstruation, genetic factors, and environmental toxins. Diagnosis involves a medical history, physical exam, ultrasound, MRI, and laparoscopy to visualize lesions. Stages range from minimal to severe based on location, size, and depth of implants. Treatment focuses on pain management and hormone therapy to suppress menstruation. Differential diagnoses include pelvic inflammatory disease, ovarian cysts, and uterine fibroids.

1. DEPARTMENT OF PRASUTI TANTRA AND STRIROGA
DAYANAND AYURVEDIC COLLEGE, JALANDHAR
SESSION 2016-17

2. CONTENTS
DEFINITION
INCIDENCE
RISK FACTORS
SITES
PATHOGENESIS
PATHOLOGY
STAGES
CLINICAL FEATURES
DIAGNOSIS
DIFFERENTIAL
DIAGNOSIS
COMPLICATIONS
TREATMENT

3. DEFINITION
Endometriosis is the medical condition
in which the functional endometrium
that grows inside uterus is present in
sites other than uterus.
With endometriosis displaced
endometrial tissues continues to act as
it normally would – it proliferates,
breaks down and bleeds with each
menstrual cycle. Because this displaced
tissue has no way to exit your body, it
becomes trapped. When endometriosis
involves the ovaries cysts called
endometriomas may form.
Surrounding tissues can become
irritated , eventually developing scar
tissue and adhesions.

4. INCIDENCE
Endometriosis is estimated to occur in roughly 6-10% of women . It is most
common in those in their 30s and 40s however can begin in girls as early as 8 yrs
old (in rare cases).
During thelast couples of decades, the prevalence of endometriosis has been
increasing.
The real cause of increasing incidence is due to delayed marriage , postponement
of first conception and adoption of small family norm.
The apparent one is due to increased use of diagnostic laparoscopy as well as
heightened awareness of this disease complex amongst the gynaecologists.
It results in few deaths estimated being 200 globally in 2013.
1 in 10 women suffer from endometriosis in India.

5. RISK FACTORS
Genetics:-
Genetic predisposition plays a role in endometriosis. Daughters or sisters of women
with endometriosis are at higher risks of developing endometriosis themselves. There is
an about 6 fold increased incidence in women with a affected first degree relative.
Individual genomic changes that have been associated with endometriosis including
changes on Chromosome 1,2,6,7,9,10 and 12.
Physical activity :-
Regular physical activity may be linked with lower levels of estrogen and reduce
endometriosis risk, and vice versa.
Environmental toxins:-
Several studies have investigated the potential link b/w exposure to exposure to dioxins
and endometriosis . Dioxins are the chemicals that includes polychlorinated biphenyls,
which is formed as accidental biproduct in bleaching industries, chemical and plastic
manufacturing industries and medical waste incineration.
Tampons and sanitary napkins are made up of rayon and bleached napkins, which
contains low levels of dioxins.Once entered in the body, it builds up in body ,
concentrates in fatty tissues over time. These dioxins interfere with cells gene processes,
influence hormone metabolism and growth factors thus affecting reproductive ,
endocrine and immune functions.

6. SITES
Sites of
endometriosis
Abdominal
Extra-
Abdominal
Remote
1. Abdominal -It can occur at any site but is usually confined to abdominal structures
below the level of umbilicus, most commonly ovaries, fallopian tubes, cul –de-sacs,
broad ligaments, uterosacral ligaments, round ligament, rectosigmoid colon, vagina,
caecum etc..
2. Extra- abdominal -The common sites are abdominal scar of hysterectomy , caesarean
section, tubectomy , myomectomy,umbilicus episiotomy scar, vagina and cervix.
3. Remote - Lungs, Pleura, Ureter, Kidney, Arms, Legs, Nasal mucosa.

7. PATHOGENESIS
While the exact cause of endometriosis remain unknown. Many theories has been
presented to better understand and explains its development . The
pathophysiology of endometriosis is likely to be multifactorial and to involve an
interplay b/w several factors.
The main theories are explained below:-
1. Sampon’s theory-proposed by John.A.Sampson. Also known as Retrograde
menstruation . According to this theory, there is retrograde flow of menstrual
blood through the uterine tubes during menstruation. The endometrial
fragments get implanted in the peritoneal surface of pelvic organs.
Subsequently cyclic growth and shedding of endometrium at ectopic sites occur
under the influence of endogenous ovarian hormones. Genetic and hormonal
favorable are necessary for successful implantation and growth of fragments of
endometrium.
This theory explains only pelvic endometriosis, it fails to explain the
endometriosis at distant sites.

