ENDOMETRIOSIS - DR SHASHWAT JANI

DR. SHASHWAT JANI
M.S. ( GYNEC )
DIPLOMA IN ENDOSCOPY.
Assistant Professor, dept. of obs – gyn,
Smt. N.h.l. municipal medical college ,
Sheth v.s. general hospital
Ahmedabad, gujarat , india..
MOB : +91 99099 44160.
E-mail : drshashwatjani@gmail.com
drshashwatjani@gmail.com 1

 INTRODUCTION OF ENDOMETRIOSIS
 SITES
 AETIOLOGY
 THEORIES FOR ENDOMETRIOSIS
 CLINICAL FEATURES
 CLASSIFIC ATION OF ENDOMETRIOSIS
 PATHO-PHYSIOLOGY
 DIAGNOSIS OF ENDOMETRIOSIS
 MANAGEMENT

 Endometriosis initially described by Von Rokitansky in 1860
 Endometriosis is a clinical and pathological entity.
 It is characterized by the presence of tissue resembling
functional endometrial glands and stroma outside the uterine
cavity.
 It is not a neoplastic condition, but malignant transformation
is possible.

ABDOMINAL
Most common site - OVARY (44% involved)
Pouch of Douglas
Uterosacral ligament
Broad ligament
Rectovaginal septum
Pelvic lymph node
Rare sites - Gut, Appendix, Ureter, Urinary Bladder

EXTRA-ABDOMINAL
Common sites - Abdominal scar of Hysterotomy,
Caesarean Section,
Tubectomy, Myomectomy
Umbilicus
Episiotomy Scar
Vagina
Cervix
Remote sites - Pleura, Lungs, deep tissues of arms, thighs

 AGE - 30-40 years(most common) - between the menarche
and menopause.
 FAMILY HISTORY -7 times greater if a 1st degree relative
affected by endometriosis.
 New study- Early menarche
 Late marriage
 SOCIAL AND ECONOMIC FACTORS- more common in
highly civilized communities.
 PARITY- 50-70 % affected women are childless.

 Retrograde menstruation (Sampson’s theory)
 Metaplasia of coelomic epithelium (Meyer and Ivanoff)
 Lymphatic dissemination
 Haematogenous Spread
 Hereditary factor
 Immunologic factor

 John Sampson first postulated that endometriosis arose
from retrograde flow of fragments of endometrial tissue
through the oviducts and into the peritoneal cavity.
 Epidemiologic data suggests that women who menstruate
more frequently, more heavily, or for a longer duration
have increased chance of disease development.
 There is retrograde flow of menstrual blood through the
uterine tube during menstruation. The endometrial
fragments get implanted in the peritoneal surface of pelvic
organs( Sites– ovaries, uterosacral ligament)
 Anomalies of the Mullerian tract, increased occurrence of
endometriosis and stenosis of external cervical os.

 In this theory, the germinal epithelia of the ovary,
endometrium and peritoneum all originate from the same
totipotential coelomic epithelium.
 In coelomic Metaplasia, these totipotential coelomic cell are
transformed by repeated exposure to hormonal or infection
stimuli.
 Development of endometriotic lesions in unusual locations.
 Prolonged treatment with estrogen.

Endometrial cell can be transported to extrauterine sites by
blood vessels or the lymphatic system or by contamination of
the pelvis or abdominal wall incision, if the uterine cavity is
surgically entered.

 In cellular immunity, can facilitate the successful
implantation of translocated endometrial cells.
 In endometriosis lymphocytes decreased cytotoxic
response to endometrial cell may be due to defect in
natural killer cell activity, such as a decreased lytic effect
toward stroma that allow ectopic development of
endometrial fragments.
There may be increased resistance of endometrium in
women with endometriosis to natural killer cytotoxicity.

 Endometriosis is an estrogen-dependent condition.
 Estradiol concentration greater than 60pg/ml is necessary for
proliferation of endometrial lesions.
 Estrogen & Progesterone receptors are found in much lower
concentrations in endometriotic tissue than in normal
endometrial tissue,
 Growth factors can originate from the peritoneal
environment to stimulate endometrial development.
 Platelet derived growth factor, macrophage secretory
products enhance endometrial stromal cell proliferation.

