Endometriosis is a condition where endometrial tissue grows outside the uterine cavity, most commonly on the ovaries and pelvic peritoneum. It causes pelvic pain and infertility and is diagnosed through laparoscopy. Treatment involves medical therapy using hormones to suppress menstruation, surgical excision or ablation of lesions, or a combination. Symptoms range from mild to severe depending on location and extent of disease.

1. ENDOMETRIOSIS
Dr. David Wol Nang
January, 2022

2. Introduction
• Definition: Condition in which endometrial tissue is
present outside the uterine cavity.
• Endometrial tissue located within the myometrium is
termed adenomyosis
• It is an estrogen-dependent disease, hormone-based rx
is a mainstay of therapy but when unresponsive to
medical management, surgery may be required.
• Implants of endometriosis are most often found on the
pelvic peritoneum, but can occur in any part of the body.
• Primary method of diagnosis is laparoscopy (gold
standard)

3. Epidemiology
True prevalence in general population is not known
• all reproductive-aged women: 10 %
• annual incidence of surgically diagnosed endometriosis is
1.6 cases per 1000 reproductive-aged women
• In asymptomatic women: 6 to 11 %
• Among patients with infertility, 20 to 50 %
• In those with CPP, it ranges from 40 to 50%

4. Risk factors
• Affects any woman regardless of age,
race, economic and child bearing status.
• Familial tendency has been identified
• Outflow tract obstruction
• lower body mass
• Early menarche, especially before age 14,
• Nulliparas.
• Environmental toxins -- estrogenic effect
(diethylstilbestrol polychlorinated biphenyl (PCB))

5. Protective Factors
• regular exercise and smoking
• Pregnancy
• Lactation
• Multiple full-term births
• Smoking

6. Pathogenesis
• The definitive cause of endometriosis remains
unknown,
• several theories are proposed.
1. retrograde menstruation through the fallopian
tubes
2. coelomic metaplasia theory
3. Vascular & Lymphatic Dissemination Theory
4. The direct transplantation theory
5. Induction theory(Hereditary Factor)
6. Autoimmune Disease Theory

7. Retrograde menstruation
• The retrograde menstruation and implantation theory
holds that endometrial tissue shed during menstruation
is transported via the fallopian tubes into the peritoneal
cavity where it implants on the surfaces of pelvic organs.
• Anatomical alterations of the pelvis that increase tubal
reflux of menstrual endometrium increases a woman's
chance of developing endometriosis “tract obstruction”

8. • Evidence supporting the implantation theory as one of the
primary mechanisms involved in the pathogenesis of
endometriosis inlcude:-
– Endometriosis is more prevalent in women with obstructing
müllerian anomalies than in women with malformations that do
not obstruct menstrual outflow.
– Viable endometrial cells recovered from the peritoneal fluid
during menses can be grown in cell culture and can attach to
and penetrate the mesothelial surface of the peritoneum.
– The incidence of endometriosis is increased in women with an
early menarche and/or short menstrual cycles.
– Endometriosis is observed most commonly in the dependent
portions of the pelvis, on the ovaries, in the anterior and
posterior cul-de-sacs, and on the uterosacral ligaments, the
posterior uterus, and the posterior surface of the broad
ligaments.

9. • Coelomic theory
– coelomic metaplasia theory holds that endometriosis
– The results from spontaneous metaplastic change in
mesothelial cells derived from the coelomic epithelium
(located in the peritoneum and the pleura).
• Induction theory
– The induction theory is a variation on the same theme and
envisions that coelomic metaplasia is induced by exposure
to menstrual effluent or other stimuli

10. Evidence supporting this theory
• Endometriosis has been described in a premenarchal girl and in
women who never have menstruated and also occurs in
adolescent girls having had relatively few menstrual cycles.
• Metaplasia in the pleura (derived from the coelomic epithelium,
like the peritoneum and the müllerian ducts), induced by steroid
hormones or chemical stimuli released by degenerating
endometrial cells into the peritoneal fluid is the more plausible
explanation.
• Metaplasia in misintegrated coelomic epithelium (adjacent to
the mesenchymal limb buds during early embryogenesis)can
explain endometriosis in unusual peripheral sites like the
extremities (thumb, thigh, knee).
• Rare cases of endometriosis have been observed in men
treated with high doses of estrogen (urinary bladder, abdominal
wall)

11. Vascular & Lymphatic Dissemination
Theory
• This theory explains endometriosis in locations
outside the pelvis and states that this likely develops
from dissemination of endometrial cells or tissue
through lymphatic channels or blood vessels.
• Vascular or lymphatic transport of endometrial cells
can also be involved in the inguinal canal, and the
umbilicus endometriosis.
• Additionally, the tendency of endometrial
adenocarcinoma to spread via the lymphatic route
indicates the ease at which endometrium can be
transported by this route

12. Direct transplantation theory
• Direct transplantation of endometrial tissue at
the time of cesarean section, other pelvic
surgery, or episiotomy repair seems the most
plausible explanation for endometriosis found
in abdominal scars and in the perineum