8. Reterograde Menstruation Theory ( Sampson’s Theory)

9. 2. Meyer and Ivanoff Theory- Also known as Coelomic Metaplasia.Chronic irritation
of pelvic peritoneum by the menstrual blood may cause coelomic metaplasia
which results in endometriosis. Coelomic cells from which endometrial and
peritoneal cells develop , undergo metaplasia(abnormal change in nature of
tissue) from one cell type to other.
This theory can explain endometriosis of the abdominal viscera , the retrovaginal
septum and the umbilicus.

10. 3. Halban’s Theory- Also known as Lymphatic Theory.It may be possible for normal
endometrium to metastasise the pelvic lymph nodes through the draining
lymphatic channels of uterus.
4. Vascular theory-It can explain endomatriosis at distant sites as lungs, arms or
thighs.
5. Direct Implantation- According to this theory, endometrial or decidual tissues start
to grow in susceptible individual when implanted in the new sites.Such sites are
the abdominal scar following hysterectomy , caesarean section, tubectomy,
myomectomy.
This theory explains endometriosis at episiotomy scar, vaginal or cervical site but
fails to clearify endometriosis at sites other than mentioned.
6. Environmental Theory- Somatic mutations of cells due to environmental factors(
pollutants and dioxins)
Thus, it is certain that not all cases of endometriosis can be explained by juat a
single theory.

11. PATHOLOGY
The endometrium in the ectopic sites has got the potentiality to undergo changes
under the action of ovarian hormones.
While proliferative changes are constantly evident , the secretory changes are
conspicuously absent in many , may be due to efficiency of steroid receptors in
ectopic endometrium.
As cyclic growth and shedding continue till menopause. The periodically shed
blood may remain encysted , the cyst becomes tense and rupture.
As the blood is irritant , there is dense tissue reaction surrounding the lesion with
fibrosis. If it happens to occur on pelvic peritoneum, it produces adhesions and
puckering of peritoneum.
If encysted , the cyst enlarges with the cyclic bleeding. The serum gets absorbed in
b/w the periods and the content inside becomes chocolate coloured. Hence,it is
called Chocolate cyst.
The term endometrial cyst or endometrioma is preferred to Chocolate Cyst.

12. Naked eye appearance:-
In the case of pelvic endometriosis , there are-
i. Small black dots called “powder burns” seen on uterosacral ligaments and
pouch of douglas.
ii. Fibrosis and scarring in the peritoneum surrounding the implants is also typical
findings.
iii. Red flame shaped areas
iv. Red polyploid areas
v. Yellow brown patches
vi. White peritoneal areas
vii. Sub ovarian adhesions
Microscopic Appearance:-
i. There is presence of endometrial tissue-both glands and stroma.Adjacent to the
linning epithelium , there may be presence of large polyhedral phagocytic cells,
laden with blood pigment haemosidrin.
ii. The cyst wall is composed of fibrous tissue and compressed ovarian cortex.

13. STAGES OF ENDOMETRIOSIS
Different factors determine the stage of the disorder. The factor includes-
i. Location
ii. Number
iii. Size
iv. Depth of endometrium implant
Stages of
Endometriosis
Minimal or
Stage 1
Mild or Stage2
Moderate or
Stage 3
Severe or
Stage 4

14. Stage 1 or Minimal endometriosis:-In Stage 1, there are small lesions or wounds
and shallow endometrial implants on ovary. There may be inflammation in or
around your pelvic cavity.
Stage 2 or Mild endometriosis:-In Stage2 there is light lesions and shallow
implants on an ovary and the pelvic lining.
Stage 3 or Moderate endometriosis:-In Stage 3 there are deep implants on ovary
and pelvic lining. There can also be more lesions.
Stage 4 or Severe endometriosis:-The most severe stage of endometriosis involves
deep implants on pelvic lining.

16. CLINICAL FEATURES
• PATIENT PROFILE :
The age is between 30-45.
Patients are mostly nulliparous or have 1-2 children long yrs prior to appearance of
symptoms.
Infertility , voluntary postponement of first conception untill at a late age.
Higher social status are often relatable.
• SYMPTOMS :
About 25% of patients with endometriosis have no symptoms, being accidently
discovered during laparoscopy or laparotomy.

