Subtle Endometriosis

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Benha university, Egypt [email protected] Aboubakr Elnashar

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Subtle Endometriosis

Transcript of Subtle Endometriosis

Page 1: Subtle Endometriosis

Benha university, Egypt

[email protected]

Aboubakr Elnashar

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History

In 1981, Chatman observed that unsuspected E.

could be found in peritoneal pockets.

In 1986 Jansen & Russel published their

observations on non-pigmented E. They concluded

that:

•Visualization of pigment is not necessary to

diagnose E.

•E. in earlier stages of histogenesis may display only

non-pigmented lesions.

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Definition

(Subtle, atypical, non-pigmented)

Endomertiotic lesions that lack the

typical black-blue, powder-burn

appearance

(Jansen & Russel,1986)

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Prevalence

Diagnosis of SE increased from 15% in 1986 to 65%

in 1988 (Nisole et al,1993).

SE are more common than the classic lesions in the

adolescents with pelvic pain (Davis et al,1993).

The incidence decreases with age (Konincks et al,1991).

The most common is white opacification of the

peritoneum

The least common, but nevertheless characteristic,

is the red flame like (Jansen & Russel,1986).

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Classification & morphology

Red lesions:

1. Red flame-like lesions, red vesicles or clear

vesicles: more commonly affecting the broad

ligament & uterosacral ligaments.

Histologically: active E surrounded by stroma

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2. Glandular excrescences resemble the mucosal

surface of the endometrium seen at hysteroscopy

Histologically: numerous endometrial glands.

3. Areas of petechial peritoneum or areas with

hypervascularization: resemble the peticheal lesions

due to manipulation of the peritoneum or to

hypervascularization of the peritoneum.

They frequently affect the bladder & the broad ligam.

Histologically: red blood cells are very rare.

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White lesions:

1. White opacification: appears as peritoneal scaring or as

circumscribed patches often thickened & sometimes raised.

Histologically: an occasional retroperitoneal glandular

structure & scanty stroma surrounded by fibrotic tissue or

connective tissue.

2. Subovarian adhesions.

Histologically: connective tissue with sparse

endometrial glands

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3. Yellow-brown peritoneal patches resembling café au lait patches.

Histologically:similar to those observed in white opacification, but haemosiderin among the stroma cells produces the café au lait colour.

4. Circular peritoneal defects: frequently occur in areas of the pelvis which overlie loose connective tissue.

80% of peritoneal defects are associated with E, either on the border of the defect or in the defect itself (Donnez et al,1992)

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NATURE

E is a dynamic disease, especially in the early

phase, with S lesions emerging & vanishing

again(Evers et al,1998). In the end however

the peritoneal defense system will prevail & the

disease will be contained in the majority of

patients.

Koninckx et al (1994) considered SE a natural

condition occurring intermittently in all women

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Biological activity

SE are thought to be more biologically

active than typical forms. Vernon et al (1986)

demonstrated that red lesions produce twice the

amount of PGF than brown lesions.

On other hand Muzii et al (2000) found that the

biologic activity of red & black lesions was

similar The sample size of their study was

relatively small to draw firm conclusions Aboubakr Elnashar

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Natural progression to

classic lesions

• Redwine (1986) showed that:

1. Clear & red lesions occur at a mean age

10 years earlier than the black lesions.

2.A progression of E: from clear to red

to white to black, with increasing age. Aboubakr Elnashar

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• Increasing age is associated with a

decreasing incidence of SE & increased

incidence of typical E, endometrioma &

deeply infiltrating E (Koninckx et al,1991).

• SE progress to pigmented E over time

(Jansen & Russel,1986). Second look

laparoscopy in untreated patients 6 to 24

months following the initial surgery,

documented pigmented lesions in areas

previously contained SE Aboubakr Elnashar

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Prognosis

1. Vascularization is one of the most important factors

of growth & invasion of endometrial glands in other

tissue (Donnez et al,1989). When compared with

typical black lesion, the vascularization was

found to be significantly higher in red

lesions & significantly lower in white lesions. This change was due to an increase (red) or decrease

(white) in the volume occupied by the vessels, as proved by

both mean capillary surface area & the ratio of

capillaries/stroma surface area. Aboubakr Elnashar

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So,

1. Red lesions are probably the first stage of

E.