 Increased concentration of macrophages derived growth
factors including vascular endothelial growth factor.
 Molecular alterations in steroidogenic enzyme function have
been implicated in the pathogenesis of endometriosis.
 Menstrual effluent contains factors that induce alterations in
the peritoneal mesothelium, facilitating adhesions of
endometrial cells.

Symptoms:-
 PELVIC- Dymenorrhoea(50%),
Abnormal menstruation(60%)
Dyspareunia, Chronic Pelvic Pain,
Premenstrual spotting
 GASTROINTESTINAL- Constipation, Diarrhea,
Hematochezia, Tenesmus
 URINARY COMPLAINTS- Flank pain, Back pain,
Abdominal pain, Urgency,
Frequency,Hematuria
 PULMONARY- Haemoptysis , Pneumothorax
 INFERTILTY

 Most common symptom
 Pain starts a few days prior to menstruation, gets worse
during menstruation( secondary dysmenorrhoea)
 Pain due to Increased secretion of PGF2α, Thromboxane β2
from endometriotic tissue.
Abnormal Menstruation
 Menorrhagia is a predominant abnormality.
Polymennorhoea, premenstrual spotting also occur.

 It is usually deep, due to stretching of the structures of the
Pouch of Douglas or direct contact tenderness found in
endometriosis of rectovaginal septum or Pouch of Douglas and
with fixed retroverted uterus.
Abdominal pain
 lower abdominal pain or backache
 May be due to inflammation in peritoneal implants due to
cystic bleeding
 Irritation or invasion of nerve
 Action of inflammatory cytokines released by the
macrophages.

Infertility
Mechanical interference---
1. Pelvic adhesions
2. Chronic salpingitis
3. Impaired oocyte pickup
4. Altered tubal motility
5. Distortion of tubo-ovarian relations
Alteration in peritoneal fluid
1. Increased concentration of prostaglandins
2. Increased number of macrophages
3. Increased production of cytokines
4. Phagocytosis of sperms
Abnormal Systemic Immune system
1. Increased cell-mediated gametes injury
2. Increased prevalence of autoantibodies
Hormonal or ovulatory dysfuntion
1. Defective folliculogenesis
2. Luteinized unruptured follicle syndrome
3. Hyperprolactinemia
4. Luteal phase deficiency
5. Implantation failure drshashwatjani@gmail.com 21

General conditions- Fair
Pallor + due to Menorrhagia
Pulse, B. P. –Normal
CVS/ RS – Normal
P/A- Mass felt in lower abdomen arising from the pelvis
Enlarged chocolate cyst or tuboovarian mass,
due to endometriotic adhesions.
The mass is tender with restricted mobility.
L/E-See Vulva and other structures
P/S- See cervix, vagina for any deposits, discharge or
growth.

o Tender uterosacral ligament
o Cul-de-sac nodularity found
o Induration of the rectovaginal septum
o Fixed retroversion of the uterus
o Adnexal masses and generalized or localized pelvic
tenderness present
o Uterosacral nodules may be found

 ASRM staging has poor correlation with
pregnancy rate.
 In 2009 new staging system was proposed called
Endometriosis Fertility Index.
 EFI is numerical measure of functional anatomy
based on assessment of tubes, fimbriae and
ovaries.
 EFI score 0 to 10
(0 – poorest and 10 – the best prognosis).

Diagnosis made by Clinical Presentation
Clinical Examination
 Clinical examination- In many women with endometriosis no
abnormality is detected during the clinical examination.
 The clinical examination may have false-negative results.
So, the diagnosis of endometriosis should be confirmed by
biopsy of suspicious lesions or by laparoscopy.

 Transvaginal or Transrectal ultrasonography is an important
diagnostic tool in the assessment of ovarian endometriotic
cysts, adnexal masses.
( Sensitivity-97% and Specificity-96% )
 Other imaging techniques are- CT/ MRI
Can be used to provide additional and confirmatory
information but they cannot be used for primary diagnosis.