18. DYSMENORRHOEA :-
Dysmenorrhoea literally means painful
menstruation but more specically
painful menstruatiom of sufficient
magnitude so as to incapacitate day to
day activities.
Dysmenorrhoea in endometriosis:-In
case of endometriosis , it is found that
concentration of the prostaglandins are
higher than in normal.
Prostaglandins (PGF2 alpha , PGE2) are
vasoconstrictors which cause ischaemia
of myometrium and increase
myometrial contractions with or
without dysrhythmia.
The pain starts a few days prior to
menstruation get worsened during
menstruation and takes time , even
after cessation of period to get relief of
pain.
PROSTAGLANDINS
Endothelins,
Leukotrienes,
PAFs
Inc.
myometrial
contractions
PAIN
Reduced
blood flow
Myometrial
‘angina’
PAIN

19. INFERTILITY:-
Infertility is defined as failure to conceive within one or more years of regular
unprotected coitus.
Endometriosis is found in 20-40% of infertile women, whereas in about 40-50%
patients with endometriosis suffer from infertility.
Infertility in endometriosis:-
Endometriosis induce a chronic inflammatory reaction, scar tissue and adhesions
, that may distort normal pelvic anatomy. Several mechanism have been proposed
to explain association b/w endometriosis and infertility.
These mechanisms include distorted pelvic anatomy, endocrine and ovulatory
abnormalities, altered peritoneal functions , altered hormonal and cell mediated
functions in endometrium.
Major pelvic adhesions disturb the tubo-ovarian lesions , tube patency can impair
oocyte release from the ovary , inhibit ovum pickup or impede ovum transport.
Thus endometriosis causes infertility.
DYSPAREUNIA:-
Dyspareunia means painful sexual intercourse. It is mostly found in
endometriosis of the rectovaginal septu, or pouch of douglas and with fixed
retroverted uterus.
It mey be due to stretching of the structures of pouch of Douglas or direct contact
tenderness.

20. ABNORMAL MENSTRUATION :-
In endometriosis , menorrhasia is the predominant abnormality.Menorrhagia is
defined as cyclic bleeding at normal intervals, the bleeding is either excessive in
amount (>80 ml) or duration(>7days) or both.
Due to congestion, increased surface area, hyperplasia of endometrium, there is
menorrhagia in pelvic endometrium.
OTHER SYMPTOMS :-
The symptoms are related to the organs involved:-
• Urinary- Increased frequency, dysuria, back pain or even haematuria.
• Sigmoid colon and rectum- Painful defecation , diarrhoea, constipation, retal
bleeding or even melena( black, stinky faeces as a result of internal bleeding)
• Chronic fatigue, perimenstrual symptoms( bloating irritability, fatigue)
• Haemotypsis, Catamenial chest pain
• Surgical scars-Cyclic pain and bleeding

21. DIAGNOSIS
A history and a physical examination can lead the health care practitioner to suspect
endometriosis.
Detailed history
Family history of endometriosis
Menstrual history -specifically the flow of blood, any sign of dysmenorrhoea.
Investigate for any other signs and symptoms related to endometriosis.
Physical examination
• Abdominal examination- Abdominal palpation may not reveal any abnormality.A
mass may be felt in lower abdomen arising from the pelvis, enlarged chocolate
cyst or tubo-ovarian mass due to endometriotic adhesions . The mass is tenser
with restricted mobility.
• Pelvic examination- Bimanual examination may not reveal any pathology . The
expected positive findings are pelvic tenderness, nodules in pouch of douglas,
nodular feet at uterosacral ligaments, or bilateral adnexal mass of varying size.
Speculum examination may reveak bluish spots in posterior fornix.
Rectal or rectalvaginal examination is often helpful to confirm the findings.

22. Clinical diagnosis & test:-
• Serum marker CA125 test-
A moderate elevation of serum CA 125 is noticed in patients with severe
endometriosis.It is significantly raised in epithelial ovarian carcinoma.
• Monocyte chemotactic Protein (MCP-1)-
MCP-1 level is increased in peritoneal fluid of women with endometriosis.
Ultrasonography:-
It isnot much helpful to the diagnosis . TVS can detect ovarian endometriomas.
TVS and endorectal ultrasound are found better for rectosigmoid endometriosis.
Biopsy:-
Biopsy confirmation of excised leison is ideal. It is done to-
Check for cancer of uterus
Find the cause of heavy , prolonged, irregular uterine bleeding.
To check whether the lining of the uterus is going through normal menstrual cycle
changes.

23. Magnetic Resonance Imaging (MRI):-
It is diagnostic tool.There is characteristic hyperintensity on T1 weighted images and
a hypintensity on T2 weighted images.It is useful for deep infiltrating
endometriosis.
CT:-
It is better compared to ultrasonography in the diagnosis , but in the case of
endometriosis, endometriomas are non specific.
Laproscopy:-
It is the good standard for detection of the endometriosis.Confirmation is done by
double puncture laproscopy or by laprotomy. Confirmation of leison with size,
shape,site , extent . Extent of adhesion could be recorded. Biopsy can be taken at
same time.

