ENDOMETRIOSIS - DR SHASHWAT JANI

drshashwatjani@gmail.com 1

ENDOMETRIOSIS

DR. SHASHWAT JANIM.S. ( GYNEC )

DIPLOMA IN ENDOSCOPY.

Assistant Professor, dept. of obs – gyn,Smt. N.h.l. municipal medical college ,

Sheth v.s. general hospitalAhmedabad, gujarat , india..

MOB : +91 99099 44160.E-mail : drshashwatjani@gmail.com

ENDOMETRIOSIS

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

INTRODUCTION

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

AETIOLOGY

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.

THEORIES FOR ENDOMETRIOSIS

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

1) Retrograde menstruation( Sampson's Theory)

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.

2) Coelomic metaplasia( Mayer and Ivanoff)

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.

3) Lymphatic theory(Vascular theory)

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.

4) Autoimmune theory

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.

Pathophysiology

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.

CLINICAL FEATURESSymptoms:-

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

Dysmenorrhoea

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.

Dyspareunia

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 adhesions2. Chronic salpingitis3. Impaired oocyte pickup4. Altered tubal motility5. Distortion of tubo-ovarian relations

Alteration in peritoneal fluid6. Increased concentration of prostaglandins7. Increased number of macrophages8. Increased production of cytokines9. Phagocytosis of sperms

Abnormal Systemic Immune system10. Increased cell-mediated gametes injury11. Increased prevalence of autoantibodies

Hormonal or ovulatory dysfuntion12. Defective folliculogenesis13. Luteinized unruptured follicle syndrome14. Hyperprolactinemia15. Luteal phase deficiency16. Implantation failure

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.

Bimanual Pelvic Examination

o Tender uterosacral ligamento Cul-de-sac nodularity foundo Induration of the rectovaginal septumo Fixed retroversion of the uteruso Adnexal masses and generalized or localized pelvic

tenderness presento Uterosacral nodules may be found

classification

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

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.

CA-125

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.

Findings are:-

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.

Medical management:-

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

Endometriosis Associated with pain Effective regimen for 6 months

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

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

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.

Gonadotropin-Releasing Hormone Agonists

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

Aromatase inhibitor (letrozole,Vorozole)

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.

Surgical management:-

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.

Surgicaltreatment

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.

Surgical procedure according to classification of Deeply Infiltratring Endometriosis 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 Laparotomy

Ovarian Endometriosis

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.

Adenomyosis--

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

Health & Medicine

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