Step by Step® Management of Endometriosis PDF

Step by Step
Management of
Endometriosis
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Step by Step
Management of
Endometriosis
Sudha Prasad
MD (AIIMS) FICOG FICMCH
Professor
Maulana Azad Medical College
New Delhi, India
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Step by Step Management of Endometriosis
2008, Jaypee Brothers Medical Publishers
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Preface
In spite of vast advances in gynecology, diagnosis of

endometriosis remains challenging. Despite an
extensive number of new laboratory tests and advances
in imaging technologies, at present there are no simple
noninvasive diagnostic tests for endometriosis.
Complete clinical assessment supported by selective
and critical use of laboratory and imaging studies may
help in the identification of a high-risk patient
population. However, in a large proportion of cases,
diagnosis of endometriosis requires careful laparoscopic
evaluation combined with a thoughtful interpretation
of histological examination of excised lesions.
Misdiagnoses and under-diagnoses of endometriosis are
not only due to the limitations of diagnostic tools but
also due to lack of recognition of the symptoms by the
patients and physicians. Although in a large proportion
of patients, early diagnosis of endometriosis is essential
for the formulation of an appropriate treatment plan,
one should keep in mind that detection of endometriosis
in asymptomatic women does not automatically
necessitate medical or surgical management. IV
pyelography, CT, MRI is not specific or adequate for
diagnosis. However, these can be performed to support
the diagnosis.
This handbook will provide the necessary clinical
knowledge to diagnose and manage this elusive disease.
Sudha Prasad
Contents
1. Introduction of Endometriosis 1
2. Etiopathogenesis of Endometriosis 5
3. Clinical Staging of Endometriosis 13
4. How to Diagnose Endometriosis? 27
5. Medical Management of Endometriosis 49
6. Surgical Management of Endometriosis 65
7. Endometriosis and Assisted Reproductive
Technologies 75
Index 81
2 MANAGEMENT OF ENDOMETRIOSIS
Endometriosis is a common, poorly understood benign

disorder. Endometriosis is the growth of endometrial
tissue, i.e. glands and stroma, outside of the uterine
cavity. It induces a chronic, inflammatory reaction on
the peritoneal lining of pelvic organs such as the ovaries
and uterus. Other parts of the body like lungs also can
be occasionally involved. Due to inflammation and
extensive fibrosis adhesion formation occurs leading to
tubo-ovarian adhesion and finally distortion of pelvic
organs in severe cases. This disease varies from small
subtle lesions to large endometriotic cyst. These cysts
subsequently thinned out and burst focally to adjacent
areas leading to further adhesion formation. These
adhesions may be flimsy to very dense one. The
condition is predominantly found in women of
reproductive age. Therefore, it leads to subfertility,
severe dysmenorrhea, deep dyspareunia and chronic
pelvic pain.
PREVALENCE
In early 18th century, there was the custom of early
marriage and early pregnancies. As retrograde
menstruation is the well-accepted etiological factor and
lactational amenorrhea used to prevent endometriosis
in young women. Hence, endometriotic nodules were
felt more often in older women. After the advent of
laparoscope early detection of endometriosis has
become easier.
INTRODUCTION OF ENDOMETRIOSIS 3
The overall true prevalence of endometriosis is

unknown because the surgery is the only reliable
method for its early diagnosis. The estimated prevalence
is approximately 8-10 percent in the reproductive age
group. The prevalence of endometriosis is found to be
higher in infertiles as the laparoscopy is the gold
standard tool for the infertility investigations. It was
observed as high as 20-40 percent among infertile
groups. 1,2 In our study at Maulana Azad Medical
College, we found 2 percent prevalence in fertile women
and 12 percent in infertile women (unpublished data).
To get the precise prevalence in general population
it is required to have laparoscopic inspection of pelvis,
skill of surgeon to do laparoscopy meticulously, and to
identify small colorless subtle endometriotic lesions and
finally confirmation of lesions histologically. Possibility
of familial tendency of endometriosis has been reported
by many investigators.3
REFERENCES
1. Cornillie FJ, Oosterlynck D, Lauweryns JM, Koninckx PR.
Deeply infiltrating pelvic endometriosis: Histology and
clinical significance. Fertil Steril 1990;53:978-83.
2. Chopin N, Ballester M, Borghese B, Fauconnier A, Foulot
H, Malartic C, et al. Relation between severity of dys-
menorrhea and endometrioma. Acta Obstet Gynecol
Scand 2006;85(11):1375-80.
3. Sung Hoon Kim, Young Min Choi, Seon Ha Choung, Jong
Kwan Jun, Jung Gu Kim, Shin Yong Moon. Vascular
endothelial growth factor gene + 405 C/G polymorphism
is associated with susceptibility to advanced stage
endometriosis. Human Reproduction 2005;20(10):2904-8.
The cause of endometriosis remains elusive even after

years of research. In the meantime, speculations
continue as to the cause of endometriosis.
One speculation is that endometrial tissue is spread
by retrograde menstruation or by vascular and/or
lymphatic spread. Another speculation that a deficiency
in the immune system allows menstrual tissue to
implant and grow in areas other than the uterine lining
or the cells lining the abdominal cavity may sponta-
neously develop endometriosis. A genetic cause
proposes that certain families may exhibit predisposing
factors that lead to endometriosis.
Some of the theories that have been put forward over
the years include:
Retrograde Menstruation
Dr Sampson postulated this theory in the early 1920s.1
He speculated that during menstruation, a certain
amount of menstrual fluid flowed backward from the
uterus to shower the pelvic organs and pelvis lining
with endometrium cells (Fig. 2.1).
Retrograde menstruation causes endometriosis is
supported by the analysis of peritoneal fluid in women.
During the perimenstrual period around 90 percent of
women have blood in the peritoneal fluid. In addition,
endometrial cells have been found in the peritoneal
fluid. The pattern of endometriosis is consistent with
retrograde menstruation and is most common in the
ovary, followed by the other dependent areas of the
ETIOPATHOGENESIS OF ENDOMETRIOSIS 7
Fig. 2.1: Retrograde menstruation -shower of the pelvic

organs and pelvis lining
pelvis. The next most frequent locations include the

uterine ligaments, pelvic cul-de-sac, pelvic peritoneum,
fallopian tubes, rectosigmoid, and bladder. Rarely,
endometriosis can be extraperitoneal, affecting the lungs
and CNS.
Staging of endometriosis depends on the degree and
complications of endometrial implants. The 1985
Revised Classification of Endometriosis, created by the
American Society for Reproductive Medicine, evaluated
the characteristics of endometrial implants, such as
location and the depth of penetration, as well as the
degree of cul-de-sac obliteration and adhesions.
Classification of Endometriosis:
(According to the Findings on Laparoscopy)
Classify patients into 4 stages:
Stage I Minimal
Stage II Mild
Stage III Moderate
Stage IV Severe.
The staging correlates with the likelihood of
achieving pregnancy but not with the severity of pain.
Critical Steps Postulated in the Development of

Endometriotic Lesions2 (Fig. 2.2)
Vascular and/or lymphatic spread is supported by
findings of the occasional distal (extraperitoneal) sites
of endometriosis, including the lungs and central
nervous system (CNS). In addition, teenage girls with
Fig. 2.2: Critical steps postulated in the development of

endometriotic lesions
obstructive uterine or vaginal anomalies show

retrograde menstrual bleeding, and endometriosis is
common in these patients.
Celomic Metaplasia
This theory holds that certain cells, when stimulated,
as in women taking estrogen replacement therapy, can
transform themselves into a different kind of cells. The
serosal epithelium of the peritoneum undergoes
metaplastic differentiation into endometrium-like
tissue. The theory that metaplasia causes endometriosis
is supported by the fact that endometrial cells and
peritoneal cells derive from the same celomic wall
epithelium. This theory also is supported by develop-
ment of endometriosis in women who lack normal
endometrial tissue (In Turners syndrome and uterine
agenesis). In addition, rare cases of endometriosis have
been found in the prostatic utricle of men. The prostatic
utricle is a mullerian remnant.
The Transplantation Theory

That endometriosis spreads via the circulatory and
lymphatic system.
Iatrogenic Transplantation
Endometriosis is accidentally transported during
surgery (Scar endometriosis). This is highly unlikely
today, due to advanced surgical management and it
does not account for the presence of the disease in the

first place.
The Hereditary Theory

Women with family members who have endometriosis
are more likely, or are susceptible to developing the
disease. Similar to this theory, the women can be born
with migrant endometrial cells in the pelvic cavity,
which in later life can develop into endometriosis.
Environmental Factors
A great deal of research is clearly highlighting that
women who are exposed to environmental toxins are
at much greater risk of developing endometriosis along
with other serious health disorders. These toxins include
PCBs, DDT and Dioxin all of which are widely spread
throughout the world today. The other major environ-
mental toxins are collectively known as xenoestrogens.
These are compounds and chemicals found in the
environment and food chain that react negatively with
the natural balance of the body, both male and female,
causing a damaging imbalance in the system.
Liver Disorders
The liver regulates and removes estrogen from the body.
If the function of the liver is compromised then serious
health problems can emerge, including endometriosis.
Autoimmune Disorder
Autoimmune diseases are now widely known to occur
based on genetic predisposition that may be triggered
by environmental and other external factors. The role
of immunologic factors and angiogenesis has evidence
in the disease pathogenesis. Women with endometriosis
appear to have altered function of peritoneal macro-
phages, natural killer cells and lymphocytes, as well as
changes in growth factors and inflammatory mediators
in the peritoneal fluid.3 Many women with endometrio-
sis are susceptible to other autoimmune diseases such
as rheumatoid arthritis, multiple sclerosis and Mnires
disease.
In women who do not have endometriosis, the
ectopic endometrium is not allowed to survive and is
destroyed by the immune system. In women with endo-
metriosis a dysfunctional immune system may permit
the continuous growth of ectopic endometrial cells,
which then develops into endometriosis.
Estrogen Dependent
Growth of endometriotic lesions is also estrogen depen-
dent, with lesions becoming inactive and gradually
undergoing regression during states of ovarian down-
regulation, such as amenorrhea or menopause.4-6
REFERENCES
1. Sampson JA. Peritoneal endometriosis due to menstrual
dissemination of endometrial tissue into the pelvic cavity.
Am J Obstet Gynecol 1927;14:422-69.
2. Seli E, Berkkanoglu M, Arici A. Pathogenesis of endo-