13. Anatomic Sites of Endometriosis
Endometriosis may develop anywhere within the pelvis and on other
extrapelvic peritoneal surfaces.
Uncommon locations.(rarely)
Inguinal canal
Abdominal or perineal scar
Pleura
Ureters.
Urinary bladder.
Kidney
Lung
Liver
Diaphragm
Pelvis: (Most commonly)
The ovary.
Anterior and posterior cul-de-sac
Posterior broad ligaments
Uterosacral ligaments.
Uterus (adenomiosis)
Fallopian tubes
Sigmoid colon
Round ligament.
Pelvic peritoneum.
Less commonly
Vagina
Cervix
Rectovaginal septum

14. Endometrial tissue Fallopian tube
Ovary
Uterus
Adhesions
Bladder
Vagina
Rectum
Principal Anatomic Sites of endometriosis found on the pelvic

15. Rare sites of endometriosis may present with
atypical cyclic symptom. For example:
 Women with urinary tract endometriosis may
describe cyclic irritative voiding symptoms and
hematuria.
 Those with rectosigmoid involvement may note
cyclic rectal bleeding.
Those with pleural lesions have been associated
with menstrual pneumothorax or hemoptysis
Anatomic Sites of Endometriosis

16. Clinical presentation
Pt can be Asymptomatic, sub fertile, or with variant degree of chronic
pelvic pain
4Ds
1) Dysmenorrhea
Cyclic pain with menstruation is noted commonly in women with
endometriosis. Typically, precedes menses by 24 to 48 hours and is less
responsive to NSAIDs and COCs.
2) Dyspareunia
• Endometriosis-associated dyspareunia is most often related to
rectovaginal septum or uterosacral ligament disease, and is less
commonly associated with ovarian involvement
3) Dysuria
• A less frequent symptom of endometriosis, cyclic urinary frequency and
urgency may be noted in affected women.
4) Dyschezia Defecatory Pain - typically reflects rectosigmoid involvement
with endometriotic implants

17. The type and severity of symptoms are dependent on the extent of
disease, the location, and the organs involved.

18. Endometriosis and infertility
Pathogenesis
• Mechanical interference
- Pelvic adhesions
- Chronic salpingitis
- Altered tubal motility
- Distortion of tubo-ovarian relations
- Impaired oocyte pickup

19. Mechanisms of Pain
• The pain associated with endometriosis
has been attributed to 3 primary
mechanisms:
The actions of inflammatory cytokines in
the peritoneal cavity.
The direct and indirect effects of focal
bleeding from endometriotic implants.
Irritation or direct infiltration of nerves in
the pelvic floor.

20. Complications of endometriosis
• Endocrinopathy. This may be mostly responsible for infertility
– Corpus luteum insufficiency
– Luteolysis due to increase in PGF2 alpha
– Luteinized unruptured follicle
– Anovulation
– Elevated prolactin level
– Double LH peak
• Rupture of cholate cyst
• Infection of cholate cyst
• Obstructive features
– Intestinal obstruction
– Ureteral obstruction; hydroureter leading to hydronephrosis and renal
failure
• Malignancy is rare, the commonest being adenocarcinoma

21. Diagnosis
• Classically, the diagnosis of endometriosis
requires surgical visualization of lesions and
histologic evidence of ectopic endometrial
glands and stroma.
• Clinical symptoms and physical examination

22. Investigations
• Non invasive methods
- CA 125 : high
- Transvaginal ultrasonography and MRI are both
highly sensitive and specific for detection of ovarian
endometriomas (GROUND GLASS) but cannot
reliably image peritoneal implants of disease
• Invasive Procedures
- Both diagnostic and therapeutic i.e. local excision,
laparoscopy, laparotomy.

23. The top, middle, and bottom series are
representative of red, white, and black
implants, respectively
Peritoneal
endometriosis

24. cont
• Biopsy findings;
- Endometrial epithelium
- Endometrial stroma
- Endometrial glands
- Haemosiderin laden with macrophages
Note ; two or more of above characteristics are
needed to make diagnosis of endometriosis

25. Differential diagnosis

26. Staging
• Classification systems for staging endometriosis are
based upon the anatomic location and severity of the
disease.
• There are various staging systems, but commonly used is
the one Introduced by the American Society for
Reproductive Medicine (ASRM)
• A point score based upon the size, depth, and location of
endometriotic implants and associated adhesions.
• The system help predict success in achieving pregnancy
following treatment of endometriosis and provide report
on operative findings.

27. 1. Minimal = stage I
2. Mild = stage II
3. Moderate = stage
III
4. Severe = stage IV
Endometriosis is classified as:

28. Surgical staging of Endometriosis
• It is surgically staged according to the revised ASRM scoring
system:
Stage I: Minimal disease is characterized by isolated implants and
no significant adhesions.
Stage II: Mild endometriosis consists of superficial implants that
are less than 5 cm in aggregate and are scattered on the
peritoneum and ovaries. No significant adhesions are present.
Stage III: Moderate disease exhibits multiple implants, both
superficial and deeply invasive. Peritubal and periovarian
adhesions may be evident.
Stage IV: Severe disease is characterized by multiple superficial
and deep implants, including large ovarian endometriomas.
Filmy and dense adhesions are usually present.

