Managemnt of endometrosis

 Introduction
 Definition
 Incidence
 Stage
 Pathophysiology
 Risk factor
 Signs & symptoms

 Clinical Evaluation of patient with endometriosis
History
Examination
Diagnosis
Treatment
Complication
Differential diagnosis
Prevention
Prognosis
Follow-up
 Conclusion

 Functional human uterus are receiving the
embryo, to give shelter to the foetus during
pregnancy and delivering the newborn at
term. The uterus is a pear-shaped, muscular,
hallow organ with a triple-layered wall:
i. Myometrium (middle tunica mucosa)
ii. Perimetrium ( outer tunica serosa)
iii. Endometrium (inner most layer)

 Endometriosis is originated from the word
endometrium.
 The endometrium is the layer in which the
implantation takes place. It experiences
morphologic and functional changes that are
closely associated with the cyclic release of
sexual hormones.
 In the light of the above, if implantation
doesn't occur the layer of the endometrium
shed and expulsed, leading to menstruation.

 Endometriosis is a benign gynaecological disease
characterized by the presence of functional
endometrial glands and stroma outside the uterus
(ectopic).
 In a typical patient, the ectopic implants are
located
in the dependant portions of the female pelvis:

Because is a chronic oestrogenic-
dependant inflammatory disease, it
therefore affects approximately 10%
of women of reproductive age.

 The public health burden of endometriosis
remain elusive because of the mode of
diagnosis of the disease, giving us a lack of
reliable data annually.
 Moreover many women are asymptomatic
and endometriosis lesions heal
spontaneously in them without a diagnosis
been previously made.

 Dysmenorrhoea
 Dyspareunia
 Chronic Pelvic pain
 Infertility
 Asymptomatic
62.2%
2.1%
80%
35-50%
20-50%

 There is a 10-folds increase incidence in women
with an affected first degree relative(family
history). And as well as monozygotic twins are
markedly concordant for endometriosis.
 Rate of endometriosis was found to increase
with age from 12% in females ages 11-13 years
to 45% in females aged 20-21years and peak
incidence between ages of 25 and 35 years.

 Endometriosis is classified into one of four
stages depending on the following;
 Size, location
 Type
 Extent
 Depth of endometriosis implants
 Presence and severity of adhesions
 Presence and size of ovarian endometriomas

 Common sites includes:
 Posterior and anterior cul-de-sac
 Ovaries (most common)
 Pelvic peritoneum
 Fallopian tubes
 Vagina
 Cervix
 Uterosacral ligaments and
 Rectovaginal septum.

 Unusual implantation sites are:
 Laparotomy scars
 Pleura, lung
 Diaphragm
 Kidney
 Spleen
 Gallbladder
 Nasal mucosa
 Spinal canal
 Stomach.

1. Superficial peritoneal lesions is typically
located on the pelvic organs /pelvic
peritoneum
subtypes:
 I. Classic bluish or blue-black lesion
(powder-burn)
 II. Non-classic lesions or clear and red or
white lesions (flame-like)
2. Endometrioma /Endometriotic Cyst
3. Deep endometriosis

 Stage I
 Stage II
 Stage III
 Stage IV
minimal 1-5
mild 6-15
moderate 16-40
severe >40

 Minimal (stage I) or mild(stage II)
endometriosis, is characterized by superficial
implants and mild adhesions. And majority of
women have these stage of endometriosis.
 While moderate(stage III) and severe(stage IV)
endometriosis is characterized by chocolate
cysts and more sever adhesions. The stages of
endometriosis is not a criteria for the presence
of severity of symptoms, in the same vain
infertility is likely with stage IV endometriosis.

1.Retrograde Menstruation
 Retrograde menstruation theory is one of the
oldest principle that explains the
aetiopathogenisis of endometriosis, this occur
due to the retrograde flow of sloughed
endometrial cells/debris via the fallopian
tubes into the pelvic cavity during
menstruation.
 However, retrograde menstruation occurs in
76%-90% of women with patent fallopian
tubes and not all of these women have
endometriosis.

 Factors obstructing menstruation are,
congenital abnormalities, including
imperforate hymen and iatrogenic
cervical stenosis etc.
 The location of superficial
endometriotic lesions in the posterior
aspect and left side of the pelvis may be
due to the effects of gravity on
regurgitated menstruation product and
the anatomical position of the sigmoid
colon.

2.Coelomic Metaplasia
 These theory postulates the origin of
endometriosis from metaplasia of specialised
cells that are present in the mesothelial lining
of the visceral and abdominal peritoneum
 Hormonal or immunological factors
stimulates the transformation of normal
peritoneal tissue/cells into endometrium-like
tissue.

