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Gyne S1 L10 Endometriosis

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GYNE • GYNECOLOGY

SHIFT
ENDOMETRIOSIS
1
Anne Catherine A. Castro, MD, Jocelyn Mariano, MD, Anne Marie C. Trinidad, MD September 22, 2022 LEC 10
○ Pelvic lymph nodes (up to 30% of cases)
LECTURE OUTLINE
○ Cervix
I. Endometriosis VI. Prognosis ○ Vagina
II. Epidemiology VII. Differential Diagnosis ○ Vulva
III. Pathology VIII. Treatment ○ Extra-pelvic endometriosis
A. Location A. Medical
■ Gastrointestinal system (common site)
B. Phenotypes B. Surgical
IV. Etiologies/Theories C. Special Considerations – Sigmoid colon
A. Retrograde Menstruation D. Treatment of Special Populations – Appendix
B. Coelomic Metaplasia IX. Case ■ Renal System
C. Benign Metastasis A. Other Important Information in the ■ Pulmonary System
D. Iatrogenic Dissemination History ■ Remote sites
E. Immunologic Changes B. Other Important Information in the – Arms, legs, nasal mucosa, and spinal column

V.
F. Genetic Predisposition
Clinical Diagnosis
A. History
History
C. Working Diagnosis
D. Diagnostic Work-Up
📕 Table 1. Anatomic Distribution of Endometriosis.
Common Sites Rare Sites
B. Physical Exam E. Treatment Options
● Ovaries (most common) ● Umbilicus
C. Imaging X. References
D. Biomarkers XI. Appendix
● Pelvic peritoneum ● Episiotomy scar
E. Endometrial Biopsy ● Ligaments of the uterus ● Bladder - cyclic hematuria
F. Endometriosis Staging ● Sigmoid colon ● Kidney

👉
important/must know
📕
book
📑
previous trans
🩺
lecturer’s key points


Appendix
Pelvic lymph nodes
● Lungs
● Arms
● Cervix ● Legs
● Vagina ● Nasal mucosa
I. ENDOMETRIOSIS
● Presence and growth of the endometrial glands and stroma of the lining of the
uterus in an aberrant or heterotopic location
● Fallopian tubes
📕
● Spinal column
Male Urinary tract

○ Any location outside the endometrium B. PHENOTYPES


● Benign disease but has characteristics of malignancy
○ Locally infiltrative
📑 3 Types

of Endometriotic Lesions (depending on the penetration)
Superficial (peritoneal)
○ Invasive ● Deep infiltrating endometriosis (DIE)
○ Widely disseminating ● Endometriomas
● Growth of endometrium is stimulated by physiologic levels of estrogen ○ Ovarian involvement
○ During menopause, endometriosis is no longer a problem because of the ○ Cyst formation
📑
📑
lack of estrogen
Classic symptoms: cyclic pain and infertility 1. SUPERFICIAL (PERITONEAL) LESIONS
Typical patient
○ Mid-30s
📑 Predominant color depends on blood supply and the amount
of hemorrhage and fibrosis
○ Nulliparous ● Also appears to be related to size of the lesion, degree of edema, and amount
○ Involuntary infertile

📑 ○ Symptoms of secondary dysmenorrhea and pelvic pain


Adenomyosis (internal endometriosis)
📑 of inspissated material
Other peritoneal lesions that are grossly similar but
histologically are not:
○ Growth of endometrial glands and stroma into the uterine myometrium at ● Necrotic areas of ectopic pregnancy
📑 least 2.5 mm from the basalis layer of the endometrium
Estrogen dependent
○ Most commonly found during the reproductive years


Fibrotic reactions to suture
Hemangiomas
● Adrenal rest
📑 ○ Exogenous estrogen – postmenopausal endometriosis
Endometriosis in teenagers
○ Should be investigated for obstructive reproductive tract abnormalities


Walthard rest
Breast cancer
● Ovarian cancer
📑 that increases retrograde menstruation
Contrasts:
○ Contraceptive steroids are usually beneficial for treatment


Epithelial inclusions
Residual carbon from laser surgery
● Peritoneal inflammation
○ Inverse relationship between pelvic endometriosis and severity of pelvic ● Psammoma bodies
📑 pain
Pelvic lesions – positive immunostaining for smooth muscle as well as nerve
cells


Peritoneal reactions to oil-based hysterosalpingogram dye
Splenosis

II. EPIDEMIOLOGY 📑
ENDOMETRIOTIC IMPLANTS
Cause a foreign-body reaction as soon as it makes contact with ectopic
📕

11% of reproductive-age women
Endometriosis has been reported in up to: 📑
surfaces,
Inflammatory reaction → prostaglandins, congestion, edema.
○ 40% of adolescents with genital tract anomalies ● Gross appearance of the implant depends on the site, activity, relationship to
○ Up to 50% of women with infertility the day of the menstrual cycle, and chronicity of the area involved.
○ Up to 70% of women and adolescents with pelvic pain ● The color of the lesion varies widely and may be red, brown, black, white,
yellow, pink, clear, or a red vesicle.
○ Related to the size of the lesion, the degree of edema, and the amount of
III. PATHOLOGY inspissated material.
○ Predominant color depends on the blood supply and the amount of
A. LOCATION hemorrhage and fibrosis
● Mostly seen in dependent portions of the female pelvis.

📑
○ Ovaries – Most common site, often bilateral.
The endometrial glands and stroma will bleed in sync with the menstrual

📑
New lesions appear small (like blebs or implants)
Less than 1 cm

cycle; lesions will be red and filled with blood (endometrioma/endometrial

📑 cyst of the ovary)


Over time, these will turn into chocolate cysts because the blood is

📑
📑
oxidized to a light/dark brown color
Older lesions become white and retracted from surrounding tissue
In 2 out of 3 women with pelvic endometriosis, there would be some
ovarian involvement Pelvic peritoneum which overlies the uterus
■ Can also be studded with endometriotic implants
○ Anterior and posterior cul-de-sac – most dependent portion.
○ Ligaments of Uterus
■ Uterosacral ligament – back of the uterus to the sacrum.
■ Round ligament – anteroinferior to the tubes.
■ Broad ligament – cover the pelvic organs. Figure 1. Superficial (peritoneal lesions).