metriosis. Obstet Gynecol Clin North Am 2003;30:41-61.
3. Gazvani R, Templeton A. Peritoneal environment,
cytokines and angiogenesis in the pathophysiology of
endometriosis. Reproduction 2002;123:217-26.
4. Bulun SE, Zeitoun K, Takayama K, Noble L, Michael D,
Simpson E, et al. Estrogen production in endometriosis
and use of aromatase inhibitors to treat endometriosis.
Endocr Relat Cancer 1999;293-301.
5. Gurates B, Bulun SE. Endometriosis: The ultimate
hormonal disease. Semin Reprod Med 2003;21:125-34.
6. Valle RF, Sciarra JJ. Endometriosis: Treatment strategies.
Ann N Y Acad Sci 2003;997:229-39.
HISTORY
Establishing the diagnosis of endometriosis on the basis
of symptoms alone can be difficult because the presen-
tation is so variable and there is considerable overlap
with other conditions such as irritable bowel syndrome
and pelvic inflammatory disease.
As a result there is often a delay of several years
between symptom onset and a definitive diagnosis.1-3
A large group of women with endometriosis is comp-
letely asymptomatic. In these women endometriosis
remains undiagnosed or is diagnosed at laparoscopy
for another indication.
The following symptoms can be caused by endo-
metriosis. Endometriosis may produce a variety of
different symptoms of varying severity and varying
extent of lesions involved. The following symptoms can
be caused by endometriosis based on clinical and patient
experience of severe dysmenorrhea; deep dysparunia;
chronic pelvic pain; ovulation pain; cyclical or peri-
menstrual (e.g. bowel or bladder associated) with or
without abnormal bleeding; infertility and chronic
fatigue.
Endometriosis should be suspected in women with
dysmenorrhea, deep dysparunia, acyclic chronic pelvic
pain and/or subfertility.
PAIN
Possible mechanisms causing pain in patients with
endometriosis include:
CLINICAL STAGING OF ENDOMETRIOSIS 15
Action of inflammatory cytokines leading to local

peritoneal inflammation.
Deep infiltration with tissue damage leading to
irritation or infiltration of nerves at pelvic floor.
Adhesion formation.
Fibrotic thickening.
Collection of shed menstrual blood in endometriotic
implants and resulting in painful traction with the
physiological movement of tissues.
Endometriotic implants were scored as:
Superficial (less than 1 mm).
Intermediate (2 to 4 mm).
Deep (greater than or equal to 5 mm).
On laparoscopy, ovaries may be observed as big as
kissing each other called Kissing ovaries(Fig. 3.1) and
it has been observed that very deep implants (greater
than 10 mm) were found exclusively in patients with
pain; superficial implants, on the contrary, were found
most frequently in patients with infertility.4
If in adult women dysmenorrhea begins after years
of pain-free menses, it may suggest of endometriosis.
The dysmenorrhea often starts before the onset of
menstrual bleeding and continues throughout the
menstrual period. In adolescents, the pain may be
present without an interval of pain-free menses after
menarche. The distribution of pain is most often bilate-
ral. Depending on the type and localization of endo-
metriosis, pain can radiate to the upper leg (ovarian),
to the perineum (rectum), or the back (uterosacral
Fig. 3.1: Bilateral endometrioma Kissing ovaries
ligaments). However, deeply infiltrating sub-peritoneal

endometriosis is associated with severe pelvic pain and
dysparunia.5-8 When there is an endometrioma, severe
dysmenorrhea is not directly related with the charac-
teristics specific to these ovarian cysts. The associated
deep infiltrating endometriotic lesions and in particular
rectal infiltration could explain these symptoms.2
SUBFERTILITY
There is an association between the presence of endo-
metriosis and subfertility. Twenty to forty percent of
women with endometriosis are infertile. When
Fig. 3.2: The American Society for Reproductive Medicine revised

classification system for endometriosis (ASRM 1996) is the most
widely accepted staging system
endometriosis is moderate or severe,9 it usually involves

the ovaries resulting in adnexal adhesions leading to
reduced tubo-ovarian motility and pick-up function.
Minimal to mild endometriosis has an increased
prevalence of sub-fertile women when compared to the
prevalence in women of proven fertility.10
The American Society for Reproductive Medicine
revised classification system for endometriosis9 is the
most widely accepted staging system (Fig. 3.2).
TABLE 3.1. Stages of endometriosis

Stage Disease Description
I Minimal A few superficial implants
II Mild More and slightly deeper implants
III Moderate Many deep implants, small
endometriomas on one or both
ovaries, and some filmy adhesions
IV Severe Many deep implants, large
endometriomas on one or both
ovaries, and many dense
adhesions, sometimes with the
rectum adhering to the back of
the uterus
Table 3.1 shows clinical stages of endometriosis.

Endometriosis implants within the fallopian tubes or
on ovary can promote inflammatory response, which
has deleterious effect on tubal function. Altered
folliculogenesis has been observed with mild endo-
metriotic patients. Luteinized unruptured follicle
syndrome with normal ovulation has been reported
with endometriosis. The moderate or severe form of
endometriosis can hamper oocytes pick-up by the
fimbrial portion of fallopian tube by distorting tubo-
ovarian relation (Fig. 3.3).
Chronic salpingitis was observed in 33 percent of
ovarian endometriosis on laparotomy (Fig. 3.4). Luteal
phase may be shortened or there may be delay in
increase in level of progesterone concentration.
The effect of endometriosis on fertilization and
implantation is well debated. There is a deleterious
Fig. 3.3: Severe degree of endometrioma with

dense adhesions
Fig. 3.4: Right endometrioma with distorted tube

effect on oocyte-sperm interaction. Peritoneal fluid in

moderate and severe endometriotic women had
decreased sperm motility leading to low fecundity rate.
A high rate of early abortion rate has been observed
with endometriosis.
Infertility is caused by various factors in endo-
metriotic women (Table 3.2).
TABLE 3.2: Causative factors related with infertility in
endometriosis
Mechanical interferance
Pelvic adhesions
Chronic salpingitis
Altered tubal motility
Distortion of tubo-ovarian relations
Impaired oocytes pick-up
Alteratations in peritoneal fluid
Increased concentration of prostaglandins
Increased number of activated macrophases
Increased production of cytokines
Enhanced phagocytosis of sperms
Abnormal immune system response
Increased cell mediated gamete injury
Increased prevalence of auto-antibodies
Anti-endometrial antibody production
Hormonal or ovulatory dysfunction
Defective folliculogenesis
Luteinized unruptured follicle syndrome
Hyperprolactinemia
Luteal phase deficiency
Fertilization or implantation failure
Early spontaneous abortion
Fig. 3.5:Proposed scoring system from American Society of

Reproductive Medicine
Many endometriotic classification systems have been

proposed to identify the endometriotic involvement in
patients and later the response of medical or surgical
management.
Proposed scoring system by American Society of
Reproductive Medicine (ASRM), (Fig. 3.5) and by the
American Fertility Society (1996).
TABLE 3.3: Classification of endometriosis

(American Fertility Society) AFS, 1996
< 1 cm 1-3 cm > 3 cm

Peritoneum
Superficial 1 2 4
Deep 2 4 6
Ovary
Rt. superficial 1 2 4
Rt. deep 4 16 20
Lt. superficial 1 2 4
Lt. deep 4 16 20
Cul-de-sac - Partial Complete
Obliteration - 4 40
Ovary <1/3 1/3 to 2/3 >2/3

Rt. flimsy 1 2 4
Rt. dense 4 8 16
Lt. flimsy 1 2 4
Lt. dense 4 8 16
Complete closure of fimbrial end = 16 (Rt. and Lt. separately)
Classification of American Society of Reproductive

Medicine was revised in 1996 for better documentation
and extent of disease (Table 3.3).
Stage 1 (minimal) 1 to 5
Stage 2 (mild) 6 to 15
Stage 3 (moderate) 16 to 40
Stage 4 (severe) > 40
A reduced monthly fecundity rate and cumulative

pregnancy rate has been observed by many workers
after husbands sperm insemination as well as donor in
women with minimal-mild endometriosis when com-
pared to those with a normal women.11-13 An enhanced
monthly fecundity rate and cumulative pregnancy rate
after surgical removal of minimal to mild endometriosis
has been assessed in a multicentric randomized trial,14
30.7 percent with treated endometriosis versus 17.7
percent non-treated, respectively. The corresponding
rates of fecundity were also 4.7 and 2.4 per 100 person-
months. Post-surgical median time to pregnancy after
ovulation induction was 65 percent within 8.5 months
and spontaneously in 60 percent.15
CHRONIC DISEASE
Endometriosis may become a chronic disease affecting
quality of life due to severe pain. It can cause infertility
and pain due to growth of implants, cyclical focal
bleeding in and around the implants and scarring. It
can affect emotional aspect of subfertility, anger about
disease recurrence, and uncertainty about the future
regarding repeated surgeries or long-term medication
and their side effects.
OTHER NON-GYNECOLOGICAL SYMPTOMS