 These theory clearly explains the occurrence of
endometriosis in pre-pubertal girls even thou
oestrogen which is the driving force of endometrial
growth is not present in them and therefore this
condition may be different from endometriosis that
is found in women of reproductive age.
 According to this theory, residual embryonic cells of
the wolffian or mullerian ducts persist and develop
into endometriotic lesions that respond to oestrogen.
these describes the hormon-dedpendent
transformation of peritoneal cells into mullerian-
type cells in adolescent.

3. Oxidative stress and
inflammation
 Reactive oxygen species (ROS) causes lipid
per-oxidation which leads to DNA damage in
endometrial cells, resulting to increase
water and electrolyte in the peritoneal fluid
which harbours the source of ROS.
 Iron overload occur in the peritoneal
cavities from the breakdown of
haemoglobin, which in turn causes redox
reaction.

 The release of the pro-inflammatory
heam products and the oxidative stress
signals generated from the ROS causes
inflammation which leads to the
recruitment of lymphocytes and
activated macrophages producing
cytokines that induce oxidizing of
enzymes and promotes endothelial
growth.

 excess proliferation of ROS is accomplished
by a decreased level of antioxidants which
usually eliminates these molecules.
 The resulting accumulation of ROS may
contributes to the propagation and
maintenance of endometriosis and
associated symptoms.

4. Immune Dysfunction
 Autoimmune disease is more
common in women with
endometriosis. This is due to
regurgitation of endometrial cells
into the peritoneum which triggers an
inflammatory response causing the
recruiting of activated macrophages
and leukocytes.

 This inflammatory response leads to a
defective immune-surveillance that prevents
elimination of the menstrual debris and
promotes the implantation and growth of
endometrial cells in the ectopic sites.
 These theory explains better why women
with endometriosis have higher
concentration of activated macrophages,
decreased cellular immunity as well as a
repressed NK cell function.

5.Stem Cells
 stem cells are undifferentiated cells,
characterized by their ability to self-renew
and differentiate into one or several types of
specialized cells.
 Due to the natural ability of the stem cells to
regenerate, the stem cells then give rise to new
Endometriotic deposits, these pathogenesis
supports the possibility of retrograde
menstruation which provides an access for the
endometrial stem cell to extra uterine
structure.

 Monthly, there is regeneration of the
endometrium after menstrual shedding and re-
epithelisation of the endometrium after
parturition or surgical curettage, these all
support the existence of a stem cell pool and
resides in the basalis layer of the endometrium.
Resulting in the formation of ectopic
endometrial lesions.
 However these stem cells may be transported
via the lymphatic or vascular pathways to
ectopic sites. Some of the endometrial stem
cells have bone marrow origin and further
supports the haematogenous dissemination
theory of these cells.

6. Apoptosis Suppression and
Alteration of Endometrial Cell Fate
 Alteration of the endometrial cell fate to favour
antiapoptotic and pro-proliferation phenotype is
paramount for the survival of the endometrial cells in
the peritoneal cavity to initiate ectopic deposits and for
the maintenance of the established lesions.
 The inhibition of the apoptosis of endometrial cells
may also be mediated by the transcription activation of
genes that normally promotes inflammation,
angiogenesis, and cell proliferation.

 Red lesions /early endometriosis
 Black lesions /advanced
endometriosis
 White lesions / healed endometriosis

 Genetics (positive family history)
 Nulliparity
 Early menarche
 Hormones
 Obesity
 Uterine retroversion
 Miscarriage.

 Although a significant number of women with
endometriosis remain asymptomatic, but
symptomatic patients can be variable and
reflects the depth and area of involvement.
 Signs and symptoms includes:
1.Pelvic pain
2.Dysmenorrhoea
3.Dsyparinuria

4.Dysuria
5.Dyschesia (pain on defecation) often with cycles of
diarrhoea and constipation
6.Lower abdominal pain or back pain (worsen during
menstrual period)
7.Inguinal pain
8.Pain during exercise
9. Heavy or irregular bleeding
10. Bloating, nausea and vomiting

 Heamaturia
 Rectal pain
 Urgency
 Haemoptysis
 Coetaneous nodules
 Hyperprolactinaemia

 History taking is an essential aspect in the
evaluation of a patient with endometriosis, the
following guidelines must be observed.
 Having completed your bio data, the necessary
important history based on the chief
complaints of the patient with endometriosis
must be asked.
Infertility/ pain is usually the chief
complains of patients with
endometriosis.

1. History of Presenting Compliant
 Onset
 Periodicity
 Duration
 Recurrence
 Aggravating & Reliving factors
 Severity

2. Menstrual History
 Menarche and menopause
 1st
day of last menstrual period
 Length of bleeding
 Frequency
 Regularity
 Bleeding between periods
 Bleeding after intercourse
 Post menopausal bleeding
 Nature of periods
Heavy?
Clots?
Flooding?