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Refer to Figure 1. Vascular spread ● Lung, nose, other distant sites
● Upper right shows active lesions (appear red) and upper left picture. Lymphatic spread ● Umbilicus, inguinal & pelvic nodes


📑○ Active lesions
Most blood-filled (upper right)
Lower left picture shows powder burn lesions (appear dark brown, dark blue,
Direct implantation ● Episiotomy & caesarian section scars

or black). A. RETROGRADE MENSTRUATION


○ Old lesions ● “Sampson’s theory”
● Lower right picture shows older lesions (appear white). ● Most popular theory.

📑○ Oldest lesion because intense scarring is already present.


Puckered or retracted from surrounding tissue.
● Reflux of menstrual blood and viable endometrial cells in the pelvis.
○ Leads to implantation of endometrial cells in the pelvic peritoneum and
under hormonal influence, grow as homologous grafts.
2. ENDOMETRIOMAS (“oma”) ● Examples/evidence:
● Ovarian cysts may range from <1 cm to large chocolate cysts greater than 8 ○ Endometriosis is discovered most frequently in areas immediately
cm in diameter. adjacent to the tubal ostia or in the dependent areas of the pelvis.


The associated adhesions may be filmy or dense.
Larger cysts are usually densely adherent to the surrounding pelvic sidewalls 📑
■ E.g. OS, cul de sac
Fibrosis and scarring will clog the fimbriated end of Fallopian tubes

📑
or broad ligament.

📑 IE usually presents as a “straight jacket”.


Apart from being usually retroverted, ovaries and fallopian tubes are

leading to infertility.
Most frequent areas:
■ Immediately adjacent to the tubal ostia

📑 palpated at the back and are immovable.


Severe form of Endometriosis - Stage IV: “frozen pelvis” - warrants a
– Fibrosis and scarring will clog the fimbriated end of Fallopian
tubes leading to infertility

📑 very long OR procedure.


Visual manifestations of endometriosis in the female pelvis are protean and ○
■ Dependent areas of the pelvis
Endometriosis is frequently found in women with outflow obstruction of

📑
have many appearances.
Depends on the site, activity, relationship to the day of the menstrual
the genitral tract
● Factors obstructing menstruation such as congenital abnormalities

📑 cycle, and chronicity of the area involved.


More emphasis has been placed on biopsy confirmation because of the
(imperforate hymen, transverse vaginal septum, and cervical
stenosis) can increase the chance for retrograde menstruation and

📑3 CARDINAL
subtle lesions.
HISTOLOGIC FEATURES OF ENDOMETRIOSIS:
📑
📑
increase risk for developing endometriosis
Extremely rapid process.
Endometriosis occurs due to the retrograde flow of slough endometrial cells or
● Ectopic endometrial glands.
debris via the fallopian tubes into the pelvic cavity during menstruation
● Ectopic endometrial stroma.
○ This is why most endometrial implants can be found in the most
○ Undergo classic decidual changes similar to pregnancy when exposed to


high physiologic or pharmacologic levels of progesterone.
Hemorrhage into adjacent tissue.
📑 dependent portions of the pelvis
Outflow tract obstruction leads to regurgitation of menstrual bleeding with
○ Large macrophages filled with hemosiderin near the periphery of the
lesion.
📑 endometrial implants out of the uterus
Endometrial implants cause a foreign-body reaction as soon as it contacts
ectopic surfaces → inflammatory reaction → prostaglandins, congestion,
○ Repetitive episodes of hemorrhage:


Severe inflammatory changes.
Glands and stroma undergoing necrobiosis secondary to
📑 edema
Viable glands may implant → during the next menstrual cycle, the endometrial
implants bleed as well → no outflow tract, just accumulates in the pelvic cavity
pressure atrophy or lack of blood supply.
→ fibrosis and scarring → fimbriated end of Fallopian tubes clogged because
● In majority of cases, aberrant endometrial glands and stroma respond in cyclic
fashion to estrogen and progesterone.
📑 of scarring → infertility


Shedding of endometrial-based adult stem cells and mesenchymal cells
Attach to the pelvic peritoneum and grow as homologous grafts through
hormonal stimulation

📑 ○ Expression of adhesion molecules and their receptors


Endometrial implants cause a foreign-body reaction as soon as it makes
contact with ectopic surfaces → inflammatory reaction → prostaglandins,
congestion, edema
PATHOPHYSIOLOGY
● Endometrial cells in menstrual fluid reach the peritoneal cavity via retrograde.
Figure 2. Endometrioma, Large Chocolate Cyst. ● Activation and infiltration of inflammatory and immune cells causing adhesion
and invasion.
3. DEEP INFILTRATING ENDOMETRIOSIS (DIE) ● Cells grow in numbers and implants leading to angiogenesis and
👉 Penetration of greater than 5 mm, represents a more progressive form of the

anti-apoptosis.
Secretions of prostaglandins, estradiol.
📑 disease.
10-15% of women with advanced disease have lesions involving the ○ Fibrosis, scarring, and pain.

📑
rectosigmoid.

📑 May lead to cyclic painful defecation.


May be difficult to differentiate grossly from primary neoplasm of he large

📑 intestine.
Deep invasive endometriosis:

👉
■ If the rectovaginal septum is invaded.
Causes dyspareunia and dysgeusia.