Women of reproductive age with endometriosis may
experience fatigue/exhaustion, abdominal bloating,
diarrhea/painful bowel movements with menstruation;
pain during or after sex, heavy or irregular bleeding,

nausea/stomach upsets with menstruation. Rectal
bleeding and hematuria during menstruation may occur
in women with infiltrating rectosigmoid and bladder
endometriosis, respectively.
CLINICAL SIGNS
On speculum examination, deeply infiltrating red or
blue colored nodules are most reliable clinical
examination especially performed during or just after
menstruation.
On pelvic examination pelvic tenderness, a fixed
retroverted uterus, tender uterosacral ligaments,
enlarged ovaries or fixed adnexal mass is suggestive of
endometriosis. The diagnosis is more certain if deeply
infiltrating nodules are found on the uterosacral
ligaments or in the pouch of Douglas, and/or visible
lesions are seen in the vagina or on the cervix.
Adhesions can obliterate the cul-de-sac, complete or
partial, which correlates with the finding of a frozen
pelvis on physical examination. Cystic masses of endo-
metriosis (endometriomas) may present as palpable
adnexal masses.
Endometriosis can cause ureteral obstruction and
hydronephrosis. This results from endometrial implants
on the distal ureter or from mass effect from endomet-
riomas.
It should always be considered that a woman with
pelvic pain and/or fertility problems may have more
than 1 disease process, such as chronic pelvic inflam-

matory disease or an adnexal neoplasm.
The endometriosis may be a underlying cause of
uterine obstruction and/or malformation in the young
women.
The findings may, however, be normal.
REFERENCES
1. Hadfield R, Mardon H, Barlow D, Kennedy S. Delay in
the diagnosis of endometriosis: A survey of women from
the USA and the UK. Hum Reprod 1996;11:878-80.
2. Arruda MS, Petta CA, Abrao MS, Benetti-Pinto CL. Time
elapsed from onset of symptoms to diagnosis of endo-
metriosis in a cohort study of Brazilian women. Hum
Reprod 2003;18:4-9.
3. Husby GK, Haugen RS, Moen MH. Diagnostic delay in
women with pain and endometriosis. Acta Obstet Gynecol
Scand 2003;82:649-53.
4. Cornillie FJ, Oosterlynck D, Lauweryns JM, Koninckx PR.
Deeply infiltrating pelvic endometriosis: Histology and
clinical significance. Fertil Steril 1990;53:978-83.
5. Chapron C, Fauconnier A, Dubuisson JB, Barakat H, Vieira
M, Breart G. Deep infiltrating endometriosis: Relation
between severity of dysmenorrhoea and extent of disease.
Hum Reprod 2003a;18:760-6.
6. Koninckx PR, Meuleman C, Demeyere S, Lesaffre E,
Cornillie FJ. Suggestive evidence that pelvic endometriosis
is a progressive disease, whereas deeply infiltrating endo-
metriosis is associated with pelvic pain. Fertil Steril 1991;
55:759-65.
7. Porpora MG, Koninckx PR, Piazze J, Natili M, Colagrande
S, Cosmi EV. Correlation between endometriosis and
pelvic pain. J Am Assoc Gynecol Laparosc 1999;6:429-34.
8. Barlow DH, Glynn CJ. Endometriosis and pelvic pain.

Baillieres Clin Obstet Gynaecol 1993;7:775-89.
9. Revised American Society for Reproductive Medicine
classification of endometriosis: 1996. Fertil Steril
1997;67:817-21.
10. DHooghe TM, Debrock S, Hill JA, Meuleman C.
Endometriosis and subfertility: Is the relationship
resolved? Semin Reprod Med 2003a;21:243-54.
11. Hughes EG. The effectiveness of ovulation induction and
intrauterine insemination in the treatment of persistent
infertility: A meta-analysis. Hum Reprod 1997;12:1865-
72.
12. Omland AK, Tanbo T, Dale PO, Abyholm T. Artificial
insemination by husband in unexplained infertility
compared with infertility associated with peritoneal
endometriosis. Hum Reprod 1998;13:2602-5.
13. Nuojua-Huttunen S, Tomas C, Bloigu R, Tuomivaara L,
Martikainen H. Intrauterine insemination treatment in
subfertility: An analysis of factors affecting outcome. Hum
Reprod 1999;14:698-703.
14. Marcoux S, Maheux R, Berube S. Laparoscopic surgery in
infertile women with minimal or mild endometriosis.
Canadian Collaborative Group on Endometriosis. N Engl
J Med 1997;337:217-22.
15. Fuchs F, Ravnal P, Salama S, Guillot F, Le Tohic A, Chis
C, et al. J Gynecol Obstet Biol Reprod Mar Reproductive
outcome after laparoscopic treatment of endometriosis in
an infertile population 2007;36(4):354-9.
Suspicion of endometriosis can be based on:

Patients history and symptoms
Gynecological findings
Investigations - transvaginal sonography, MRI
Laparoscopy and biopsy are required to confirm the
diagnosis.
Differential Diagnosis for Endometriosis

Diagnosis of endometriosis is supported by careful
history and physical examination findings and one
should be able to differentiate from following:
Pelvic infection
Ovarian cyst
Ovarian torsion
Ovarian neoplasm
Ectopic pregnancy.
LAPAROSCOPY
Laparoscopy and histological examination are the gold
standard investigations for a definitive diagnosis,
disease staging and for surgical treatment of endometrio-
sis, unless disease is visible in the vagina or elsewhere.
ASRM or AFS classification is required to score the
disease after the confirmation of diagnosis (Fig. 4.1).
Timing to perform the laparoscopy is very important
at a specific time in the menstrual cycle: During or just
after menstruation.
Endometriosis typically appears as superficial
powder burn or gunshot lesions on the ovaries
(Fig. 4.2), serosal surfaces and peritoneum - black, dark-
HOW TO DIAGNOSE ENDOMETRIOSIS? 29
Fig. 4.1: Laparoscopic view of endometrioma of right ovary
Fig. 4.2: Powder burn or Gun shot endometriotic lesion

Fig. 4.3: Laparoscopic view: Clear vesicle (white arrow)

Black vesicle (black arrow)
brown, or bluish puckered lesions (Fig. 4.3), nodules or

small cysts containing old hemorrhage surrounded by
a variable extent of fibrosis.
Atypical or subtle lesions are also common,
including red implants (petechial, vesicular, polypoid,
hemorrhagic, red flame-like) and serous or clear vesicles
(Fig. 4.4). Other appearances include white plaques or
scarring and yellow-brown peritoneal discoloration of
the peritoneum (Fig. 4.5).
Pelvic adhesions can be the result of pelvic inflam-
mation, endometriosis or surgical trauma obliterating
Fig. 4.4: Hemorrhagic red flame petechial implants (arrows)
Fig. 4.5: Endometrial tissue implanted in the peritoneum has a

varied appearance: (a) blue black lesions, (b) white plaques and
clear vesicles, and (c) newly formed blood vessels
Fig. 4.6: Obliterated cul-de-sac due to endometrioma
the cul-de-sac (Fig. 4.6). Other etiologies include

infection, chemical irritation or foreign body reactions
(Fig. 4.7).
Endometriomas usually contain thick fluid like tar
(arrow in Figure 4.8); such cysts are often densely
adhered to the peritoneum of the ovarian fossa and the
surrounding fibrosis may involve the tubes and bowel.
Deeply infiltrating endometriotic nodules extend
more than 5 mm beneath the peritoneum and may
involve the uterosacral ligaments, vagina, bowel,
bladder or ureters (Fig. 4.9). The depth of infiltration is
related to the type and severity of symptoms.1-3
Fig. 4.7: Laparoscopic findings: Adhesion at right

ovarian fossa
Fig. 4.8: Ovarian endometriotic cyst

Fig. 4.9: Deeply infiltrative endometrioma
TRANSVAGINAL HYDROLAPAROSCOPY
Transvaginal hydrolaparoscopy, using a needle-cannula
system inserted into the posterior fornix and injection
of saline for peritoneal distention, was recently
introduced as an office screening technique for infertile
women. Interestingly, it was reportedly more accurate
than traditional laparoscopy in diagnosis of early
endometriotic lesions.4,5
HISTOLOGY
Positive histology confirms the diagnosis of endo-
metriosis but negative histology does not exclude it.
Visual inspection is usually adequate but histological
Fig. 4.10: Ovarian stroma with the part of a cyst wall with a few
granulosa and theca cells (H & E 250)
confirmation of at least one lesion is ideal (Fig. 4.10). In

cases of ovarian endometrioma (> 4 cm in diameter),
and in deeply infiltrating disease, histology should be
obtained to identify endometriosis and to exclude rare
instances of malignancy.
Microscopically, endometriotic implants consist of
endometrial glands and stoma with or without hemo-
siderin-laden macrophages (Arrow in Figure 4.11).
The value of histological confirmation of the
laparoscopic view for the diagnosis of endometriosis
has to be further evaluated. Endometriotic lesions are
often either extremely small or consist mainly of fibrotic
tissue (Fig. 4.12); hence, biopsies may miss microscopic
Fig. 4.11: Organized hemorrhage with macrophages containing