 Cancer Antigen-125, a high molecular weight glycoprotein
expressed on the cell surface of some derivatives of embryonic
coelomic epithelium.
 It is elevated towards the end of the luteal phase and during
menstruation.
 In many other conditions elevated CA-125 concentration like
PID, adenomyosis, uterine leiomyoma, menstruation,
pregnancy, epithelial ovarian cancer, pancreatitis, chronic liver
disease.

 80% of women with pelvic pain and endometriois had a CA-
125 titre greater than 16 U/ml
 6% of patients with pelvic pain and without endometriosis
had an increased CA-125.
 The result of most studies suggest that CA-125 is not
sufficiently sensitive to identify lesser stages of
endometriosis.
 CA-125 is not reliable as a screening test.

Diagnostic Laparoscopy is the gold standard
investigation for Endometriosis.
 In laparoscopy examination, we classify the extent and severity of
disease.
 In laparoscopy evaluation, a double puncture technique is essential.
 The forceps placed through the lower abdomen sheath permits
mobilization of the tube and ovaries.
 Inspect the lateral side wall, all ovarian surface, both sides of the broad
ligament, the bladder, bowel serosa, inferior aspect of cul-de-sac,
evaluation of the uterosacral ligaments and rectal serosa.
 To avoid under diagnosis it should not be performed during or within 3
months of hormonal therapy.

 Typical “powder-burn or “gunshot” lesions on the serosal
surface of the peritoneum. These lesions are black, blue or
dark brown, nodules or small cysts containing old
hemorrhage surrounded by variable degree of fibrosis.
 White lesions are predominantly fibromuscular. Scarring
with scattered glandular and stromal elements.
 Brown lesions are mainly haemosiderin deposits. Peritoneal
defect and subovarian adhesions contain endometriosis in
40% -70%.

 For ovarian endometriosis- Large ovarian endometriotic cysts
are usually located on the anterior surface of the ovary and
associated with retraction, pigmentation and adhesions to the
posterior peritoneum. Size smaller than 12 cm in diameter for
diagnosis.
 Ovarian endometriotic cyst contain a thick, viscous dark
brown fluid.(Chocolate fluid)
Chocolate cysts– sometimes it is confused with
hemorrhagic corpus luteum cysts and
neoplastic cysts. Biopsy must be done.

Pelvic pain & suspected endometriosis
NSAID or OCP Success Continue drug therapy
Failure
Empirical GnRH agonist
therapy + estrogen
success progestin add back therapy failure
continue drug therapy operative laparoscopy
GnRH agonist therapy + estrogen progestin add back therapy

Progestogens : Route Dose Frequency
Medroxy progesterone acetate oral 30mg Daily
Megestrol acetate oral 40 mg Daily
Lynoestrenol oral 10mg Daily
Dydrogesterone oral 20-30mg Daily
Antiprogestins :
Gestrinone oral 1.25/2.5mg Twice weekly
Danazol oral 400mg Daily
Gonadotropin-releasing Hormone
Leuprolide s.c. 500mg Daily
I.M. 3.75mg Monthly
Goserelin S.C. 3.6 mg Monthly
Buserelin Intranasal 300ug Daily
Nafarelin Intranasal 200ug Daily
Triptorelin I.M. 3.75mg Monthly

 Progestogens suppress ovarian steroidogenesis and promote
endometrial glandular atrophy, apoptosis and extensive
decidual transformation to the stroma.
 Progestogens oppose the growth-promoting effect of estrogens
on the endometrial tissue by altering the clearance of the
nuclear estrogen, receptor and inducing 17 β hydroxysteroid
dehydrogenase which convert estradiol to the weaker estrone.
 They- prevent reflux menstruation
- prevent implantation and growth
of regurgitated endometrium.
- Progestogens have anti-inflammatory effect.
Side effects weight gain, edema, irritability.

