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SUBTLE
ENDOMETRIOSIS
contents
• History
• Definition
• Typical lesions
• Atypical (subtle) lesions
• Non-visible endometriosis
• Prevalence
• Biological activity
• Clinical picture
• Diagnosis
• Differential diagnosis
• Treatment
History
• In 1981 , Chatman observed that unsuspected
Endometriosis could be found in peritoneal
pockets.
• In 1986 , Jansen & Russel published their
observations on non-pigmented Endometriosis.
• They concluded that:
Visualization of pigment is not necessary to
diagnose E.
Endometriosis in earlier stages of histogenesis
may display only non-pigmented lesions.
synonyms
•Atypical endometriosis.
•Non pigmented endometriosis
Definition
•Endometriosis: The presence of functional
endometrium outside the uterine cavity.
•Atypical (Subtle) endometriosis:
Endometriotic lesions that lack the typical black-
blue, powder-burn appearance.
(Jansen & Russel,1986)
Typical lesions
Black or bluish lesions:
• It results from tissue bleeding and retention
of blood pigment.
Typical lesion
SUBTLE LESIONS
I- RED lesions:
• Red flame-like lesions: more commonly affecting
the broad ligament & uterosacral ligaments.
Histologically: active E surrounded by stroma
• Glandular excrescences: resemble the
mucosal surface of the endometrium.
Histologically: numerous endometrial glands.
• Areas with hypervascularization: resemble the
peticheal lesions due to manipulation of the
peritoneum or to hypervascularization of the
peritoneum.
II- White lesions:
• 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.
• Subovarian adhesions:
 Histologically: connective tissue with sparse
endometrial glands
• 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.
• 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)
Non-visible endometriosis
• Biopsies were taken from visually normal
peritoneum of the uterosacral ligaments.
• Histological study revealed the presence of
endometriotic tissue in about 6% of infertile
women without endometriosis.
Nezhat F et al, 1991, Walter AJ et al, 2001.
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).
Biological activity
• Subtle endometriosis are thought to be
more biologically active than typical forms.
• The red petechial implants produce twice
the amount of PGF than brown lesions,
which in turn produce more PGF than typical
powder-burn implants.
Clinical picture
1.Infertility.
2.Pain:
• Chronic pelvic pain.
• Dysparunia.
• Dysmenorrhea.
3.PREMENSTRUAL BLEEDING
•Infertility:
SE is the most common single cause of
unexplained infertility.
(Propst & Laufer,1999).
•Pain:
Endometriosis occurs in approximately 70%
of adolescent girls with chronic pelvic pain not
responding to conventional medical therapy
and the majority of patients have stage I
disease.
(Ivo Brosens et al, 2013)
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
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).
3.PREMENSTRUAL
SPOTTING:
In the absence of classic E at laparoscopy,
premenstrual spotting was highly predictive
of SE (Jansen & Russel,1986) .
Diagnosis
•Standard laparoscopy:
Negative laparoscopy results do not mean
that the patient has no E (Martin,1999)
•Laparoscopy under hydroflotation:
Using lactated Ringer or normal saline
introduced into the pelvis (Laufer,1997).
•Near-contact laparoscopy
Visualization at magnifications of 1- to 7-
power (Redwin,1987)
•Peritoneal blood painting :
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. (Redwin,1989)
•E. Bubble test :
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. (Amer A & Omar M., 2002)
•Transvaginal hydrolaparoscopy:
Superior to standard laparoscopy for detection
of Subtle endometriotic adhesions of the
ovary(Brosen et al,2001)
•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)
•Histopathologic examination:
Biopsy taken from suspected lesions.
Differential diagnosis
• Hemangiomas.
• Old suture.
• Reaction to oil-contrast medium.
• Epithelial inclusions.
• Secondary breast & ovarian cancer.
• inflammatory cystic inclusions.
• Walthard rests, adrenal rests
 Differentiation between SE & above lesions may be
impossible visually but may be achieved histologically
TREATMENT
• Aim of treatment:
Reduce pain.
Increase the possibility of pregnancy.
Delay recurrence for as long as possible.