Figure 3. Deep Infiltrating Endometriosis. Figure 4. Pathophysiology of Retrograde Menstruation


IV. ETIOLOGIES / THEORIES
📑 Some women develop endometriosis and others do not
○ Complex interplay between a dose-response curve of the amount of
📕
B. COELOMIC METAPLASIA
Metaplasia of the coelomic epithelium or proliferation of embryonic rests.
retrograde menstruation and an individual woman’s immunologic
response

📑
Theory of embryonic Mullerian rests, or mullerianosis.
Histogenesis of endometriosis in peritoneal pockets of the posterior
pelvis results from congenital anomaly of rudimentary duplication of the
📕 ■ May depend on ethnic and genetic variability
No single theory adequately explains all the manifestations of the disease
Mullerian system.
■ Posterior aspects of the broad ligament.
📑 Table 2. Theories and Involved Sites ●
■ Cul-de-sac.
The metaplasia hypothesis postulates that the coelomic epithelium retains the
THEORY INVOLVED SITES
Retrograde flow ● Ovaries, tubes, cul-de-sac of Douglas, uterosacral ligaments, 📑
ability for multipotential development.
Ovarian endometriosis - from metaplasia of the coelomic epithelium that

👉
rectosigmoid colon, urinary bladder, pelvic peritoneum, invaginates into the ovarian cortex.
rectovaginal septum Metaplasia occurs after an “induction phenomenon” has stimulated the

📕
Coelomic metaplasia ● Peritoneum, pleura, pericardium multipotential cell.
Immunologic ● Peritoneum Induction substance may be a combination of menstrual debris and the
Genetic ● Peritoneum influence of estrogen and progesterone.

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📑 Also proposes that residual embryonic cells of the Wolffian or Mullerian ducts

📑 may persist and develop into endometriotic lesions that respond to estrogen
Abnormalities in the embryological development of the following:
○ Peritoneal cavity (most common)
○ Pleural cavity
○ Pericardial cavity (least common)
● Examples: Discovery of endometriosis in:
○ Prepubertal girls.
○ Women with congenital absence of the uterus.
○ Very rarely in men.
○ Decidual reaction of isolated areas of peritoneum during pregnancy.

C. BENIGN METASTASIS (LYMPHATIC AND VASCULAR METASTASIS)


📕 Helps
📕 to explain rare and remote sites of endometriosis such as:

📕 The spinal column


Nose


📕
Pelvic lymph nodes
30% of women with the disease
Forearm
○ Thigh Figure 6. Hypothesis regarding pathophysiologic characteristics of human peritoneal
○ Multiple lesions in the lung macrophages in endometriosis

📑

📕
The spread is through the lymph nodes to the blood vessels
Catamenial hemothorax: bloody pleural fluid occuring during menses
Hematogenous dissemination of endometrium is the best theory to explain
Refer to Figure 6.
Upper Box:
endometriosis of the forearm and thigh, as well as multiple lesions in the lung. ● It is a peritoneal macrophage with no endometriosis
● In which there is lack of membrane function, lack of enzymes and there is no
D. IATROGENIC DISSEMINATION (Direct Implantation) increase in size
● Endometriosis of the anterior abdominal wall after cesarean delivery. Lower Box:
○ Hypothesis: Endometrial glands and stroma are implanted during a ● With endometriosis, the peritoneal implant grows at the same it activates
surgical procedure. ● The hyperactive cells will secrete growth factors enzyme and cytokines and all
○ Found subcutaneously at the abdominal incision. of these contribute to the development of the endometrial cells
○ Symptoms: Nonhealing CS wound, cyclic inflammation and bleeding of ● Endometrial cells would implant and attract more monocytes
CS wound.
○ Treatment: Excision STEROID INTERACTIONS
● Examples: ● Steroid interactions also enhances the progression of the disease
○ CS Scar endometriosis (subcutaneous layer) ● Estrogen production is enhanced locally, and there is evidence for upregulation

📑
Episiotomy scar endometriosis
Do an excision biopsy to definitively diagnose

of aromatase activity, increased COX-2 expression, and deficiency in
17β-dehydrogenase II activity favoring local estradiol production.
Enhanced aromatase activity appears to be the result of overexpression of the
orphan nuclear steroidogenic factor-1 (SF-1) lesions.
● The local production of estrogen through aromatase activity explains why

● 📑
progression of lesions may occur even with ovarian suppression.
Progesterone “resistance”
○ Dysregulation of the isoform B of the progesterone receptor

Figure 5. Endometriosis of anterior abdominal wall after cesarean delivery

E. IMMUNOLOGIC CHANGES
📕 Changes in the immune system, especially altered function of the
immune-related cells (peritoneal macrophages) are directly related to the
pathogenesis of endometriosis.
○ Primary immunologic change: Alteration of peritoneal macrophages
function.
○ Peritoneal macrophages are prevalent in the peritoneal fluid of patients
with endometriosis.
● Abnormalities in cell-mediated and humoral components of the immune
system in both peripheral blood and peritoneal fluid.
● Women with no endometriosis have monocytic-type macrophages in their Figure 7. Normal Endometrium and Endometriosis.

📕 peritoneal fluid that have a short life span and limited function.
Women who developed endometriosis have more peritoneal macrophages that
are larger. These hyperactive cells secrete multiple growth factors and
Refer to Figure 7.
A. Endometrium in Disease-Free Women
cytokines that enhance the development of endometriosis. ● Normal COX-2 enzyme → low level of prostaglandin.
○ Chemokines (chemotactic cytokines) – attraction of leukocytes to specific ● No aromatase in the endometrium → no local production of estrogen.

📕 areas ● 17β-Hydroxysteroid dehydrogenase 2 (HSD17B2) converts estradiol


Enhanced aromatase activity appears to be the result of overexpression of the (active form of estrogen) to less active form of estrogen which is
orphan nuclear receptor steroidogenic factor-1 (SF-1) in lesions.
👉 estrone.