 Danazol is a synthetic derivative of 17α-ethinyl
testosterone that was introduced into clinical practice
by Greenblatt in 1971.
 The pharmacologic action of Danazol is complex,
directly inhibiting GnRH secretion. Midcycle LH surge
is ablated although basal gonadotropin concentrations
are maintained.
 Direct inhibitions of steroidogenesis, increased
metabolic clearance of estradiol and progesterone.
Side effects- Weight gain, muscle cramps, increase
breast size, vasomotor symptoms.

 GnRH agonists bind to pituitary GnRH receptors and
stimulate LH and FSH synthesis and release.
 Agonists have much longer biologic half-life(3-8 hours) and
GnRH have(3-5 mint) continuous exposure of GnRH
receptors to GnRH agonist activity.
 Ovarian steroid production is suppressed.
Side effects- Hypoestrogenism, hot flushes,
vaginal dryness, osteoporosis

 This drug act by interrupting local estrogen
formation
 With in the endometriosis implant themselves they
also inhibit estrogen production in the ovary,brain
and other source.
Side effect : Bone loss,development of multiple
follicles cyst at ovulation.

 When medical measures fail surgical intervention is needed.
 In most women with endometriosis, preservation of
reproductive function is most important.
 The goal of surgery is to excise all visible endometriotic
lesions and associated adhesions like peritoneal lesions,
ovarian cysts, deep rectovaginal endometriosis and restore
normal anatomy.
 Laparotomy should be reserved for patients with advanced
stage disease, who cannot undergo a laparoscopic procedure
and for those in whom fertility conservation is not necessary.

 Conservative resection of disease by Laparotomy is most
valuable in case of extensive dense pelvic adhesions or
endometriomas greater than 5 cm in diameter.
 Deep involvement of the rectovaginal septum with fibrotic
extension into perirectal fossa. Invasion of the bowel
muscular and endometriotic infiltration in the region of
uterine vessels and ureter. Are generally best approched
through the open abdomen.
 Peritoneum – Small lesions of superficial peritoneal
endometriosis less than 5 mm in diameter are easily treated
with laser or bipolar coagulation or constant stream of
irrigation.

DIE CLASSIFICATION OPERATIVE PROCEDURE
(A) Anterior DIE
A1 : Bladder Laparoscopy partial cystectomy
(P) Posterior DIE
P1 : Uterosacral Laparoscopic resection of ligament
uterosacral ligament
P2 : Vagina Laparoscopic assisted vaginal
resection of DIE infiltrating
the posterior fornix.
P3 : Intestine
w/o vaginal infiltration ---- Intestinal resection
by laparoscopy or by Laparotomy
with vaginal infiltration ---- Laparoscopically assisted vaginal
intestinal resection or by Laparotomy
Multiple intestinal location ---- Intestinal resection by Laparotomydrshashwatjani@gmail.com 46

 Surgical treatment of endometriosis less than 4-5 cm in
diameter.
 Technique is initiated by longitudinally incising the cortex
overlying the cyst after achieving full mobilization of the
ovary.
 Incision is made along the inferior pole on the opposite side
to the hilus to preserve the opposite side of ovarian tissue to
the fimbria.
 The cyst contents are immediately drained with suction
cannula and cavity is irrigated and inspected for papillary
structure.
 Very small endometriosis less than 1-2 cm in size may be
effectively treated by electro coagulation of the mucosal
lining.

 Also called uterine endometriosis, in which islands of
endometrium are found in the wall of the uterus.
 Observed commonly in elderly women.
 Often coexists with uterine fibromyomas, pelvic
endometriosis, endometrial carcinoma.
 Gross- Uterus appears symmetrically enlarged.
 Histology- Islands of endometrial glands surrounded by
stroma.
 C/F- Menorrhagia, progressively increasing
dysmenorrhoea, pelvic discomfort, backache,
dyspareunia.

 C/E- Symmetrical enlargement of uterus, tender uterus.
 Treatment- Diagnostic Hysteroscopy combined with
curettage.
 Elderly- Total hysterectomy
-NSAID’s
-Hormonal therapy.
Drugs- Danazol, GnRH.

THANK YOU

ENDOMETRIOSIS - DR SHASHWAT JANI

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