brown hemosiderin (arrow) compatible of chocolate cyst (H &E
160)
Fig. 4.12: Congested blood vessels with fibrous tissue and

mild inflammation indicative of scar tissue (H & E 150)
endometriotic glands and stroma and turned to be

negative.
MARKERS
CA-125
Ideal serum markers for endometriosis should have
high sensitivity and specificity. It should provide a good
correlation between severity of disease and its level.
Hence, these markers should be used not only for the
diagnosis of disease but also for monitoring the response
of the treatment. Multiple attempts have been made to
identify serum markers for endometriosis.
However, to date, none of the evaluated serum
proteins, including CA-125, has adequate sensitivity
and specificity to function as a screening tool. At
present, there is limited evidence supporting selective
use of laboratory tests for therapy follow-up and
monitoring of endometriosis recurrence in selected
populations at risk.
Although CA-125 is often elevated in advanced
endometriosis, the low sensitivity of this assay limits
its usefulness in the detection of minimal and mild
disease. However, sensitivity increases if done during
mid follicular phase of menstrual cycle.6
The elevated CA-125 is not specific for endometriosis
and is also associated with many epithelial cancers as
well as with benign gynecologic and non-gynecologic
disorders like adenexitis, pancreatitis, pregnancy and
ovarian hyperstimulation syndrome.
Several studies performed in populations at high-

risk for endometriosis have demonstrated that serum
CA-125 has good specificity (86-100%) but poor
sensitivity as low as 13 percent. 7 Sensitivity was
improved with the introduction of the new CA-125 II
assay as well as other assay modifications. 8,9 The
combination of elevated serum CA-125 with positive
clinical findings (detection of pelvic nodularities) further
improved the diagnostic power of this test, achieving a
sensitivity of 87 percent.10 Serial of CA-125 determina-
tion may be useful to predict the clinical improvement
or recurrence of endometriosis after therapy.
OTHER LABORATORY MARKERS

The search for a reliable marker for endometriosis has
been extended to various proteins either naturally
secreted by the endometrium or produced in the course
of an immune reaction to endometrial and endo-
metrium-related tissues.
Markers evaluated for their diagnostic potential in
detection of endometriosis comprised CA-72, CA-15.3,
TAG-72, and CA-19.9, all of which demonstrated
unacceptably low sensitivity.11-13
Serum levels of tumor-associated trypsin inhibitor
(TATI) were found to be elevated in patients with
endometriosis and few workers described positive
correlation with the stage of endometriosis. TATI is
not a useful screening test, but it may constitute an
adjunct diagnostic tool because its combination with the
CA-125 assay showed a sensitivity of 59 percent in

detection of all stages of endometriosis and 89 percent
for stage III/IV.14
Elevated levels of acute inflammatory phase proteins
(C-reactive protein and serum amyloid A) have also
been demonstrated in severe endometriosis, but the
usefulness of these assays remains to be elucidated.15
Serum interleukin (IL)6, peritoneal fluid necrosis factor
alpha (TNF-), anti-endometrial antibodies, anti-
carbonic anhydrase antibodies and increased leptin
levels in serum and peritoneal levels failed to confirm
the association of endometriosis.
IMAGING TECHNIQUES
Selective use of imaging studies may be helpful in
identifying patients with endometriosis. Detection of
large endometriotic implants and endometriomas may
be accomplished by transvaginal ultrasonography and
magnetic resonance imaging (MRI). Other techniques,
such as computed tomography, while occasionally
helpful in localizing lesions, often yield nonspecific
findings.
Ultrasound
Ultrasonographic examination is the most common
imaging modality used to evaluate women suspected
of having endometriosis.
Ultrasound is particularly helpful in the evaluation
of endometriotic cysts but cyst smaller than 2 cm cannot
Fig. 4.13: Endometriotic cyst on transvaginal ultrasonography
be detected by trans vaginal ultrasonography and has

a limited role in the diagnosis of adhesions or superficial
peritoneal implants.16 Transvaginal ultrasound should
be performed preferably using high-frequency probes
(6-7.5 MHz) and with the aid of color Doppler imaging
(Fig. 4.13).
The characteristic features of endometriomas are the
presence of diffuse low-level internal echoes and hyper-
echoic foci in the wall (Figs 4.14 and 4.15).
Endometriomas are associated with poor blood
supply where as ovarian cysts and malignant ovarian
are characterized by a rich vascular supply (Figs 4.16
to 4.18).
Fig. 4.14: Presence of low-level internal echo
Fig. 4.15: Presence of diffuse echo of endometrioma

Fig. 4.16: Echo showing absence of intracystic solid tissue
Fig. 4.17: Internal iliac vessel with absence of

blood supply in endometrioma
Fig. 4.18: Doppler study with no blood flow in

endometriotic cyst
In selected cases, such as abdominal wall endo-

metriosis and bladder endometriosis, a transabdominal
approach may also be useful.17,18
Dermoid cysts, hemorrhagic cysts, and cystic
neoplasms may resemble endometriomas and must be
considered in the differential diagnosis. 19,20 The
application of three-dimensional ultrasound may allow
better visualization of the topography of the surface and
internal echoes as well as the vasculature of cystic
ovarian tumors. The three-dimensional technique may
provide better differentiation of endometriomas from
other benign and malignant masses.21,22 Transrectal

ultrasonography was reported to be a useful tool in the
diagnosis of deep infiltrating endometriosis. The use of
rectal ultrasound with a 6.5-MHz biplane convex probe
had a sensitivity of 97 percent and 80 percent and a
specificity of 96 percent and 97 percent in detection of
rectovaginal endometriosis and uterosacral ligament
infiltration, respectively, as confirmed by surgery and
histopathological findings.23
MAGNETIC RESONANCE IMAGING (MRI)

MRI is particularly helpful in identification of endo-
metriomas. Occasionally, it may also visualize solid
endometriotic implants and adhesions. It is an adjunc-
tive noninvasive examination, useful in a preselected,
high-risk population.
Endometrial implants are often small and their signal
intensity is variable. They usually express intensity
similar to that of normal endometrium. Pelvic magnetic
resonance may also be useful in monitoring the effects
of medical therapy as well as in predicting treatment
outcome in patients with endometriomas prior to
therapy initiation.
Pelvic magnetic resonance may also be useful in
monitoring the effects of medical therapy as well as in
predicting treatment outcome in patients with
endometriomas prior to therapy initiation.
OTHER IMAGING TECHNIQUES

Various additional imaging procedures may be occa-
sionally useful in the diagnosis of endometriosis.
Computed tomography can detect lesions in pleura,
brain, and other uncommon locations. 24,25 Barium
enema, especially with double contrast, can demons-
trate bowel infiltration. 26,27 If bladder or ureteral
involvement is suspected, intravenous pyelography,
cystoscopy, or ureteroscopy may be performed.28,29
However, the findings of these techniques are
nonspecific.
REFERENCES
1. Chapron C, Fauconnier A, Dubuisson JB, Barakat H, Vieira
M, Breart G. Deep infiltrating endometriosis: Relation
between severity of dysmenorrhoea and extent of disease.
Hum Reprod 2003a;18:760-6.
2. Koninckx PR, Meuleman C, Demeyere S, Lesaffre E,
Cornillie FJ. Suggestive evidence that pelvic endometriosis
is a progressive disease, whereas deeply infiltrating
endometriosis is associated with pelvic pain. Fertil Steril
1991;55:759-65.
3. Porpora MG, Koninckx PR, Piazze J, Natili M, Colagrande
S, Cosmi EV. Correlation between endometriosis and
pelvic pain. J Am Assoc Gynecol Laparosc 1999;6:429-34.
4. Gordts S, Campo R, Brosens I. Office transvaginal
hydrolaparoscopy for early diagnosis of pelvic endo-
metriosis and adhesions. J Am Assoc Gynecol Laparosc
2000;7:45-9.
5. Brosens I, Campo R, Gordts S, Brosens J. An appraisal of
the role of laparoscopy: Past, present, and future. Int J
Gynaecol Obstet 2001;74(suppl 1):S9-S14.
6. Mol BWJ, Bayram N, Lijmer JG, et al. The performance of