📕Table 3. Cytokines and Growth Factors in Peritoneal Fluid


Overall effect: Low PGE2 locally and low level of estradiol.
B. Endometrium in Women with Endometriosis
CYTOKINES AND GROWTH FACTORS IN PERITONEAL FLUID ● Increased level of COX-2 enzyme → moderate level of prostaglandin.
INCREASED ● There is an aromatase enzyme → androgen is converted to estrogen.


Complement
Eotaxin


IL-6
IL-8


RANTES
Soluble ICAM-1
C.
👉● Estradiol is converted to estrone due to (HSD17B2).
Overall effect: Moderate level of PGE2 locally and low level of estradiol.
Ectopic Endometriotic Tissue
● Glycodelin ● MCP-1 ● TGF-β
● Increased level of COX-2 enzyme → high level of prostaglandin.
● IL-1 ● PDGF ● VEGF
● There is an aromatase enzyme → androgen is converted to estrogen →
UNCHANGED high estrogen.
● EGF ● Interferon-𝛄 ● IL-4
● Basic FGF ● IL-2
DECREASED
● IL-12 👉● No HSD17b2, therefore estradiol is not converted to estrone.
Overall effect: High level of PGE2 and estradiol locally.

● IL-13

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PROGESTERONE RESISTANCE 👉 Extent of pelvic pain is often inversely proportional to the amount of
endometriosis in the female pelvis.
● Other symptoms include:
○ Dyschezia
○ Hematochezia
○ Massive ascites (rare)

📑FROM
👉 2023 TRANS
Classical Triad of Endometriosis:

👉 3D’s of○○ Endometriosis:


Dysmenorrhea, Dyspareunia, Infertility/Subfertility

Dysmenorrhea, Dyspreunia, Dyschezia


● Minor symptoms: Women with large, fixed, adnexal masses
● Moderate to severe pain: Only a few small foci with deep infiltration
○ Infiltrative endometriosis
■ Involves extensive areas of retroperitoneal space
● Infertility (25-50%)
○ Fallopian tubes are blocked by adhesions | ��
○ Secondary to pelvic scarring and adhesions
● Abnormal bleeding (15-20%)
○ Premenstrual spotting and menorrhagia
Figure 8. Progesterone Resistance. ○ May be related abnormalities in endometrium but NOT associated
with anovulation
Refer to Figure 8. ● Dyschezia
● Presence of progesterone resistance in the endometriotic lesions due to lack ○ Pain with defecation
of progesterone receptors. ● Hematochezia
● The stromal cells of the endometriosis are not capable of responding to ○ Bleeding with defection
progesterone due to deficiency in progesterone receptors. ● Massive ascites: RARE but important because the disease process initially
○ This leads to formation of insufficient quantities of retinoic acid hence the masquerades as ovarian carcinoma
loss of paracrine signaling to induce HSD17B2 expression. ○ Ovulatory dysfunction if the ovary is involved
● When the HSD17B2 promoter epithelial cell is not activated, there would be ○ Dysuria/hematuria if the bladder is involved
resulting high levels of estradiol. ○ Painful defecation/diarrhea if the rectum is involved

📕 ○ Since there is no enzyme available to convert the estradiol to estrone.


This is occasioned by a dysregulation of the isoform B of the progester- one
receptor in most endometriotic lesions, where levels may be undetectable.

○ Massive ascites (rare)
1/3 of the patients are asymptomatic

AUTOIMMUNITY
● Autoimmunity may exist in women with endometriosis.
● There are reports of increased B and T cells, and serum immunoglobulins
(IgG, IgA, and IgM) autoantibodies in endometriosis.
● Evidence of higher prevalence of other autoimmune diseases.

F. GENETIC PREDISPOSITION
📕 Familial predisposition to endometriosis with groupings of cases of

📕 endometriosis in mothers and their daughters.


Sevenfold increase in incidence of endometriosis in first-degree relatives.

📕 ○ Women with severe endometriosis have been thought to be 7%.


Women who have a family history of endometriosis are likely to develop the
Figure 9. Most Common Preoperative Symptoms .
📕 disease earlier in life and to have more advanced disease.
Deletions of genes, most specifically increased heterogenecity of

📕 chromosome 17 and aneuploidy.


The genetic heritability of endometriosis has been estimated at 52% based on ●
B. PHYSICAL EXAM
The classic pelvic finding of endometriosis is a fixed retroverted uterus, with
📕
📕
twin studies
Endometriosis is a polygenic disease, with various susceptibility factors
Loci on 7p and 10q have also been found to increase the susceptibility
📑 scarring and tenderness posterior to the uterus
Small areas of endometriosis in the cervix or upper vagina may be evident in
speculum exam
📑FROM

2023 TRANS
Reflux of matrix metalloproteinases (MMPs) into the peritoneal cavity at
● There is immobility of the pelvic organs and during coital activity there is direct
pressure on the areas of endometriosis
● The characteristic tender nodularity of the uterosacral ligaments and
menstruation may contribute to peritoneal attachment. cul-de-sac, and induration of rectovaginal septum may be palpated on RVE
● Genetic predisposition or exposure to environmental factors may program ● The ovaries may be enlarged and tender and are often fixed to the broad
fetal progenitor cells in an epigenetic way to overexpress SP-1 and estrogen ligament or lateral pelvic sidewall
receptor-β, which increase the risk of developing endometriosis ○ This is what we call the “chocolate cysts”
● Asian women – ninefold increase.