24. DIFFERENTIAL DIAGNOSIS
Pelvic Inflammatory Disease(PID):-
• The patient’s description of pelvic pain during menstruation , dysuria and
dyspareunia are often symptoms of PID.
• PID is the medical condition in which there is infection of the upper part of
female reproductive system including uterus, fallopian tube, ovaries and inside
the pelvis.
• Differentiating Symptoms-
Fever, Nausea , Acute pain along with malodorous vaginal discharge and cervical
motion tenderness. Adnexal tenderness is typical for acute PID.
• PID would be ruled out with a vaginal swab to test for any organisms that might
have caused the infection, cervical cultures,pelvic ultasonography may show
complex adnexal masses.

25. Ovarian cyst :-
• The presentation of pelvic pain during menstruation , dyspareunia, dysuria are
common symptoms of ovarian cysts.
• Ovarian cysts are fluid filled sacs in the ovary. They are common and generally
have no symptoms. When cysts grow large or multiply is when they can cause
pain or other problems.
• Differentiating Symptoms-
May be asymptomatic with an incidental pelvic mass or present with acute rather
than chronic pain.
• To rule out an ovarian cyst, a pelvic exam can be performed to palpate for swollen
masses on the ovaries. Ultrasound can also be performed to visually verify.

26. Uterine myoma :-
• Uterine myoma also known as Uterine fibroid are benign smooth muscle tumors
of the uterus.
• The presentation of abnormal uterine bleeding heavy or painful periods,
abdominal discomfort in some cases infertility and dyspareunia are common
symptoms of uterine myoma.
• Differentiating Symptoms-
Most cases are asymptomatic but often present with heavy or irregular menstrual
bleeding.Pelvic examination may show an enlarged nodular pelvic mass that can
vary in size and shape.
• To rule out TVS is done. It shows concentric, solid, hypoechoic (dark) mass with in
endometrium or myometrium. Small myoma may be isoechoic but if calcified,
myoma can be hyperechoic.

27. Adenomyosis:-
• It is medical condition characterized by abnormal presence of endometrial tssue
within the myometrium . In contrast when endometrial tissue is present entirely
outside the uterus, it is called endometriosis.
• Symptoms may be identical to those of endometriosis.
• To rule out , pre-operative MRI findings may show diffuse or focal widening of
the junctional zone , islands of endometrial tissue , mass within
myometrium.Histopathological evaluation of uterus after hysterectomy shows
endometrial glands in the myometrium.
• Laproscopy may reveal a normal pelvis or concurrent endometriosis.

28. COMPLICATIONS
Various complications of endometriosis include:-
Malignant transformation :- It is a well defines although rare complication of
endometriosis.
Endometrioma Rupture:- Rupture of endometrioma is rare condition. The
condition most commonly occurs during pregnancy because of rapid growth
from hormonal stimulation of endometrial stromal elemrnts. Due to presence of
blood from rupture of the endometrium may cause peritoneal inflammation.
Endometrioma Infection:- An endometrioma most commonly becomes infected
after surgical drainage or aspiration.Infection may also result from spread from
adjacent inflammation or may spread haematologically in patient with
bacteremia.
Decidualization of Endometrioma during pregnancy:- Decidualization refers to
hypertrophy of stromal cells of endometrium that occurs during pregnancy to
form vascular decidual lining of gravid uterus. The process results primarily from
the efects of progesterone.
Obstructive features:-
It may cause –
• Intestinal obstruction
• Ureteral obstruction -->Hydroureter -->Hydronephrosis --> Renal infection

29. TREATMENT
Endometriosis needs to be treated as it is a progressive disease(30-60%).
TREATMENT
Preventive Curative

30. Preventive Treatment:-
• To avoid tubal pregnancy test immediately after curettage or around the time of
menstruation.
• Forcible pelvic examination should not be done during or shortly after
menstruation.
• Married women with family history of endometriosis are encouraged not to delay
the first conception but to complete the family.
Curative treatment:-
The objectives are-
• To abolish or minimize the symptoms – pelvic pain and dyspareunia
• To improve fertility
• To prevent recurrence
Treatment options:-
• Expectant management
• Medical therapy
• Surgery
• Combined therapy

31. Determinants of Treatment Options:-
• Age of patients
• Size and extent of leisons
• Severity of symptoms
• Location of disease
• Desire for fertility
• Results of previous therapy
Expectant therapy:-
• Endometriosis is a progressive disease in about 30-60% of women. Some form of
treatment is often needed regardless of clinical profile and to arrest the progress
of the disease.
• Case Selection for expectant treatment :-
1. Minimal endometriosis with no other abnormal finding
2. Unmarried
3. Young married who are ready to start family
4. Approaching menopause.