3. Past Gynaecological History
 Gynaecological symptoms
 Gynaecological diagnosis
 Gynaecological surgery
 Date & result of cervical smears
 Conception

4. Past Obstetrics History
 Gravity & Parity
 Dates of deliveries
 Length of pregnancy
 Mode of delivery
 Weight of babies
 Sex of babies
 Complication before, during & after delivery
 Days spent before discharged.

5. Past Medical History
 Current or past illnesses
 Hospital admission
 Past surgeries

6. Drug History
 Current medication
 Prescribed/ over the counter medication
 Herbal Remedies
 Recreational drugs
 Any known drug allergies.

7. Contraception
 Types of contraception
 Side effects of contraception
 Any history of unprotected intercourse

8. Family History
 History of endometriosis (occurs 10 times in
someone with positive family history)
 Gynaecological condition
 Malignancies
 Consanguinity
 History of demise, causes and age at demise.

9. Social History
 Occupation
 Alcohol, how often and quantity
 Smoking, how often.

10. Other history
 Sleep pattern
 Change in bowel movement
 Micturation
 Defecation
 Weight loss/gain
 Addiction

 Majority of patient with endometriosis do not
frequently present with physical findings beyond
tenderness related to the site of involvement. The
hallmark of finding on examination of a patient
with endometriosis is pelvic examination. Major
finding:
 On pelvic examination
 Tender nodular masses
 Adenexia mass
 Bluish nodule is seen as a result of infiltration
from the posterior vagina wall.
 Cervicities
 Foul smelling vaginal discharge

 Methods of diagnosis
1. Invasive diagnosis
a. Laparoscopy
b. Microlaparoscopy
2. Non invasive diagnosis
a. Therapeutic trials
b. Imaging: USS,CT, MRI
c. Endometrial nerve fibers
d. Serum markers
v. Other.

Invasive Diagnosis
Laparoscopy: is the gold standard diagnostic
test.
Advantages
1. Excludes other condition e.g. ovarian cancer
2. Treatment of endometriosis
Disadvantages
1. requirement for surgery and anaesthesia
2. risk of major complications (bowel perforation)
3. visible inspection doesn't detect deep
endometriosis.

Technique
It has two approaches which includes;
 Inspection of D pouch, US lig, Pelvic side
walls, Anterior surface of the ovary
(adhesion). It endure complete evaluation,
inspection of the pelvic is in a clockwise
fashion.
 Biopsy in case there is a doubt.

 Findings:
A. Peritoneal
i. Typical endometriosis : Black-blue, powder-burn
appearance, and doesn't require any biopsy.
ii. Atypical endometriosis: Lesion that lacks the
typical black-blue, powder-burn appearance but
however diagnosis may be difficult with standard
laparoscopy so biopsy is necessary for confirmation
of diagnosis.
B. Endometrioma

1. Near-contact: it magnifies the peritoneal area
2. Peritoneal blood painting: flowing erythrocytes
outline surface irregularities.
3. Examined from different angles and at
different degrees of illumination: it shows
vesicles or whitish lesions.
4. Direct vision
5. Laparoscopic visualization of peritoneal lesions
is of limited accuracy, and biopsy confirmatory.
6. Bubble test: posterior cul de sac is irrigated with
short bursts of saline under controlled pressure. It
increases the level of triglycerides in the
peritoneal fluid.

Microlaparoscopy:
 out patient procedure
 Local anaesthesia
 Pain mapping
 For adolescent endometriosis

Non Invasive Diagnosis
 Therapeutic trials
i. Pain suggestive of endometriosis
ii. Women not trying to conceive
iii. No pelvic mass
 Chronic pelvic pain
i. Unrelated to menstruation
ii. Unrelieved by NSAID & antibiotics
iii. Is clinically suspected.

 Imaging
1. Transvaginal ultrasound
 First line investigational tool for the suspecting
endometriosis
 Visualization of deep nodules (retrovaginal
septum)
 Results :
 Anechoic to echogenic cysts
 Masses containing multiple septations & solid
tissue
 Cysts with low-level echoes ( this is the
commonest finding 0f about 95%).

 2. Transrectal ultrasound: it detect
 Rectal involvement
 Depth of infiltration
 Lesions on the posterior bladder wall.
 3. CT : it has an important role in detecting an
unrelated involvement and possible renal
insufficiency.
 It has been replaced by MRI due to,
 poor specificity
 High radiation

4. MRI: it helps to detect pigmented hgic lesion and
inadequately localized lesions.
 Posses greater sensitivity which detects about
75% of mild disease
 Evaluation of deep lesions
 Is also superior to ultrasound in diagnosis
rectosigmoid lesions and bladder of the
endometriosis
 Disadvantages
 It is expensive
 And not readily available

 5. Endometrial nerve fibers: they are
reported to be small unmyelinated
sensory C fibers in the functional layer
of endometrium which are identified by
their staining with PGP9.5, VIP, and
substance P, but not with neurofilament

 6. Serum makers: is a useful marker for
monitoring treatment.
 Others:
 Cystoscopy : for bladder endometriosis
 Sigmoidoscopy or colonoscopy: for transmural
bowel lesions
 Ultrasound-guided fine needle aspirate: for
endometriosis in the rectosigmoid ,
rectovaginal septum, or in abdominal scars.
 IVP, barium study.