V. CLINICAL DIAGNOSIS
🩺 ○


If severe, can be found at the back of the uterus
Best time to do pelvic exam: Day 1 or 2 of the menses
This is the time of maximum swelling and tenderness in the areas of

A. HISTORY 📑 ○
endometriosis
In advanced cases:
There is lateral displacement or deviation of the cervix towards one side
● Classic symptoms of endometriosis are cyclic pelvic pain and infertility.
○ Cyclic pelvic pain due to: (indicative of intense scarring and adhesions)
■ Sequential swelling and extravasation of blood.
■ Chemical mediators such as prostaglandin and cytokine.
● Chronic pelvic pain usually presents as secondary dysmenorrhea or

🩺
dyspareunia, or both.
Dyspareunia
■ Has to be deep.

■ 📑
“May parang tinatamaan ba sa loob na masakit pag may contact”.

📑 Pain during penetration/painful coitus |



■ 📑 Pain deep in pelvis
Caused by immobility of pelvic organs during coital activity or
direct pressure on areas of endometriosis in the uterosacral


■ 📑
ligaments of cul-de-sac
Acute pain may continue for several hours following intercourse
Secondary dysmenorrhea usually begins 36 to 48 hours prior to the onset of
Figure 10. Left: Small endometriosis in the cervix/upper vagina; Right: (A) Normal
appearance, (B) Lateral deviation of the cervix towards one side.


📑
menses.
○ Secondary dysmenorrhea
Dull ache to severe pelvic pain, may be unilateral or bilateral and
📑CLASSICAL

FINDINGS IN INTERNAL EXAMINATION
Fixed or immobile retroverted uterus secondary to adhesions.
may radiate to lower back, legs, and groin ● Scarring and tenderness posterior to the uterus.
■ Pelvic heaviness or a perception of internal organs being swollen ● Adnexa: Presence of endometrial cysts or endometriomas.
■ Pain may last for many days, including several days before and ○ Cystic lesions that tend to be fixed to the broad ligament of lateral pelvic
after menstrual flow sidewall.
● Approximately ⅓ of patients with endometriosis are asymptomatic. ○ Tender.

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📑CLASSICAL

FINDINGS ON RECTOVAGINAL EXAMINATION
Implants on the cul de sac or uterosacral region
MAGNETIC RESONANCE IMAGING (MRI)
● Provides the best overall diagnostic tool for endometriosis but is not always
● Tender nodularities on examining finger a practical modality for diagnosis
● Advanced cases: extensive scarring & narrowing of the posterior vaginal fornix ● The use of MRI seems logical for equivocal ultrasound findings, especially if

📑
surgery is planned for excision of deeply infiltrating endometriosis, possibly
CLASSICAL
ENDOMETRIOSIS
FINDINGS OF ADENOMYOSIS CONCOMITANT WITH
📑
requiring rectal or bladder resection
Characteristic hyperintensity on T1-weighted images, and a hypo intensity on
T2-weighted images
● Diffusely enlarged uterus that is tender and boggy in consistency
● Very thick anterior and posterior myometrium with pinpoint hemorrhages
○ Represents the endometrial glands and stroma that are infiltrating the FOUR ULTRASONOGRAPHIC STEPS TO THE EVALUATION OF THE PELVIS WITH
myometrium SUSPECTED ENDOMETRIOSIS
1. Traditional evaluation of the uterus and adnexa for adenomyosis or
C. IMAGING endometriomas
● Imaging can be a useful adjunct to the clinical presentation and physical exam a. Adenomyosis is observed more frequently in women with deep
for evaluation of endometriosis endometriosis lesions compared with those with superficial lesions
○ Especially for patients with Deep Infiltrating Endometriosis (DIE) b. Measure the thickness of the endometrium wall
■ Adenomyosis >2.5 cm


👉
TRANSVAGINAL / TRANSRECTAL ULTRASOUND
First line diagnostic imaging
Most cost effective
2. Ultrasound probe is used to determine the location of specific tender spots
that may reflect disease-specific sites to be investigated at the time of surgery
3. Evaluate the cul de sac (pouch of Douglas) to determine whether there is
● Has the highest sensitivity and specificity in identifying ovarian deeply infiltrating disease or obliteration by the “sliding sign”, in which
📑
endometriomas
Appears as unilocular cyst, ground-glass appearance with diffuse
low level internal echo (looks gray)
pressure is placed on the cervix with the probe to see whether the anterior
rectum moves freely across the area of the vagina next to the posterior cervix
and upper uterus
● Helpful in differentiating solid from cystic lesions and may help distinguish an a. (+) Sliding = No endometriosis
endometrioma from other adnexal abnormalities b. (-) Sliding = Endometriosis
● Because the lesions are vascular, increased Doppler flow may be 4. Evaluation for nodules of the anterior compartment (bladder) and posterior
📑 📑
demonstrated in endometriosis.
Visualize ovarian cysts
compartment
a. The posterior compartment includes the uterosacral ligaments (which are
📑
📑
Low to medium echogenicity
Visualize the retroverted uterus
not seen by ultrasonography unless there is a nodule), the rectovaginal
septum, vaginal wall, and rectum.
📑 Ultrasound by itself is quite accurate already
Ultrasound examination shows no specific pattern to screen for pelvic D. BIOMARKERS

📑 endometriosis
An increased doppler flow may be demonstrated because the lesions are
vascular Biomarker
Table 4. Biomarkers
INFORMATION
CA-125 ● Levels are elevated in most patients with endometriosis and
increases incrementally with advanced stages
● Low specificity
● Increase with other pelvic conditions such as leiomyomas, acute
pelvic inflammatory disease, and the first trimester of pregnancy.
● Usually used for ovarian cancer also
Glycodelin ● Previously known as placental protein 14, has been shown to be
elevated in endometriosis and is produced in endometriotic

📕
📕
lesions.
Levels also fall with removal of the disease
Great variability in levels
○ not proved to be useful clinically.
Figure 11. Transvaginal Ultrasound showing unilocular cyst, ground-glass appearance
with diffuse low level internal echo. IL-1
👉
● Predictive marker
MOST useful marker
Chemoattractant ● Predictive marker
protein-1