32. • Protocols for expectant management:-
Observation with administration of non-steroidal anti-inflammatory drugs or
prostaglandins synthetase inhibiting drugs are used to relieve pain.
Ibuprofen 800-1200 mg or Mefanamic Acid 150-600 mg a day is quite effective.
The married women are encouraged to have conception.
Pregnancy usually cures the condition . This is due to absence of shedding and
decidual changes in ectopic endometrium causing its necrosis and absorption.
Hormonal Treatment:-
The aim of hormonal treatment is to induce atrophy of endometriotic implants . It
should be considered suppressive rather than curative because of high recurrence
rate.
The mechanism of endometrial atrophy is either by producing ‘psuedopregnancy’
( Combined oral pills) or by ‘ psuedomenopause’(Danazol) or by ‘medical
oophorectomy(GnRH agonists). The hormonal use is gratifying in superficial
peritoneal implants and endometriomas of less than 1 cm.
The drugs used are combined oestrogen and progesterone ( oral pills) ,
progesterone, danazol and GnRH analogues.
All the drugs are used continuously to produce amenorrhoea ans as such
individualisation of the dose is required.

33. • Combined Oestrogen and Progesterone:-
The low dose contraceptive pills may be prescribed either in cyclic or continuous
fashion with advantages in young patients with mild disease who want to defer
pregnancy . It may induce amenorrhoea relieves dysmenorrhoea.
• Progesterone:-
It causes decidualisation of endometrium and atrophy. High doses may suppress
ovulation and induce amenorrhoea.
Oral Route is commonly used .Injectible preparation as depot form should be
withheld in patients wishing to concieve . Ovulation may remain suspended for
several months following withdrawl of therapy.The drug is comparitvely cheaper
than danazol. Progesterone Antagonists(Mifepristone 50-100 mg/day) has also
been found effective.
• Levonorgestrel- releasing IUCD, wjen used isfound to reduce dysmenorrhoea,
pelvic pain, dyspareunia and menorrhagia significantly. It is specially useful for
rectovaginal endometriosis.

34. • Danazol-
Danazol therapy is to be started from the day 5 of menstrula cycle.The dose (600-
800 mg daily) is variable and depends upon the extent of the leisons but should be
adequate enough to produce amenorrhoea.
The patirnt should use barier method of contraception to avoid virilisation of a
female fetus in accidental pregnancy.
Gestrinone has got the same mechanism of action like that of danazol.
Administration is simple, twice a week.
• GnRH analogues-
When used continuously act as medical oophorectomy , a state of hypo-
oestrinism and amenorrhoea. The goal is to maintain a reduced level of oestrogen
so that growth of endometrium is suppressed.

36. Agent Dose Route Frequency
Danazol 600-800 mg Oral Daily(limited to 6
months)
Combined Oral
Contraceptive pills
30-35 μg Oral Daily
GnRH agonists
i) Leuprolide 1mg / day SC Injection Daily
ii) Tripotrelin 3mg IM Monthly
iii) Goserelin 3.6mg SC Monthly
iv) Buserelin 300-400 μg Intranasal TDS
v) Naserelin 200-400 μg Intranasal BD

37. Agent Dose Route Frequency
Progestins
i) Dydrogesterone 60mg Oral 12 days per cycle
ii) Gestrinone 2.5 – 5 mg Oral Daily
iii) Megestral acetate 40 mg Oral Daily
iv) Norethindrone
acetate
5mg Oral Daily
v) MPA 30mg Oral Daily
vi) DMPA-150 150 mg IM Every 3 months

38. Surgical Treatment:-
• Indiacations-
i. Endometriosis with severe symptoms unresponsive to hormone therapy.
ii. Severe and deep infiltrating endometriosis to correct distortion of pelvic anatomy
iii. Endometriosis of more than 1 cm.
• Conservative surgery-
It is planned to destroy the endometriotic leison in attempt to improve the
symptoms.
Laproscopy is commonly done to destroy endometriotic leisons by excision or
abalation by electrodiatherapy or by laser vapourisation.
It is done in minimal to mild endometriosis , improves fertility outcomes.

40. THANK YOU