CA-125 measurement in the detection of endometriosis:
A meta-analysis. Fertil Steril 1998;70:1101-8.
7. Patton P, Field C, Harms R, Coulam C. Ca-125 levels in
endometriosis. Fertil Steril 1986;45:770-3.
8. Hornstein MD, Harlow BL, Thomas PP, Check JH. Use of
a new CA 125 assay in the diagnosis of endometriosis.
Hum Reprod 1995;10:932-4.
9. Pittaway DE. Assay characteristics of the immuno-
radiometric method for CA-125. Fertil Steril 1989;51:348-
50.
10. Koninckx PR, Meuleman C, Oosterlynck D, Cornille FJ.
Diagnosis of deep endometriosis by clinical examination
during menstruation and plasma CA-125 concentration.
Fertil Steril 1996;65:280-7.
11. Muscatello R, Cucinelli F, Fulghesu A, et al. Multiple
serum marker assay in the diagnosis of endometriosis.
Gynecol Endocrinol 1992;6:265-9.
12. Molo MW, Kelly M, Radwanska E, Binor Z. Preoperative
serum CA-125 and CA-72 in predicting endometriosis in
infertility patients. J Reprod Med 1994;39:964-6.
13. Abrao MS, Podgaec S, Pinotti JA, de Oliveira RM. Tumor
markers in endometriosis. Int J Gynaecol Obstet 1999;66:
19-22.
14. Medl M, Ogris E, Peters-Engl C, et al. Serum levels of the
tumour-associated trypsin inhibitor in patients with
endometriosis. Br J Obstet Gynaecol 1997;104:78-81.
15. Abrao MS, Podgaec S, Filho BM, et al. The use of bio-
chemical markers in the diagnosis of pelvic endometriosis.
Hum Reprod 1997;12:2523-7.
16. Friedman H, Vogelzang RL, Mendelson EB, Neiman HL,
Cohen M. Endometriosis detection by US with laparo-
scopic correlation. Radiology 1985;157:217-20.
17. Alexiadis G, Lambropoulou M, Deftereos S, et al.
Abdominal wall endometriosis-ultrasound research: A
diagnostic problem. Clin Exp Obstet Gynecol 2001;28:
121-2.
18. Balleyguier C, Chapron C, Dubuisson JB, et al. Com-
parison of magnetic resonance imaging and transvaginal
ultrasonography in diagnosing bladder endometriosis. J
Am Assoc Gynecol Laparosc 2002;9:15-23.
19. Athey PA, Diment DD. The spectrum of sonographic
findings in endometriomas. J Ultrasound Med 1989;8:487-
91.
20. Patel M, Feldstein V, Dillon C, Lipson S, Filly R.
Endometriomas: Diagnostic performance of US.
Radiology 1999;210:739-45.
21. Hata T, Yanagihara T, Hayashi K, et al. Three-dimensional
ultrasonographic evaluation of ovarian tumours: A
preliminary study. Hum Reprod 1999;14:858-61.
22. Kurjak A, Kupesic S, Anic T, Kosuta D. Three-dimensional
ultrasound and power Doppler improve the diagnosis of
ovarian lesions. Gynecol Oncol 2000;76:28-32.
23. Fedele L, Bianchi S, Portuese A, Borruto F, Dorta M.
Transrectal ultrasonography in the assessment of recto-
vaginal endometriosis. Obstet Gynecol 1998;91:444-8.
24. Elliot DL, Barker AF, Dixon LM. Catamenial hemoptysis.
New methods of diagnosis and therapy. Chest 1985;
87:687-8.
25. Thibodeau LL, Prioleau GR, Manuelidis EE, Merino MJ,
Heafner MD. Cerebral endometriosis. Case report. J
Neurosurg 1987;66:609-10.
26. Shah M, Tager D, Feller E. Intestinal endometriosis
masquerading as common digestive disorders. Arch
Intern Med 1995;155:977-80.
27. Forsgren H, Lindhagen J, Melander S, Wagermark J.
Colorectal endometriosis. Acta Chir Scand 1983;149:431-
5.
28. Donnez J, Spada F, Squifflet J, Nisolle M. Bladder endo-
metriosis must be considered as bladder adenomyosis.
29. Zanetta G, Webb MJ, Segura JW. Ureteral endometriosis
diagnosed at ureteroscopy. Obstet Gynecol 1998;91:857-
9.
In most women with endometriosis, preservation of

reproductive function is desirable. The least invasive
and least expensive approach that is effective with the
least risks in the long run should be chosen. The option
should be left with the women to decide about the
treatment options. Analgesics, hormones, surgery,
assisted reproduction or a combination of these can be
the option to treat symptomatic endometriosis patients.
As endometriosis is a chronic disease, elimination
of the endometriotic implants by surgical or medical
treatment often provides only temporary relief.
Therefore, the goal should be to eliminate the
endometriotic lesions and, more importantly, to treat
the symptoms (pain and subfertility) and prevent
recurrence. Many women with endometriosis have pain
and subfertility at the same time, which complicates the
choice of treatment and as endometriosis is a chronic
disease and the recurrence rate is high after both
hormonal and surgical treatment.
Therefore, the principal objective in treating
endometriosis should be:
Symptom-relief management.
Prevent or delay the disease progression by reducing
endometriotic implants through surgical treatment
or medically induced atrophy of the implants.
To improve fertility rates substantially in women
with endometriosis. Endometriosis-associated
infertility in confirmed disease may be treated by
hormonal or surgical treatment.
MEDICAL MANAGEMENT OF ENDOMETRIOSIS 51
SYMPTOMATIC RELIEF
Non-steroidal Anti-inflammatory Drugs (NSAIDs)

NSAIDs (specifically naproxen) are effective in
managing pain caused by endometriosis.1 These have
significant side effects, including gastric ulceration and
an anti-ovulatory effect when taken at mid-cycle. Other
analgesics may be effective but there is insufficient
evidence to make recommendations.
Drugs other than non-steroidal anti-inflammatory
agents, androgenic agents (danazol), GnRH analogues,
estrogen/progestin combined oral contraceptives
(COCs) and progestins are used in various form in cases
of endometriosis (Table 5.1).
Progestins
Progestins exert an antiproliferative effect by causing
initial decidualization of endometrial tissue followed
by atrophy. They can be considered as a first choice for
the treatment of endometriosis because they are as
effective in reducing AFS scores and pain. In most
studies, the effect of treatment has been evaluated after
3 to 6 months of therapy. Medroxyprogesterone acetate
(MPA) has been found the most effective in relieving
pain. Starting dose of MPA may be 30 mg/day and
increasing the dose based on the clinical response and
bleeding patterns.2,3 Pain was reduced significantly
during luteal phase treatment with 60 mg dydroges-
terone and this improvement still was evident at
TABLE 5.1: Various drugs used in endometriosis

Agent Dose Route Dosing Common side
frequency effects
Combined 30-35 g Oral Daily Irregular bleeding,
oral con- ethinyl (cyclic or weight gain,
traceptives estradiol, conti- bloating, breast
plus nuous) tension and
progestin headache
Androgen 400-800 mg Oral Daily Androgenic/
Danazol (duration anabolic (weight
limited to gain, fluid
6 months retention, breast
by side atrophy, acne, oily
effects) skin, hot flashes
and hirsutism)
GnRH (Duration
agonists limited to
6 months
due to BMD
effects)
Leuprolide 1 mg/day SC Daily Hypoestrogenic
injection (hot flashes,
vaginal dryness,
emotional lability,
loss of libido and
BMD decline)
Leuprolide 3.75 mg IM Monthly
depot injection
11.75 mg IM Every
injection 3 months
Triptorelin 3 mg IM injection Monthly
Triptorelin 11.25 mg IM injection Every
depot 3 months
Goserelin 3.6 mg SC implant Monthly
Buserelin 300-400 g Intranasal tid
Nafarelin 200-400 g Intranasal bid
Contd...
Contd...
Agent Dose Route Dosing Common side

frequency effects
Progestins
Dydroges- 60 mg Oral 12 days
terone per cycle*
Gestrinone 2.5-5 mg Oral Daily/twice
weekly
Megestrol 40 mg Oral Daily Irregular bleeding,
acetate weight gain,
bloating and
edema
Norethin- 5 mg Oral Daily
drone
acetate
MPA 30 mg Oral Daily
DMPA-IM 150 mg IM injection Every
150 3 months
DMPA-SC 104 mg SC injection Every
104 3 months
BMDBone mineral density; DMPADepot medroxyprogesterone

acetate; IMIntramuscular; MPAMedroxyprogesterone acetate;
SCSubcutaneous.
*During the luteal phase.
Starting dose, with gradual dose escalation.
Also with transient BMD decline.
12 months follow-up.4 Other progestogens, such as

desogestrel, are now being looked at as alternative
treatments.
Side effects of progestogens include nausea, weight
gain, fluid retention and breakthrough bleeding due to
hypoestrogenemia. Breakthrough bleeding, is usually

corrected by short-term (7 days) administration of
estrogen. Depression and other mood disorders are a
significant problem in approximately 1 percent of
women taking these medications.
An intrauterine device releasing 20 mug/day of
levonorgestrel in women with endometriosis and after
the first year of use, a 70-90 percent reduction in
monthly blood loss is observed. Local progesterone
treatment with a levonorgestrel-releasing intrauterine
system in endometriosis-associated dysmenorrhea
during 12 months result in a significant reduction in
dysmenorrhea, pelvic pain and dyspareunia.5-9 It also
significantly reduces the volume of rectovaginal endo-
metriotic nodules.10 The use of a depot preparation of
Medroxyprogesterone acetate (DMPA-SC 104) demons-
trates that pain reduction is as effective as that observed
with GnRH analogues.11
COMBINED ORAL CONTRACEPTIVES (COCs)
Continuous Administration
Low-dose combination oral contraceptive pill contain-
ing 30-35 mg of ethinyl estradiol used continuously (to
achieve amenorrhea) can be effective in the manage-
ment of endometriosis. Symptomatic relief of
dysmenorrhea and pelvic pain is reported in 60-95
percent of patients.
Cyclical Administration
The cyclical use of combination oral contraceptives may
provide prophylaxis against either the development or
recurrence of endometriosis. COCs also have been
shown to down-regulate cell proliferation and increase
apoptosis in the eutopic endometrium of women with
endometriosis.12
Cyclical COCs reduces menstrual bleeding and
regularizes the cycle in women with endometriosis.13
COCs are widely used in endometriosis and are
generally well tolerated with less metabolic impact than
danazol or GnRH analogues.14 COCs results in ovula-
tion inhibition, decreased gonadotropin levels, reduced
menstrual flow and decidualization of endometriotic
implants.14 But women older than 35 years who smoke
and use OCs containing estrogen may be at increased
risk of myocardial infarction, stroke or venous
thromboembolism.15
Gestrinone
Gestrinone is a 19-nortestosterone derivative with
androgenic, anti-progestagenic, anti-estrogenic, and
anti-gonadotropic properties. It results in the cellular
inactivation and degeneration of endometriotic
implants.16 Amenorrhea occurs in 50-100 percent of
women and is dose-dependent.
The standard dose has been 2.5 mg twice a week,
although it has been reported that 1.25 mg twice weekly
is equally effective.17 The clinical side effects include