📕
IFN-Gamma ● Predictive marker
P53 Explains association of Endometriosis with ovarian cancer

E. 📕ENDOMETRIAL BIOPSY
● Enhanced aromatase expression and progesterone resistance
● Aid in the outpatient diagnosis of endometri sis
● B-cell lymphoma 6 (BCL6), which is only minimally expressed in the normal
secretory endometrium of women withut endometriosis
○ enhanced expression has been found in the eutopic endometrium of
women with endometriosis
Figure 12. Transvaginal Ultrasound of adenomyosis shows an enlarged uterus, thickening ○ Using an immunochemical staining score for BCL6, the receive
of myometrium (white arrows), cystic or anechoic spaces within myometrium operating characteristic (ROC) curve showed a sensitivity of about 94%
representative of endometrial glands and stroma, lack of homogeneity of myometrium. ○ Although there is a commercially available test for this marker, it is still
not universally accepte

👉
LAPAROSCOPY
Gold standard
○ Not all patients will agree to a surgical procedure → not routinely done F. ENDOMETRIOSIS STAGING
● Diagnosis can be confirmed in most cases by direct laparoscopic visualization
of endometriosis 1. ASRM(AFS) STAGING
● Biopsy of selected implants can be done to confirm diagnosis
● However, this is expensive Table 5. ASRM (AFS) Staging
● When laparoscopy is undertaken to establish the diagnosis of endometriosis, it PROGRESSION TISSUE DESCRIPTION IMAGE
is important to describe systematically the extent of the pathology
● Diagnostic of choice for special populations
○ Patients with infertility who have tubal endometriosis I Minimal Presentation of 2-3 superficial implants.
○ Can be done concomitantly with chromopertubation
■ Inject a dye intracervically and expect spillage of the dye in to the
pelvic cavity in patients with patent fallopian tubes
● The American Society for Reproductive Medicine developed a point-scoring Appearance of more implants that occur within
designed primarily to record the extent of the disease in fertility patients II Mild
deeper layers of tissue.
○ The focus here was intended to provide characterization of disease
extent for fertility and not for pain assessment
● Endometriosis Fertility Index (EFI): focuses on the fertility potential of Many deep implants in combination with
patients with endometriosis, and it has been shown in prospective evaluation III Moderate minor/small endometriomas on one or both
to correlate with pregnancy rates ovaries. May also present filmy adhesions.

Persistence of deep implants, enlargement of


RECTAL WATER CONTRAST TRANSVAGINAL ULTRASOUND
IV Severe endometriomas on one or both ovaries,
● Can increase the probability of detecting a DIE lesions, which is now
development of dense adhesions.
considered to the more sensitive technique for the diagnosis of DIE.

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2. ENZIAN STAGING 👉 Primary Long term goals


Supplement to ASRM (AFS) Staging
Grades the disease by the diameter of the nodules and localization
📑 ○ Prevent progression or recurrence of the disease process
Selection of an optimal treatment is based on multiple factors including:
○ Patient age
○ Patient preference
○ Reproductive plans
○ Pain severity
○ Degree of disease
○ Treatment cost and intended duration
○ Treatment risks/side-effect profiles
○ Accessibility

A. MEDICAL
● The main objective of medical management is to prevent recurrence and
Figure 13. Enzian Staging reduce symptoms, thereby eliminating the need for surgery (or repeat
surgery) or prolonging the time between surgeries.
3. ENDOMETRIOSIS FERTILITY INDEX (EFI) STAGING ● Aim: suppression of lesions and associated symptoms, particularly pain.

👉
● Newest staging ● The goal of hormonal treatments is to induce a local hypoestrogenic state
Estimates the woman’s chances of pregnancy after doing a laparoscopic or by suppressing ovulation (menstrual suppression) → amenorrhea
open surgery to remove the endometriotic lesions. ● The resulting amenorrhea or hypomenorrhea reduces the conversion of
● Scores are plotted based on historical and surgical categories to get the final arachidonic acid to prostaglandins with menses and subsequently lessens
EFI Score. dysmenorrhea and pelvic pain.
● Identify who are the best candidates for IVF ● Medical therapy usually suppresses symptomatology and prevents
● Factors to consider are: progression of endometriosis, but it does not provide a long-lasting cure of
○ ASMR Staging the disease.
○ Age of the patient ● Unfortunately, once suppressive therapy is stopped, symptoms tend to recur at
○ Duration of infertility variable rates.
○ Previous pregnancy 1. ORAL CONTRACEPTIVES
○ Lesions in the fallopian tube, fimbriae, and ovary 👉
📑 Pseudopregnancy effect
Creation of a high progesterone effect, producing decidual changes in the
endometrial implants (edema and eventual shrinkage)
● It has been accepted that the most economical regimen for the treatment of
women with mild or moderate symptoms of endometriosis has been

👉 continuous daily oral contraceptives for 6 to 12 months.


Continuous dose regimens are aimed at more complete suppression and the
only concern is with breakthrough bleeding.
● One potential risk of using oral contraceptives or progestogens is that there is

📑
some risk of rupture if a large endometrioma is present.
Rupture of large endometriomas may result in an acute surgical
abdomen during the first 6 weeks of oral contraceptive therapy.
● During prolonged therapy the endometrial glands atrophy and the stroma
undergoes a marked decidual reaction.
● Some smaller endometriomas (<3 or equal to 3 cm) can undergo
necrobiosis and resorption.
● Most common side effects
○ Weight gain
Figure 14. EFI Staging. ○ Breast tenderness
VI. PROGNOSIS ● Examples:
● 📑 American Society for Reproductive Medicine (ASRM) scoring for severity of
Pelvic Endometriosis (See appendix)
○ Continuous low dose monophasic COC daily for 6 to 12 months to
prevent menstruation (produce amenorrhea) and cause atrophy of the
endometrial implants.
● 📑


Used for patients with infertility
Score:
< 15 = minimal to mild (stage I-II)
■ Monophasic COC- contain a constant amount of estrogen .