• Ideal Goal (ASRM recommendation):
 Endometriosis should be viewed as a
chronic disease that requires a life-long
management plan
with the goal of maximizing the use of
medical treatment and avoiding repeated
surgical procedures. Fertil & Steril, 2008
Advances in
treatment
dienogest mirena
SPRM
Aromatase
inhibitor
Angiogenesis
inhibitor
Dienogest (Visanne)
• Synthetic oral progestogen with unique
pharmacological properties.
• highly selective for the progesterone
receptor .
Dienogest
• 2mg once-daily.
• Can start at any day of menstrual
cycle.
• Must be continued regardless of vag.
Bleeding.
• Advantages:
Dienogest appears to be safe and effective
when taken for up to 2 years.
Dienogest is an oral therapy.
Treatment of endometriosis with dienogest
is not inferior to that with GnRH agonists.
Meirina ( LNG-IUD)
• Treatment of choice for endometriosis
associated pain in women who do not
wish to conceive:
 Effective for at least 5 ys.
Can be reapplied every 5 ys.
No modifications in estrogen levels.
Low-cost therapy.
Fewer side effects than other
progestogenic agents.
Aromatase inhibitors
• Idea of use:
In Normal endometrium: No detectable
levels of aromatase activity
In endometriosis: An increased expression
of cytochrome P450 aromatase in
endometrial tissue.
• Disadvantages:
Cost
Osteoporosis {decrease E in local
tissues}. Controversial
Selective Progesterone
receptor modulators
(SPRM)
• Asoprisnil:
It reduce pelvic pain as well as
dysmenorrhea.
Its effect on bleeding pattern is dose-
dependent. (Chwalisz et al, 2004).
• Advantage: No estrogen deprivation.
Angiogenesis inhibitors
• Statins:
Inhibit the growth of human endometrial
stromal cells in vitro (Piotrowski et al, 2006).
• Thalidomide:
Angiostatic & Immunomodulatory
Effective in women with relapsing
endometriosis (Scarpellini et al, 2002).
Surgical management:
• Laparoscopy:
Destruction or ablation of the
endometriotic implants
Lysis of adhesions
Made by
•Ahmed khalaf el-said
•Ahmed hamdy
•Ahmed hussein
•Ahmed el-said aref

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subtle-endometriosis.pptx

  • 2. contents • History • Definition • Typical lesions • Atypical (subtle) lesions • Non-visible endometriosis • Prevalence • Biological activity • Clinical picture • Diagnosis • Differential diagnosis • Treatment
  • 3. History • In 1981 , Chatman observed that unsuspected Endometriosis could be found in peritoneal pockets. • In 1986 , Jansen & Russel published their observations on non-pigmented Endometriosis. • They concluded that: Visualization of pigment is not necessary to diagnose E. Endometriosis in earlier stages of histogenesis may display only non-pigmented lesions.
  • 5. Definition •Endometriosis: The presence of functional endometrium outside the uterine cavity. •Atypical (Subtle) endometriosis: Endometriotic lesions that lack the typical black- blue, powder-burn appearance. (Jansen & Russel,1986)
  • 6. Typical lesions Black or bluish lesions: • It results from tissue bleeding and retention of blood pigment.
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  • 9. SUBTLE LESIONS I- RED lesions: • Red flame-like lesions: more commonly affecting the broad ligament & uterosacral ligaments. Histologically: active E surrounded by stroma • Glandular excrescences: resemble the mucosal surface of the endometrium. Histologically: numerous endometrial glands. • Areas with hypervascularization: resemble the peticheal lesions due to manipulation of the peritoneum or to hypervascularization of the peritoneum.
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  • 14. II- White lesions: • 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. • Subovarian adhesions:  Histologically: connective tissue with sparse endometrial glands
  • 15. • 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. • 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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  • 19. Non-visible endometriosis • Biopsies were taken from visually normal peritoneum of the uterosacral ligaments. • Histological study revealed the presence of endometriotic tissue in about 6% of infertile women without endometriosis. Nezhat F et al, 1991, Walter AJ et al, 2001.
  • 20. 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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  • 22. Biological activity • Subtle endometriosis are thought to be more biologically active than typical forms. • The red petechial implants produce twice the amount of PGF than brown lesions, which in turn produce more PGF than typical powder-burn implants.