nausea, muscle cramps, and androgenic effects such as
weight gain, acne, seborrhea, oily hair/skin, and
irreversible voice changes.
Danazol
Danazol is an oral agent with both androgenic and
anabolic properties that induces amenorrhea through
suppression of the hypothalamic-pituitary-ovarian
(HPO) axis, accompanied by increased serum androgen
concentrations and low serum estrogen levels.18,19 After
surgical management in endometriosis, Danazol and
MPA significantly alleviated postoperative pelvic pain
compared with placebo.20 In a more recent, 6 months
randomized trial, both leuprorelin acetate and danazol
significantly (P < 0.001) improved endometrial lesions
and pain symptoms in 81 women with endometriosis,
with no significant differences between groups.
Danazol has poor tolerability represents the major
drawback of danazol as a treatment for endometriosis
The major side effects of danazol:19,21
Weight gain
Edema
Myalgia
Acne
Oily skin
Hirsutism.
The duration of treatment is for 6 months. Due to its
side effects the use of this drug has been in decline in
recent years.19 Danazol is contraindicated in women

with liver disease or hyperlipidemia.
Gonadotropin-releasing Hormone Agonists

GnRH agonists bind to pituitary GnRH receptors and
initially stimulate LH and FSH synthesis and release.
However, prolonged stimulation causes down regu-
lation of gonadotropic activity leading to suppress
ovarian steroid production, providing a medically
induced and reversible state of pseudo menopause or
medical menopause by down-regulating hypothalamic-
pituitary GnRH receptors. Hence, decreases gonado-
tropin secretion, suppression of ovulation and reduced
serum estrogen levels.19,22
Various GnRH agonists have been developed and
used in treating endometriosis. These include leupro-
relin buserelin, nafarelin, histrelin, goserelin, deslorelin,
and tryptorelin. These drugs are inactive orally and
must be administered intramuscularly, subcutaneously,
or intranasally.
The side effects of GnRH agonists are caused by
hypoestrogenism and include hot flushes, vaginal
dryness, reduced libido, and reduction in bone density
especially if treatment periods of longer than 6 months.
Side effects can be ameliorated by the use of add-
back. The goal of add-back is to effectively treat endo-
metriosis and endometriosis-associated pain, while
preventing vasomotor symptoms and bone loss may
lengthen the duration of time that these agents can be
administered.23
Add back can be achieved by progestogens only:

Norethisterone 1.2 mg
Norethindrone acetate 5 mg
Tibolone 2.5 mg/day
Estrogen/progestogen combination, i.e. conjugated
estrogens 0.625 mg combined with medroxypro-
gesterone acetate 2.5 mg
Norethindrone acetate 5 mg
Estradiol 2 mg and norethisterone acetate 1 mg
Draw-back therapy - 400 microgram nafarelin /
day for 1 month followed by 5 months 200 micro-
gram nafarelin/day for 6 months showed similar
estradiol levels (30 pg/mL) but less loss of bone
mineral density.
Aromatase Inhibitors
There is persistence of local aromatase enzyme in
endometriotic tissue, which converts adrenal precursors
in to estrogen. Therefore, theoretically aromatase
inhibitors may have a role to play in the medical
management of endometriosis, particularly in post-
menopausal women.23-25
It is likely that if aromatase inhibitors do find a role
in the management of endometriosis then it will be as
part of a combination therapy with other ovarian
suppressant drugs.23 There are pilot data suggesting
that the aromatase inhibitor, letrozole, may be effective
although it is associated with significant bone density
loss.26
RECENT ADVANCES UNDER TRIALS
Anti-angiogenic Therapies
Currently available medical therapies are designed to
suppress estrogen synthesis, inducing atrophy of
ectopic endometriotic implants or interrupting the cycle
of stimulation and bleeding. Oral contraceptive,
androgenic agents, progestins and gonadotropin-
releasing hormone analogues have all been successfully
used in the treatment of endometriosis. However, none
of these drugs can eradicate the disease.
Angiogenesis is a prerequisite for the development
of endometriosis. According to the transplantation
theory27 shed endometrial fragments lodged in the
peritoneal cavity require the establishment of a new
blood supply for the survival of implants and the
development of the disease.
In one study, endometriotic lesions were allowed to
form in mice for over 3 weeks after transplantation of
human endometrial tissue before evaluating the effect
of angiostatic agents.28 It has been seen that angiostatic
agents like TNP470, endostatin, anginex and anti-
human VEGF antibody significantly decreased
microvessel density and the number of established
endometriotic lesions. 29 Hence, administration of
antiangiogenic drugs has been proved to reduce the
establishment, maintenance and progression of
endometriotic lesions in different laboratory and animal
models; however, further investigations are required
before clinical trials can be planned in humans.30
Progesterone Antagonists
Antiprogesterones, such as mifepristone, have been
suggested as potential treatments for endometriosis but
limited data is available to advocate wider use.
Selective Progesterone Receptor Modulators

There is also little data to support the use of selective
progesterone receptor modulators although their
potential use has been advocated.
Genistein
The endometriotic implants were treated with oral
Genistein and the histological assessment revealed that
the histopathological score of the regression of endo-
metriotic implants was observed statistically significant
at the end of the treatment in the rat model.31
Atorvastatin
High-dose (2.5 mg/kg) Atorvastatin caused a significant
regression of endometriotic implants by decreasing
vascular endothelial growth factor (VEGF) level in
peritoneal fluid and histological score in rat model.
REFERENCES
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inflammatory drugs for pain in women with endo-
metriosis (Cochrane Review). The Cochrane Database of
Systematic Reviews 2005;4:CD004753.
2. Moghissi KS, Boyce CR. Management of endometriosis
with oral medroxyprogesterone acetate. Obstet Gynecol
1976;47:265-7.
3. Luciano AA, Turksoy RN, Carleo J. Evaluation of oral
medroxyprogesterone acetate in the treatment of
endometriosis. Obstet Gynecol 1988;72:323-7.
4. Overton CE, Lindsay PC, Johal B, Collins SA, Siddle NC,
Shaw RW, et al. A randomized, double-blind, placebo-
controlled study of luteal phase dydrogesterone
(Duphaston) in women with minimal to mild endo-
metriosis. Fertil Steril 1994;62:701-7.
5. Vercellini P, Aimi G, Panazza S, De GO, Pesole A,
Crosignani PG. A levonorgestrel-releasing intrauterine
system for the treatment of dysmenorrhea associated with
endometriosis: A pilot study. Fertil Steril 1999a;72:505-8.
6. Vercellini P, Vigano P, Somigliana E. The role of the levo-
norgestrel-releasing intrauterine device in the manage-
ment of symptomatic endometriosis. Curr Opin Obstet
Gynecol 2005;17:359-65.
7. Lockhat FB, Emembolu JO, Konje JC. The efficacy, side-
effects and continuation rates in women with symptomatic
endometriosis undergoing treatment with an intrauterine
administered progestogen (levonorgestrel): A 3 years
follow-up. Hum Reprod 2005;20:789-93.
8. Petta CA, Ferriani RA, Abrao MS, Hassan D, Rosa E Silva
JC, et al. Randomized clinical trial of a levonorgestrel-
releasing intrauterine system and a depot GnRH analogue
for the treatment of chronic pelvic pain in women with
endometriosis. Hum Reprod 2005;20:1993-8.
9. Varma R, Sinha D, Gupta JK. Non-contraceptive uses of
levonorgestrel-releasing hormone system (LNG-IUS) - A
systematic enquiry and overview. Eur J Obstet Gynecol
Reprod Biol, Epub 2005 Dec 1.
10. Fedele L, Bianchi S, Zanconato G, Portuese A, Raffaelli R.
Use of levonorgestrel-releasing intrauterine device in the
treatment of rectovaginal endometriosis. Fertil Steril 2001;
75:485-8.
11. Crosignani PG, Luciano A, Ray A, Bergqvist A. Subcuta-