2. White lesions could be latent stages of E

as suggested by the poor vascularization

observed. They are probably non-active

lesions which have been quiescent for a

long time

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2. Mitotic index: Mitotic processes permit

the maintenance & the growth of peritoneal

E.

MI is significantly different in typical &

subtle E .

The absence of mitosis in white

lesions proves their low activity

(Nisolle et al,1993) Aboubakr Elnashar

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American Society for Reproductive

Medicine (ASRM) classification of E

The only difference between the 1985 AFS classification &

1996 ASRM classification is that the latter includes

information on the morphologic appearance of the

disease.

In the new ASRM classification, peritoneal & ovarian

implants are categorized into 3 subgroups:

1. Red (red, red-pink & clear lesions)

2. White (white, yellow-brown & peritoneal defects)

3. Black (black & blue lesions). Aboubakr Elnashar

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The percentage of surface involvement of each

implant type (red, white, & black) must be recorded

on the opposite form.

The new ASRM classification of E is the gold standard to clearly document the extent & location of the disease

(Muzii et al,2000)

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Clinical features

• SE has the same (possibly PG related)

symptoms that characterize classic E (Jansen

& Russel,1986)

1. IFERTILITY

2. PAIN: dysmenorhea, dysparunia,

ch.pelvic pain

3. PREMENSTRUAL BLEEDING Aboubakr Elnashar

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1.INFERTILITY:

SE is the most common single cause (70%) of

unexplained infertility

(Propst & Laufer,1999).

SE can be etiologically important in infertility.

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2. PAIN:

• Acquired deep dysparunia was

found in 18% of SE (Jansen &

Russel,1986).

On other hand Vercellini et al(1996)

observed that deep dysparunia was

associated only with typical E & not with

SE Aboubakr Elnashar

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•Increasing dysmenorrhea suggestive of active

E is present in 64% of SE (Tansen &

Russel,1986).

The number of typical or S implants did not correlate with the severity

of dysmenorrhea (Muzii et al,1997). The S forms, however, were

considered together & were not categorized into red & white

subgroups , as in the new ASRM classification.

Recently Muzi et al (2000) found no correlation between the ASRM

classification of E & associated dysmenorrhea.

White implants are associated with milder

pain symptoms than the black or red

lesions. Aboubakr Elnashar

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•Chronic pelvic pain: SE is

the most common single

cause of chronic pelvic pain

not responding to medical

treatment (Propst &

Laufer,1999). Aboubakr Elnashar

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3.PREMENSTRUAL

SPOTTING: In the absence

of classic E at laparoscopy,

premenstrual spotting was

highly predictive of SE

(Jansen & Russel,1986) . Aboubakr Elnashar

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Diagnosis

The ability to diagnose SE is directly related to the

experience & skill of the surgeon(Cook & Rock,1993)

1. Laparoscopy:

A. Standard laparoscopy:

Negative laparoscopy results do not mean that the

patient has no E

(Martin,1999)

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B. lactated Ringer or normal saline

introduced into the pelvis

(Laufer,1997).

Laparoscopic visualization of of clear vesicles can be

facilitated by the use of the three-dimensional effect

of the fluid. The laparoscope is submerged so that

the optical distension medium is now liquid as

opposed to CO2. The magnification focal length of

the laparoscope is adjusted for the new refractory

index through the liquid. Vesicles are no longer

falsely interpreted as light reflection.

