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Subtle Endometriosis

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Subtle Endometriosis Powered By Docstoc
					                     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.
          Definition
     (Subtle,atypical,
       non-pigmented)

Endometriotic lesions that lack the
typical black-blue, powder-burn
appearance (Jansen &
Russel,1986)
                     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 next most common is a glandular-like excrescence.
The least common, but nevertheless characteristic, is the
red flame like (Jansen & Russel,1986).
Classification & morphology
Red lesions:
1.Red flame-like lesions or red vesicular
  excrescences: more commonly
  affecting the broad ligament &
  uterosacral ligaments.
Histologically: active E surrounded by
  stroma
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.
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
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)
                 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
               Biological activity

SE are thought to be more biologically active
than typical forms. Vernon et al (1986)
demonstrated that red peticheal implants produce
twice the amount of PGF than brown lesions, which
in turn produce more PGF than typical powder-burn
implants.

On other hand Muzii et al (2000) found that the
biologic activity of red & black implants was
similar The sample size of their study was
relatively small to draw firm conclusions
   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.
• 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
                   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.
So,
1. Red lesions are probably the first stage of
   early implantation of endometrial glands
   & stroma.
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
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)
    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).
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))
          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
1.INFERTILITY: SE is the most
common single cause (70%) of
unexplained infertility (Propst &
Laufer,1999).
SE can be etiologically important in
infertility.
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 lesions &
not with atypical fresh clear implants.
•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. .
•Chronic pelvic pain: SE is
the most common single
cause of chronic pelvic pain
not responding to medical
treatment     (Propst     &
Laufer,1999).
3.PREMENSTRUAL
SPOTTING: In the absence of
pigmented E at laparoscopy,
premenstrual spotting was
highly predictive of SE (Jansen
& Russel,1986) .
                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)
B. lactated Ringer or normal saline introduced into
   the pelvis (Laufer,1997). Laparoscopic visualization
   of of clear vesicular lesions 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. Vesicular lesions are no
   longer falsely interpreted as light reflection.
C. Near-contact laparoscopy (Redwin,1987):
Visualization at magnifications of 1- to 7-power
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.
E. Bubble test (Amer A & Omar M., 2002)
 During laparoscopy, the posterior 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.
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.
              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)
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.
                     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.
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
1.    Endometriosis & pain:
a. Medical management: Several drugs are effective in
temporarily relieving pain associated with E. Non-steroidal anti-
inflammatory drugs may be effective in reducing the pain
associated with E. The choice between the combined oral
contraceptive, progestagens, danazol & GnRH agonists depends
principally upon their side-effect profiles because they relieve
pain associated with E. equally well. It seems sensible to
prescribe the safest & cheapest therapy.
b. Surgical management: Although there are limited data available from
RCT assessing the effectiveness of surgery in relieving pain, it is clearly
effective for many women. However, clinical experience shows that some
women fail to respond to surgical treatment either because of incomplete
excision or because of post-operative disease recurrence.
2.    Endometriosis & infertility:
a. Medical management: There is no role for medical
therapy with hormonal drugs in the treatment of E
associated infertility. Ovarian stimulation with intrauterine
insemination (IUI) is more effective than either no
treatment or IUI alone in infertile women with minimal or
mild E.
b. Surgical management: In infertile women with minimal
or mild E. detected at laparoscopy, destruction or
ablation of the endometriotic implants & lysis of
adhesions at that time is recommended to improve the
chance of pregnancy.
1. SE are more common than the classic dark blue-
   black lesions in adolescents
2. The most common type of SE is white opacification
   the next most common is glandular-like
   excrescence.
3. SE progress to pigmented E over time
4. Red lesions are probably the first stage of early
   implantation of endometrial glands & stroma &
   white lesions could be latent stages of E.
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, whether its lesions are pigmented or not, does
   not itself demand treatment unless it is causing, or
   it is likely to cause symptoms.

				
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