 Treatment for endometriosis can be
expectant, medical, or surgical depending on
location, depth, severity of symptoms and as
well as the desire of the patient to maintain or
restore fertility.
Medical treatment:
Is used in patients with pelvic pain or
dyspareunia and the aim of treatment is to
focus on hormonal manipulation of the
menstrual cycle to create the state of
pseudopregnancy, pseudomenopause, or
chronic anovulation..

 Medication includes
1. Danazol
2. Gonadotropin-releasing hormone agonists
3. Oral contraceptive pills and other
4. Progestational agents

Surgical treatment can be :
A. Conservative
B. Definitive
A. Conservative Surgery
 These can be performed with laparoscopy or
laparotomy
 And the success rate is however high, but
implant recurrence occurs in 28% of patient
at 18 months after surgery and 40% by 9
years.
 Adhesion recur in 40-50% of patients

B. Definitive surgery
 These include
 Hysterectomy and oophorectomy
 Is usually reserved for women with
intractable pain. And in one severe cases, one
ovary may be retained.
 Endometriosis may recur with exogenous
estrogens replacement therapy, even in
patient who has undergone oophorectomy.

 Complications of endometriosis includes the
following:
1. Bleeding : forming bands of scar tissue leading to
adhesion which then attaches to the organs in the
pelvis and abdomen.
2. Infertility : usually of unknown origin, and may be
caused by adhesions forming on or close to the
ovaries and fallopian tubes.
3. Miscarriage or premature birth
4. Cancer (most esp. Ovarian cancer)
5. Blocked or twisted bowel : due to endometriosis
of the intestine
6. Adhesion

1. Ovarian cysts
2. Tuberculosis peritonitis
3. Ovarian cancer
4. Pelvic inflammatory disease

 Prevention of endometriosis includes a wide
range of activities known as interventions
 Its aim is to reduce risks of threats to health.
These leads us to the three categories of
prevention of endometriosis;
1. Primary prevention
2. Secondary prevention
3. Tertiary prevention

Primary prevention:
 Its aim at preventing disease or injury of
endometriosis before it ever occurs.
 This is done by;
i. Preventing exposures to hazards that can cause
disease or injury which alters unhealthy
behaviours that can lead to endometriosis.
ii. Enforcement to ban or control the use of
hazardous substances.
iii. Education about healthy and safe habits.

2. Secondary prevention:
 Aims to reduce the impact of endometriosis or
injury that has already occur. This is done by;
i. Regular examination and screening to detect
endometriosis in its earliest stage.
ii. To treat endometriosis as soon as possible to slow
its progression.
ii. Encouraging personal strategies to prevent re-
injury or recurrence, and implementing programs
to return people to their original health.
iv. To prevent long-time complications of
endometriosis.

3. Tertiary prevention:
 Aim to reduce the impact of an ongoing illness or
injury that has lasting effects, and is done by;
i. Helping people to manage long-term, often-
complex health problems and injuries, in order to
improve as much as possible their ability to
function, their quality of life and life expectancy.
ii. Support groups that allow people to share
strategies for living well
iii. Vocational rehabilitation programs to recover as
early as possible.

 The recurrence rate five years following surgery
is between 20% and 40%, providing menopause
has not been reached and hysterectomy has not
been performed
 Women who have undergone treatment for
endometriosis needs to attend periodic
examinations so they can be monitored using
sonography
 Note that endometriosis may recur after surgery
or medical intervention if the underlying p causes
is not probably treated.

 Endometriosis is often a chronic disease, and
thorough discussions to ensure a good level of
patient understanding is essential.
 It’s important to assess your level of symptoms,
your desire to have children in the future, as well as
your social and occupational needs for better health.
 Comprehensive follow-up will aid in the assistance
of total rehabilitation.

 Majority of patients with endometriosis will
have increasing fertility problems.
Fortunately, the results of assisted
reproduction (such as IVF) after treatment
for endometriosis are very good.
 While some of these patients , even if they
have an initial problem with their fertility,
end up becoming pregnant after adequate
and carefully monitored treatment.

 In the same vain, some patients will require
a higher level of technology to achieve a
pregnancy, such as IVF or GIFT.
 Note that, pregnancy is not a complete and
definitive cure for endometriosis, the
combination of pregnancy and breastfeeding
significantly slows down the course of the
disease and may even get rid of it entirely.

Managemnt of endometrosis

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