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C. Near-contact laparoscopy

(Redwin,1987)

Visualization at magnifications of 1- to 7-power

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D. Peritoneal blood painting

(Redwin,1989):

SE can be seen more easily by painting the

peritoneal surface with bloody peritoneal fluid. The

physical- chemical properties of blood cause it to

interact with S. physical deformities of the

peritoneal surface in such a way as to cause

flowing erythrocytes to outline surface

irregularities.

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E. Bubble test

(Amer A & Omar M., 2002)

During laparoscopy, the cul de sac is irrigated with

short bursts of saline under controlled pressure.

Development of dense soap like bubbles staying for

at least 5 seconds indicates a positive test. The

positivity of the test is apparently related to

increased level of triglycerides in peritoneal fluid in

cases of E.

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2. Transvaginal hydrolaparoscopy is superior to

standard laparoscopy for detection of S

endometriotic adhesions of the ovary (Brosen et

al,2001)

3. Elevated serum levels of endometrial

secretory protein (placenta protein 14). The

highest levels in patients with E are found on

days 1 to 4 of the cycle (Seppala et al,1989)

4. Histopathologic examination of biopsy taken

from suspected lesions. Aboubakr Elnashar

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Differential diagnosis

Not all abnormalities of the peritoneum represent E (Cock &

Rock,1993). Stripling et al (1988) confirmed E in

91% of white lesions,

75% of red lesions,

33% of haemosiderin lesions, &

85% of other lesions

1. White E should be differentiated from postoperative

scaring & from fibrotic adhesions resulting from inflammatory

disease (Cock & Rock,1993)

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2.Other lesions which may mimic E include

hemangiomas, old suture, residual carbon from laser

surgery, reaction to oil-contrast medium, epithelial

inclusions, secondary breast & ovarian cancer,

inflammatory cystic inclusions,Walthard rests, adrenal

rests(Cock & Rock,1993).

Differentiation between SE & other lesions may

be impossible visually but may be achieved

histologically through excision or biopsy. An

abnormality of the peritoneum, no matter what its size,

shape, or appearance, should suggest the possibility of E.

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Treatment

E, whether its lesions are pigmented or not, does not

itself demand treatment unless it is causing, or it is

likely to cause symptoms. SE should receive the

same pathophysiological & therapeutic attention that

classic lesions do.

There is a substantial difference between the expectant

management of the isolated lesions found incidentally in a

woman towards the end of reproductive years & the active

management for a widespread non-pigmented lesions in a

teenager with many years of ovulation before her.

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The first question to be asked is whether

treatment is appropriate at that time

(Kim,1999). If it is, a comprehensive plan

should be formulated that takes into account

the woman’s primary complaint (infertility or

pain) & reproductive desires.

The guidelines of the Royal College of

obstetricians & Gynaecologists in

management of E.( july, 2000) Aboubakr Elnashar

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1. Endometriosis & pain:

a. Medical management:

Non-steroidal anti-inflammatory drugs may be effective.

Combined oral contraceptive, progestagens, danazol &

GnRH agonists relieve pain associated with E. equally

well. It seems sensible to prescribe the safest & cheapest

therapy.

b. Surgical management: Surgery is clearly effective for

many women. However, some women fail to respond to

surgical treatment either because of incomplete excision or

because of post-operative disease recurrence. Aboubakr Elnashar

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2. Endometriosis & infertility:

a. Medical management:

No role for medical therapy

In minimal or mild E: Ovarian stimulation IUI

b. Surgical management:

In minimal or mild E. laparoscopy, destruction

or ablation of the endometriotic implants & lysis

of adhesions

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1. SE are more common than the classic dark

blue-black lesions in adolescents

2. The most common type of SE is white

opacification

3. SE progress to classic E over time

4. Red lesions are probably the first stage of

early E & white lesions could be latent stages

of E.

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5. In the new ASRM classification, peritoneal &

ovarian implants are categorized into red,

white & black

6. SE has the same symptoms that

characterize classic E.

7. Negative laparoscopy results do not mean

that the patient has no E

8. E. does not itself demand treatment unless it

is causing, or it is likely to cause symptoms.

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