Subtle Endometriosis
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Transcript of Subtle Endometriosis
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.
Aboubakr Elnashar
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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Aboubakr Elnashar
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
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
• 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
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
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
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
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
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
•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
•Chronic pelvic pain: SE is
the most common single
cause of chronic pelvic pain
not responding to medical
treatment (Propst &
Laufer,1999). Aboubakr Elnashar
3.PREMENSTRUAL
SPOTTING: In the absence
of classic E at laparoscopy,
premenstrual spotting was
highly predictive of SE
(Jansen & Russel,1986) . Aboubakr Elnashar
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
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
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
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.
Aboubakr Elnashar
Aboubakr Elnashar