neous depot medroxyprogesterone acetate versus
leuprolide acetate in the treatment of endometriosis-
associated pain. Hum Reprod 2006;21:248-56.
12. Meresman GF, Aug L, Baraao RI, Lombardi E, Tesone
M, Sueldo C. Oral contraceptives suppress cell prolife-
ration and enhance apoptosis of eutopic endometrial tissue
from patients with endometriosis. Fertil Steril 2002;
77:1141-7
13. Cramer DW, Wilson E, Stillman RJ, Berger MJ, Belisle S,
Schiff I, et al. The relation of endometriosis to menstrual
characteristics, smoking and exercise. JAMA 1986;255:
1904-8.
14. Rice VM. Conventional medical therapies for endometrio-
sis. Ann N Y Acad Sci 2002;955:343-52.
15. WHO Collaborative Study of Cardiovascular Disease and
Steroid Hormone Contraception. Acute myocardial
infarction and combined oral contraceptives: Results of
an international multicentre case-control study. Lancet
1997;349:1202-9.
16. Brosens IA, Verleyen A, Cornillie F. The morphologic
effect of short-term medical therapy of endometriosis. Am
J Obstet Gynecol 1987;157:1215-21.
17. Hornstein MD, Gleason RE, Barbieri RL. A randomized
double-blind prospective trial of two doses of gestrinone
in the treatment of endometriosis. Fertil Steril 1990;53:237-
41.
18. Rotondi M, Labriola D, Rotondi M, Ammaturo FP, Amato
G, Carella C, et al. Depot leuprorelin acetate versus
danazol in the treatment of infertile women with sympto-
matic endometriosis. Eur J Gynaecol Oncol 2002;23:523-
6.
19. Valle RF, Sciarra JJ. Endometriosis: Treatment strategies.
Ann N Y Acad Sci 2003;997:229-39.
20. Telimaa S, Rnnberg L, Kauppila A. Placebo-controlled
comparison of danazol and high-dose medroxyproges-
terone acetate in the treatment of endometriosis after
conservative surgery. Gynecol Endocrinol 1987b;1:363-71.
21. Biberoglu KO, Behrman SJ. Dosage aspects of danazol
therapy in endometriosis: Short-term and long-term
effectiveness. Am J Obstet Gynecol 1981;139:645-54.
22. Rotondi M, Labriola D, Rotondi M, Ammaturo FP, Amato
G, Carella C, et al. Depot leuprorelin acetate versus dana-
zol in the treatment of infertile women with symptomatic
endometriosis. Eur J Gynaecol Oncol 2002;23:523-6.
23. Child TJ, Tan SL. Endometriosis: Aetiology, pathogenesis
and treatment. Drugs 2001;61:1735-50.
24. Attar E, Bulun SE. Aromatase inhibitors: The next gene-
ration of therapeutics for endometriosis? Fertil Steril
2006;85:1307-18.
25. Bulun SE, Zeitoun KM, Takayama K, Sasano H. Molecular
basis for treating endometriosis with aromatase inhibitors.
Hum Reprod Update 2000;6:413-8.
26. DHooghe TM. Immunomodulators and aromatase inhi-
bitors: Are they the next generation of treatment for endo-
metriosis? Curr Opin Obstet Gynecol 2003b;15:243-9.
27. Ailawadi RK, Jobanputra S, Kataria M, Gurates B, Bulun
SE. Treatment of endometriosis and chronic pelvic pain
with letrozole and norethindrone acetate: A pilot study.
28. Sampson JA. Peritoneal endometriosis due to menstrual
dissemination of endometrial tissue into the pelvic cavity.
Am J Obstet Gynecol 1927;14:422-69.
29. Nap AW, Dunselman GA, Griffioen AW, Mayo KH, Evers
JL, Groothuis PG. Angiostatic agents prevent the
development of endometriosis-like lesions in the chicken
chorioallantoic membrane. Fertil Steril 2005;83:793-5.
30. Ferrero S, Ragn N, Remorgida V. Antiangiogenic therapies
in endometriosis. British Journal of Pharmacology 2006;
149:133-5.
31. Yavuz E, Oktem M, Esinler I, Toru SA, Zeyneloglu HB.
Genistein causes regression of endometriotic implants in
the rat model. Fertil Steril 2007;88:1129-34.
OBJECTIVE OF SURGICAL TREATMENT

Direct visualization of endometrioma, pelvic
adhesions.
To restore normal tubo-ovarian anatomical relation-
ship who desires to preserve fertility.
To fulgurate or excise all visible endometriotic
implants.
Chromopertubation in stage 1 and 2 (pre-requisite
for IUI) (Fig. 6.1).
Fig. 6.1: Stage 2 endometrioma with patent right tube

SURGICAL MANAGEMENT OF ENDOMETRIOSIS 67
Fig. 6.2: Endometrioma on laparoscopy
Surgical management can be provided by laparo-

scopy as well as laparotomy. But laparoscopy provides
better visualization; less tissue handling and less
adhesions postoperatively. Hence, provides better
fertility goal (Fig. 6.2).
Adhesions should be excised by sharp dissection as
it contains disease (Fig. 6.3).
Peritoneal implants can be ablated by unipolar or
bipolar electrosurgical instruments or laser. Skilled
person should do it to prevent the complications. Stage
1 and 2 endometrioma can be treated by laparoscopic
electrocauterization. Women with moderate to severe
endometriosis are treated most effectively by ablating
or excising as many implants as possible to preserve
fertility (Fig. 6.4). But no RCTs or meta-analyses are
Fig. 6.3: Adhesions between uterus and omentum

on laparoscopy
Fig. 6.4: Severe form of endometriosis

Fig. 6.5: Severe endometriosis before surgical excision
available to answer the question whether surgical

excision of moderate to severe endometriosis enhances
pregnancy rate (Fig. 6.5).
Based upon three studies1-3 there seems to be a
negative correlation between the stage of endometriosis
and the spontaneous cumulative pregnancy rate after
surgical removal of endometriosis (Fig. 6.6). Microsurgi-
cal techniques are used to prevent adhesions if women
desire to preserve fertility.
Laparoscopy can be used to remove lesions;
peritoneal or ovarian lesions can sometimes be electro-
cauterized, excised, or vaporized with a laser (Fig. 6.7).
After this treatment, fertility rates are 40 to 70 percent
and are inversely proportional to severity of the
Fig. 6.6: Laparoscopic removal of left endometrioma
Fig. 6.7: Ovarian endometrioma dark thick tarry fluid seen

coming out from left ovary
Fig. 6.8: Puckered scar seen on the ovary
endometriosis. If resection is incomplete, use of oral

contraceptives or GnRH agonists may increase fertility
rates. But folliculogenesis will be hampered if ovaries
are puckered due to fibrosis (Fig. 6.8).
While doing laparoscopic surgery for endomet-
rioma, it is important one should try to excise out the
complete pseudocapsule (Fig. 6.9). It has been observed
that laparoscopic cystectomy for ovarian endomet-
riomas > 4 cm diameter improves fertility compared to
drainage and coagulation.4,5
Coagulation or laser vaporization of endometriomas
without excision of the pseudocapsule is associated with
a significantly increased risk of cyst recurrence.6,7
Fig. 6.9: Removal of pseudocapsule of endometrioma
Persistence of pelvic pain may be relieved by:

Ovarian cystectomy than drainage and ablation of
cyst.
Ablation of implants.
Pre-sacral neurectomy or laparoscopic uterine nerve
ablation (LUNA) relieves the pain associated with
endometriosis, which is not relieved by medical
treatment.
Laparoscopic resection of the uterosacral ligaments
with electrocautery or a laser may reduce midline
pelvic pain.
Adhesions in cul-de-sac.
Hysterectomy should usually be reserved for
patients who have intractable pelvic pain and who have
completed childbearing. If women < 50 require
hysterectomy with oophorectomy, supplemental estro-
gen should be considered. There may be persistence of

symptoms if without removal of fibrotic tissues
hysterectomy with bilateral salpingo-oophorectomy is
preceded. It may be due to persistence of local
aromatase enzyme, which converts adrenal precursors
in to estrogen.
Second-look Laparoscopy
Women who have gone through laparoscopy or
laparotomy for the resection of endometrioma should
have second look laparoscopy after 8 days to 6 weeks
interval of initial surgery. It allows the separation of de
novo flimsy adhesions or small endometrioma.
Recurrence of endometrioma has been observed in 15
to 20 percent of women.
Combination of Medical and Surgical Therapy

Preoperative and postoperative medical therapy gives
adjunct to conservative resection of endometrioma and
enhanced the fertility rate. Preoperative suppression of
disease with hormones reduces the tissue vascularity
and suppresses the corpus luteum and hence facilitates
the surgical procedure. In controlled clinical trial, a
3 months course of GnRH agonist treatment before
laparoscopy significantly reduces the operative time
and recurrence of endometrioma. Postoperative medical
therapy inhibits the activity of residual disease but it
postpones the attempt of conception. Postoperative
GnRH agonist therapy for 6 months significantly delay
the endometriotic related pain and it can also be
achieved after low dose cyclical oral contraceptives

received for 6 months.8
REFERENCES
1. Adamson GD, Hurd SJ, Pasta DJ, Rodriguez BD. Laparo-
scopic endometriosis treatment: Is it better? Fertil Steril
1993;59:35-44. Pubmed ID: 8419220.
2. Guzick DS, Silliman NP, Adamson GD, Buttram-VC J,
Canis M, Malinak LR, et al. Prediction of pregnancy in
infertile women based on the American Society for
Reproductive Medicines revised classification of
endometriosis. Fertil Steril 1997;67:822-9. Pubmed ID:
9130885.
3. Osuga Y, Koga K, Tsutsumi O, Yano T, Maruyama M,
Kugu K, et al. Role of laparoscopy in the treatment of
endometriosis-associated infertility. Gynecol Obstet Invest
2002;53(Suppl 1):33-9. Pubmed ID: 11834866.
4. Beretta P, Franchi M, Ghezzi F, Busacca M, Zupi E, Bolis
P. Randomized clinical trial of two laparoscopic treatments
of endometriomas: Cystectomy versus drainage and
coagulation. Fertil Steril 1998;70:1176-80. Pubmed ID:
9848316.
5. Chapron C, Vercellini P, Barakat H, Vieira M, Dubuisson
JB. Management of ovarian endometriomas. Hum Reprod
Update 2002;8:6-7. Pubmed ID: 12498427.
6. Vercellini P, Chapron C, De Giorgi O, Consonni D,
Frontino G, Crosignani PG. Coagulation or excision of
ovarian endometriomas? Am J Obstet Gynecol 2003b;188:
606-10. Pubmed ID: 12634628.
7. Hart R, Hickey M, Maouris P, Buckett W, Garry R.
Excisional surgery versus ablative surgery for ovarian
endometriomata: A Cochrane Review. Hum Reprod
2005;20:3000-7. Pubmed ID: 16246860.
8. Hornstein MD, Hemmings R, Yuzpe AA, et al. Use of
naferelin veruses placebo after reductive laparoscopic
surgery for endometriosis. Fertil Steril 1997;68:860.
Although it is well indicated that laparoscopic surgery

is the first choice in endometriotic related infertility. But,
it does not show homogenous result.
There is lack of RCTs to support the few following
evidences:
There is no relation between AFS scoring and fertility
rate.
There is no association between size of endo-
metrioma and adenexal adhesions.
Relation of adenexal and tubal adhesion with
pregnancy rate.
Assisted Reproductive Technologies includes