  • 23. Clinical picture 1.Infertility. 2.Pain: • Chronic pelvic pain. • Dysparunia. • Dysmenorrhea. 3.PREMENSTRUAL BLEEDING
  • 24. •Infertility: SE is the most common single cause of unexplained infertility. (Propst & Laufer,1999).
  • 25. •Pain: Endometriosis occurs in approximately 70% of adolescent girls with chronic pelvic pain not responding to conventional medical therapy and the majority of patients have stage I disease. (Ivo Brosens et al, 2013)
  • 26. 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 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).
  • 27. 3.PREMENSTRUAL SPOTTING: In the absence of classic E at laparoscopy, premenstrual spotting was highly predictive of SE (Jansen & Russel,1986) .
  • 28. Diagnosis •Standard laparoscopy: Negative laparoscopy results do not mean that the patient has no E (Martin,1999) •Laparoscopy under hydroflotation: Using lactated Ringer or normal saline introduced into the pelvis (Laufer,1997). •Near-contact laparoscopy Visualization at magnifications of 1- to 7- power (Redwin,1987)
  • 29. •Peritoneal blood painting : 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. (Redwin,1989) •E. Bubble test : 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. (Amer A & Omar M., 2002)
  • 30. •Transvaginal hydrolaparoscopy: Superior to standard laparoscopy for detection of Subtle endometriotic adhesions of the ovary(Brosen et al,2001) •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) •Histopathologic examination: Biopsy taken from suspected lesions.
  • 31. Differential diagnosis • Hemangiomas. • Old suture. • Reaction to oil-contrast medium. • Epithelial inclusions. • Secondary breast & ovarian cancer. • inflammatory cystic inclusions. • Walthard rests, adrenal rests  Differentiation between SE & above lesions may be impossible visually but may be achieved histologically
  • 32. TREATMENT • Aim of treatment: Reduce pain. Increase the possibility of pregnancy. Delay recurrence for as long as possible.
  • 33. • Ideal Goal (ASRM recommendation):  Endometriosis should be viewed as a chronic disease that requires a life-long management plan with the goal of maximizing the use of medical treatment and avoiding repeated surgical procedures. Fertil & Steril, 2008
  • 35. Dienogest (Visanne) • Synthetic oral progestogen with unique pharmacological properties. • highly selective for the progesterone receptor .
  • 36. Dienogest • 2mg once-daily. • Can start at any day of menstrual cycle. • Must be continued regardless of vag. Bleeding.
  • 37. • Advantages: Dienogest appears to be safe and effective when taken for up to 2 years. Dienogest is an oral therapy. Treatment of endometriosis with dienogest is not inferior to that with GnRH agonists.
  • 38. Meirina ( LNG-IUD) • Treatment of choice for endometriosis associated pain in women who do not wish to conceive:  Effective for at least 5 ys. Can be reapplied every 5 ys. No modifications in estrogen levels. Low-cost therapy. Fewer side effects than other progestogenic agents.
  • 39. Aromatase inhibitors • Idea of use: In Normal endometrium: No detectable levels of aromatase activity In endometriosis: An increased expression of cytochrome P450 aromatase in endometrial tissue.
  • 40. • Disadvantages: Cost Osteoporosis {decrease E in local tissues}. Controversial
  • 41. Selective Progesterone receptor modulators (SPRM) • Asoprisnil: It reduce pelvic pain as well as dysmenorrhea. Its effect on bleeding pattern is dose- dependent. (Chwalisz et al, 2004). • Advantage: No estrogen deprivation.
  • 42. Angiogenesis inhibitors • Statins: Inhibit the growth of human endometrial stromal cells in vitro (Piotrowski et al, 2006). • Thalidomide: Angiostatic & Immunomodulatory Effective in women with relapsing endometriosis (Scarpellini et al, 2002).
  • 43. Surgical management: • Laparoscopy: Destruction or ablation of the endometriotic implants Lysis of adhesions
  • 44.
  • 45. Made by •Ahmed khalaf el-said •Ahmed hamdy •Ahmed hussein •Ahmed el-said aref