○ > 15 = moderate to severe (stage III-IV) 2. PROGESTOGENS


● Indications:
VII. DIFFERENTIAL DIAGNOSIS ○ For women who fail combined hormone therapy
○ Smokers older than 35 years,
● Although a benign disease, endometriosis exhibits characteristics of both
○ Women with predisposing risk factors for myocardial infarction,
malignancy and sterile inflammation
○ Stroke,
● Therefore, the common considerations in the differential diagnosis include:
○ Thromboembolic events.
○ Chronic pelvic inflammatory disease
● May be given through oral, intrauterine, parenteral, or implantable routes and
○ Ovarian malignancy
all have breakthrough bleeding as their most common side effect.
○ Degeneration of myomas
● Breakthrough bleeding can be ameliorated with a 7- to 14-day course of oral
○ Hemorrhage or torsion of ovarian cysts – torsion results in loss of blood
estrogen.
supply to the adnexa, causing the pain.
● Some authors suggest that progestin-only methods such as norethindrone
○ Adenomyosis – endometriosis interna.
acetate and dienogest may be superior to COCs and can be considered
○ Primary dysmenorrhea – no pathology seen and yet there is
first-line, especially in women with rectovaginal and extrapelvic endometriosis
dysmenorrhea
● Examples:
○ Functional bowel disease
○ Medroxyprogesterone acetate (Provera)/ Progesterone: 20-30 mg
● Occasionally a large endometrioma of the ovary may rupture into the
PO daily- Give continuously from day 1 (not cyclic).
peritoneal cavity.
○ Depot medroxyprogesterone acetate (Depo-Provera): 150 mg IM
● This results in an acute surgical abdomen and brings into the differential
every 3 months to a maximum of 200 mg every month will produce a
diagnosis conditions such as:
prolonged amenorrhea.
○ Ectopic pregnancy
○ Norethindrone acetate: 10-40 mg OD; has a similar symptom profile to
○ Appendicitis
that of continuous medroxyprogesterone.
○ Diverticulitis
○ Gestrinone: 2.5 - to 7.5 mg/week. -acts as an agonist-antagonist of
○ Bleeding corpus luteum cyst
progesterone receptors and an agonist of androgen receptors; binds
weakly to estrogen receptors.
VIII. TREATMENT
📑
○ Dienogest: 2mg OD is a selective progestogen that causes anovulation,
Endometriosis should be viewed as a chronic disease that requires a lifelong has an antiproliferative effect on endometrial cells, and may inhibit
management plan with the goal of maximizing the use of medical treatment cytokine secretion.

📑 and avoiding repeated surgical procedures. ■ Indicated for young patients with dysmenorrhea and small
Treatment of endometriosis can be medical, surgical, or usually a combination endometriomas.

📕 of both. ■ Lipid-friendly, less androgenic side effects.


Disease is heterogeneous, with vast differences in the spectrum of clinical ■ Contraindicated in patients with thromboembolism or
symptoms and extent of disease from one woman to another. cardiovascular diseases.

👉 ○ Treatment plan must be individualized


Primary Short term goals
○ Provide pain relief
○ Treat the infertility/ promotion of fertility

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3. GnRH AGONISTS
👉 Medical oophorectomy or induction of pseudomenopause.

📑

○ an effect of chronic use.
Usually NOT given to young, reproductive-age patients;
Dramatic reduction occurs in serum estrone, E2, testosterone, and
androstenedione to levels similar to the hormonal levels in oophorectomized

📑
women.
GnRH is usually secreted in a pulsatile fashion, but this drug involves
giving a large amount of GnRH agonist which provides a continuous

📑 supply for the pituitary gland.


Initially, a state of gonadotropin hypersecretion or “flare effect” occurs.
This is then followed by desensitization of the pituitary gland and
suppression of FSH and LH secretion.
● GnRH agonists have no effect on sex hormone-binding globulin. Thus, the
androgenic side effects from Danazol caused by the increase in free serum
testosterone are not observed.
● Similarly, no significant changes occur in total serum cholesterol, HDL, or LDL
levels during therapeutic periods of as long as 6 months. 👉Figure 15. Medical Management of Endometriosis Summary
● The side effects associated with GnRH agonist therapy are primarily those

📕
associated with estrogen deprivation, similar to menopause.
decrease in bone density associated with 6 months of therapy is

B. SURGICAL
Surgical management is indicated for the following:
📕 completely recovered between 12 and 24 months
The three most common symptoms are:
○ Hot flushes, vaginal dryness (Atrophic Vaginitis), insomnia.


After failure of empiric therapy
Failure, or intolerance of medical management
○ For purposes of diagnosis and immediate treatment
● Examples:
○ For diagnosis and treatment of an adnexal mass
○ Leuprolide acetate: 3.75 mg IM q monthly or a 11.25-mg depot injection
○ Treatment of infertility in some patients.
every q 3 months
● Foundation of treatment for women with moderate or severe endometriosis,
○ Nafarelin acetate nasal spray is given in a dose of one spray (200 mg)
especially those with adhesions and when the disease involves
in one nostril in the morning and one spray (200 mg) in the other nostril
nonreproductive organs.
in the evening up to a maximum of 800 mg daily.
○ Goserelin acetate: 3.6 mg every 28 days SQ.
CONSERVATIVE SURGERY
● Involves the resection or destruction of endometrial implants, lysis of
4. NSAIDS
👉