29. Examples of the classification of
endometriosis

30. American Society for
Reproductive Medicine
revised classification of
endometriosis

31. Treatment
• Depends on;
- Fertility desires
- age of the patient
- severity of the symptoms
- location of the lesion

32. cont
• Rx can either be;
1. Expectant Management
2. Medical
3. Surgical
4. Combination therapy

33. Expectant Management
Avoiding specific therapy is considered when patients:
- have minimal or no symptoms
- have suspected minimal or mild endometriosis
 NSAIDs/Analgesics: Minor pain may be controlled
Cyclic or continuous oral contraceptives: retard
progression of the disease and protect against unwanted pregnancy.
Infertile women having suspected limited disease may
be observed without treatment
Perimenopausal women may be managed expectantly
even when the disease is advanced, because
endometriotic implants usually regress in the absence of
ovarian hormone production after menopause.

34. Medical therapy
Endometriotic implant growth is highly dependent on ovarian
steroids.
 Medical therapy attempts to induced pseudopregnancy or
menopause
Drugs:
Progestins
Continuous oral contraceptives
Danazol
GnRH analogues

35. Effects of progestagens
- Inhibits pituitary release of LH
- Suppresses Steriodogenesis
- Promotes endometrial glandular atrophy
- Opposes estrogen effects
- Induces 17 B-hydroxysteroid dehydrogenases
to convert estrogen to weaker estrone
Examples; depo provera, norethindrone, IUD

36. Medical therapy
Danazol
Mechanisms of action:
(a)inhibition of pituitary gonadotropin secretion
(b)direct inhibition of endometriotic implant growth.
(c)direct inhibition of steroidogenic enzymes.
Doses:
- orally in divided doses from: 400 to 800 mg
daily/for 6 months.
Most women taking danazol have side effects.
Endometriomas and adhesions do not respond well
to danazol treatment

37. Medical therapy
Side effects of Danasol:
weight gain
 muscle cramps
 decreased breast size
 acne
 hirsutism
 oily skin
 decreased high-density lipoprotein levels
increased liver enzyme levels
 hot flashes
 mood changes
depression.

38. Medical therapy
The GnRH analogues:
Mechanism:
• profoundly suppress ovarian estrogen production by
inhibiting pituitary gonadotropin secretion
• Desensitization of gonadotrope receptors
• Reversible down regulation of pituitary-ovarian axis
Doses: (nasal spray or depot injections).
 400 to 800 mg daily for nasal nafarelin
 3.60 mg for monthly subcutaneous goserelin
3.75 mg for monthly intramuscular leuprolide.

39. Side effects of the hypoestrogenemia are common:
 hot flashes
 vaginal dryness
 decreased libido
 insomnia
 breast tenderness
 depression
 headaches
transient menstruation.
In addition, GnRH analogue treatment for the recommended 6-
month period decreases bone density and total body calcium, but
most of the bone loss is reversible.
Medical therapy
Side effects of GnRH analogues:

40. Surgical therapy
Laparoscopy or Laparotomy
Conservative: retains uterus and ovarian tissue
Definitive: removal of uterus and possibly ovaries
Indications for Surgery:
 when the symptoms are severe
 incapacitating
 when the disease is advanced.
 anatomic distortion of the pelvic organs
 endometriotic cysts
 obstruction of the bowel or urinary tract.
Women who are older than 35 years, infertile, or symptomatic
following expectant or medical management should be
treated surgically.

41. Surgical therapy
Laparoscopy: is the preferred to perform conservative surgery
Conservative surgery involves:
excision
fulguration
laser ablation of endometriotic implants
removal of associated adhesions
Definitive surgery is indicated when:
significant disease is present and pregnancy is not desired
when incapacitating symptoms persist following medical therapy
or conservative surgery
and when coexisting pelvic pathology requires hysterectomy
The ovaries may be conserved in younger women to avoid
the need for estrogen replacement therapy.

42. Combination therapy
Combination Medical and Surgical Therapy
Medical therapy is used before surgery:
-to decrease the size of endometriotic implants.
-reduce the extent of surgery.
Postoperative medical therapy:
When complete removal of implants is not possible or advisable
is used to treat residual disease.
Progestin, danazol, or GnRH analogues may be used in conjunction
with conservative or definitive surgery.
Preoperative medical therapy may decrease the amount
of surgical dissection required to remove implants.

43. Summary Points
The pathogenesis of endometriosis is poorly understood, but
emerging evidence supports the role of retrograde
menstruation and implantation of endometrial tissue.
Endometriosis is common in women with pelvic pain and/or
infertility.
Laparoscopy is the optimal technique to diagnose pelvic
endometriosis.
In most cases, surgical therapy at the time of initial diagnosis
effectively relieves pain and may enhance fertility.
Alternatively, medical therapy with progestins, progestin-
releasing intrauterine devices, danazol, or GnRH analogues
will ameliorate pelvic pain, but they do not enhance fertility.
Endometriosis is a recurrent disease, and definitive treatment
with removal of pelvic organs may be necessary.