IUI (intrauterine insemination)
IVF
ICSI (Intracytoplasmic sperm injection)
Oocytes donation.
If spontaneous conception does not occur after
expectant management of 6 to 9 months in stage one
and two endometriosis, ovarian stimulation with IUI
should be offered. If semen count is relatively good
(according to WHO classification), IUI should be done
by swim-up and simple sperm-washing which provides
a good result (Figs 7.1A and B). Insemination should be
done gently within 36 to 38 hours of ovulation trigger
(Figs 7.2A and B).
But maternal age more than 38 and in advanced
stages of endometriosis, IVF/ICSI should be offered
immediately after the laparoscopic treatment. There is
ENDOMETRIOSIS AND ART 77
Figs 7.1A and B: (A) After semen wash motile sperms as

pellet (arrow) (B) motile sperms after wash
Figs 7.2A and B: Insemination of washed sperms

ENDOMETRIOSIS AND ART 79
no role of IUI in advanced endometriosis due to

distorted tubo-ovarian relation and associated chronic
salpingitis.
For IVF/ICSI cycles, it is better to drain endomet-
rioma because chances of puncturing endometrioma are
very high during ovum-pick-up. It may leads to abscess
formation. Hence, before IVF drainage of endometrioma
followed by long acting gonadotropin (Depot) is
recommended for 3 to 6 cycles. After the last cycle of
gonadotropin analogue, ovarian stimulation is done
with follicle stimulating hormone (FSH, 200mIU) with
hMG. After stimulation, IVF procedure is performed.
Cycle fecundity rates with COH/IUI therapy
associated with endometriosis have ranged from 9 to
13 percent and give higher pregnancy rates with
6 weeks of GnRH suppression. Infertility related
endometriosis stage 1 and 2 demonstrated the live birth
of 11 percent in treatment group and 2 percent in control
group. When ovarian stimulation with IUI fails for 3 to
4 cycles, IVF is recommended in these women (Table
7.1). The fertilization rate in IVF cycle is slightly reduced
than the any other factor. But we prefer after
laparoscopic treatment, IVF should be offered in
immediate cycle in stage three and four. Endometriosis
has been observed a responsible factor for high
miscarriage rate. After laparoscopic treatment, GnRH
analogues are offered for 3 to 6 months. During the last
cycle stimulation to be started with FSH and hMG
before the IVF procedures. Ultrashort protocols showed
TABLE 7.1: Management of endometriosis related

infertility
Ovarian stimulation with clomiphene citrate (CC) from

day 2/3rd for 5 days

Injection human menopausal gonadotropin(hMG)
75to150 mIU (Subcutaneously) from 7/8th)

Follicular monitoring (Preferably TVS) from day 10th till
follicular size 18 to 20 mm

Ovulation triggered by injection human chorionic
gonadotropin (hCG)

After 36 to 38 hours, IUI to be done with washed sperms

Luteal support with micronized progesterone

Failed IUI cycles (3 to 4 cycles)
Plan for IVF / ICSI
better pregnancy rate than the standard protocol.

Hence, the clinical history must be carefully weighed
when planning a sequence of therapy for the infertile
patient with endometriosis.
Index
A other laboratory markers
38
Aromatase inhibitors 58 transvaginal hydrolaparo-
Autoimmune disease 11 scopy 34
C E
Clinical staging of
endometriosis 13 Endometriosis 1
chronic disease 23 prevalence 2
clinical signs 24 Endometriosis and assisted
other non-gynecological reproductive technolo-
symptoms 23 gies 75
subfertility 16 ICSI (intracytoplasmic
sperm injection) 76
D IUI (intrauterine insemina-
tion) 76
Diagnosis of endometriosis 27
IVF 76
differential diagnosis 28
oocytes donation 76
ectopic pregnancy 28
Etiopathogenesis of endomet-
ovarian cyst 28
riosis 5
ovarian neoplasm 28
celomic metaplasia 9
ovarian torsion 28
pelvic infection 28 estrogen dependent 11
histology 34 hereditary theory 10
imaging techniques 39 autoimmune disorder
magnetic resonance 11
imaging (MRI) 44 environmental factors
other imaging 10
techniques 45 liver disorders 19
ultrasound 39 retrograde menstruation 6
laparoscopy 28 transplantation theory 9
markers 37 iatrogenic transplanta-
CA-125 37 tion 9
F selective progesterone
receptor modulators
Fertilization of implantation 60
failure 20 symptomatic relief 51
non-steroidal anti-
H inflammatory drugs
Hormonal or ovulatory (NSAIDs) 51
dysfunction 20 progestins 51
I O
Infertility 20 Objective of surgical
treatment 66
M Ovarian endometriotic cyst 33
Medical management of Ovarian stroma 35
endometriosis 49
combined oral contracep- P
tives (COCs) 54
aromatase inhibitors 58 Pelvic adhesions 30
continuous adminis-
tration 54 R
cyclical administration
55 Retrograde menstruation 7
danazol 56
gestrinone 55 S
gonadotropin-releasing
hormone agonists 57 Surgical management of
recent advancesunder endometriosis 65
trials 59 objective of surgical
anti-angiogenic treatment 66
therapies 59 combination of medical
atorvastatin 60 and surgical therapy
genistein 60 73
progesterone antago- second-look laparo-
nists 60 scopy 73

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Step by Step

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

Step by Step Management of Endometriosis

2008, Jaypee Brothers Medical Publishers

First Edition: 2008

Typeset at JPBMP typesetting unit

In spite of vast advances in gynecology, diagnosis of

Endometriosis is a common, poorly understood benign

The overall true prevalence of endometriosis is

The cause of endometriosis remains elusive even after

Fig. 2.1: Retrograde menstruation -shower of the pelvic

pelvis. The next most frequent locations include the

Critical Steps Postulated in the Development of

Fig. 2.2: Critical steps postulated in the development of

obstructive uterine or vaginal anomalies show

The Transplantation Theory

does not account for the presence of the disease in the

The Hereditary Theory

2. Seli E, Berkkanoglu M, Arici A. Pathogenesis of endo-

Action of inflammatory cytokines leading to local

Fig. 3.1: Bilateral endometrioma Kissing ovaries

ligaments). However, deeply infiltrating sub-peritoneal

Fig. 3.2: The American Society for Reproductive Medicine revised

endometriosis is moderate or severe,9 it usually involves

TABLE 3.1. Stages of endometriosis

Table 3.1 shows clinical stages of endometriosis.

Fig. 3.3: Severe degree of endometrioma with

Fig. 3.4: Right endometrioma with distorted tube

effect on oocyte-sperm interaction. Peritoneal fluid in

Fig. 3.5:Proposed scoring system from American Society of

Many endometriotic classification systems have been

TABLE 3.3: Classification of endometriosis

< 1 cm 1-3 cm > 3 cm

Cul-de-sac - Partial Complete

Ovary <1/3 1/3 to 2/3 >2/3

Classification of American Society of Reproductive

A reduced monthly fecundity rate and cumulative

OTHER NON-GYNECOLOGICAL SYMPTOMS

pain during or after sex, heavy or irregular bleeding,

than 1 disease process, such as chronic pelvic inflam-

8. Barlow DH, Glynn CJ. Endometriosis and pelvic pain.

Suspicion of endometriosis can be based on:

Differential Diagnosis for Endometriosis

Fig. 4.1: Laparoscopic view of endometrioma of right ovary

Fig. 4.2: Powder burn or Gun shot endometriotic lesion

Fig. 4.3: Laparoscopic view: Clear vesicle (white arrow)

brown, or bluish puckered lesions (Fig. 4.3), nodules or

Fig. 4.4: Hemorrhagic red flame petechial implants (arrows)

Fig. 4.5: Endometrial tissue implanted in the peritoneum has a

Fig. 4.6: Obliterated cul-de-sac due to endometrioma

the cul-de-sac (Fig. 4.6). Other etiologies include

Fig. 4.7: Laparoscopic findings: Adhesion at right

Fig. 4.8: Ovarian endometriotic cyst

Fig. 4.9: Deeply infiltrative endometrioma

confirmation of at least one lesion is ideal (Fig. 4.10). In

Fig. 4.11: Organized hemorrhage with macrophages containing

Fig. 4.12: Congested blood vessels with fibrous tissue and

endometriotic glands and stroma and turned to be

Several studies performed in populations at high-

OTHER LABORATORY MARKERS

CA-125 assay showed a sensitivity of 59 percent in

Fig. 4.13: Endometriotic cyst on transvaginal ultrasonography

be detected by trans vaginal ultrasonography and has