First intervention for Pain relief and control of bleeding
Rationale: lesions of endometriosis have been found to express high levels of

adhesions, and attempts to restore normal pelvic anatomy.
Preferably done by laparoscopy
○ Gold standard
COX-2. ○ Better than laparotomy because of shorter recovery period; also,

📑

📑
For short-term goal only.
For endometrial implants < 2.5 cm
Give NSAIDs for both primary and secondary dysmenorrhea (to prevent ●

laparotomy causes more post-surgical adhesions than laparoscopy
Both diagnostic and therapeutic
Conservative surgery has as its goal the removal of all macroscopic, visible
prostaglandin formation) areas of endometriosis with the preservation of ovarian function and

📑 AROMATASE INHIBITORS
restoration of normal pelvic anatomy.
5. ● Conservative operations include removal or destruction of implants, removal of
endometriomas, lysis of adhesions, appendectomy, and sometimes presacral
● Recent studies advocate for the use of aromatase inhibitors neurectomy.
● Still experimental treatment ● If the patient has midline pain, such as dysmenorrhea or dyspareunia →
● MOA: Inhibits the conversion of testosterone to estradiol. presacral neurectomy or resection of the uterosacral ligaments may be
● May inhibit growth and relieve pain performed.
● Examples: ● Ablation of the uterosacral nerves when performed via the laparoscope is
○ Anastrozole 1 mg called laser uterosacral nerve ablation (LUNA).
○ Letrozole 2.5 or 5 mg ● Presacral neurectomy relieves only midline pain and does not diminish pain in
other areas of the pelvis..
6. ANDROGEN RECEPTOR AGONISTS (DANAZOL)

👉
● Attenuated androgen (active when given orally) DEFINITIVE SURGERY
Produces a hypoestrogenic and hyperandrogenic effect on steroid-sensitive ● AKA Extirpative Surgery

📕 end organs. ● Involves the removal of both ovaries, the uterus, and all visible ectopic foci of
Prescribed for women with benign cystic mastitis, menorrhagia, and hereditary endometriosis.
angioneurotic edema ○ Analogous to cytoreductive surgery in ovarian carcinoma
● Androgenic and anabolic effects have limited its modern-day use. ● Ovarian cystectomy/ oophorocystectomy: for endometriotic cysts,
● Induces atrophic changes in the endometrium of the uterus and similar Oophorocystectomy is done if there are cysts in the ovary; only the cysts are
changes in endometrial implants. removed, not the entire ovary (so that any remaining ovary can still function)

📕
● It may also modulate immunologic function. ● Total hysterectomy with bilateral salpingo-oophorectomy (THBSO): for
Dose: 400 - 800 mg daily for 6-9 months, but many clinicians reduce the total women not desirous of pregnancy

📑 SPECIAL CONSIDERATIONS
daily dosage of the drug down to 200, and even 100 mg daily because of side

📑
📑
effects.
Usually begun during menses (Day 1 to 5)

C.
In cases of extensive pelvic disease, in vitro fertilization/ embryo transfer
📑 Standard length of treatment: 6-9 months
Side effects of the hormonal changes are encountered by 80% (10-20%

(IVF-ET) is a necessary approach.
When pelvic pain is not a significant issue, the removal of endometriomas is of
📑
discontinue Danazol):

📑 Deepening of voice that did not resolve after discontinuation


Mild elevation in serum liver enzyme levels ●
no benefit and may be harmful in that it may compromise ovarian reserve
Some studies suggest improved fertility outcomes with prolonged GnRH
agonist use when administered prior to assisted reproductive treatment.
● Stage I/II endometriosis
○ Excision or ablation of endometriosis has been shown to increase live
birth and ongoing pregnancy rates and is therefore recommended when
visible lesions are present
● Stage III/IV endometriosis
○ Surgical treatment has also been suggested to increase pregnancy rates
● Endometriomas
○ Conservative management has potential risks such as infection of the
endometriomas, interfering with response to infertility treatments and
oocyte retrieval, risks of complications in pregnancy, and malignancy
○ Endometriomas may also decrease ovarian reserve
○ Excision of endometriomas has been shown to increase clinical
pregnancy rates.
○ In patients failing to conceive spontaneously after the initial surgery,

📑 assisted reproductive therapy is recommended


If all visible normal ovarian tissue is replaced by endometriomas
(typically endometriomas around 4 cm or greater), do SURGICAL

📑 EXCISION
Surgery for endometriomas does not improve IVF rates, therefore
surgery should only be selected for individual basis

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📑 HOW SOON
PREGNANT?
AFTER SURGERY WILL YOU ADVISE THE PATIENT TO GET 👉 Dyspareunia
○ Reflux of menstrual blood to dependent portion
● First menstruation after surgery ■ Dependent portion is usually in the uterosacral portion or
● Advise the patient to conceive within the 12 months after the operation: best cul-de-sac.
period - Endometrial implants cause scarring and fibrosis making the
○ You do not need to wait for it to heal! Sex na agad pag kaya! uterus immovable.
● Give fertility agents to hasten ovulation during this time - Pain is felt when there is pressure or contact on the implants
● A patient may still get pregnant even though she has an active endometrioma located at the uterosacral portion.
in an ovary, because some follicles may remain active
📑
○ Onset (at which point during the sexual activity does the pain manifest?)
Is the pain during or after sexual activity?
D. 📑TREATMENT OF SPECIAL POPULATIONS ○ Site of Dyspareunia:
■ Deep dyspareunia: If you elicit location as deep or pelvic
● Infertility dyspareunia, think of organic condition like endometriosis or PID
○ Surgery (laparoscopy, laparotomy) and artificial reproductive technology - May be caused by processes or structures (nodularities)
(ART) affecting the cul-de-sac
● Endometrioma ■ Introital dyspareunia (just outside) or insertional (during the
○ Medical therapy does not resolve endometriomas beginning), it might indicate vulvitis, there is inflammation in the
■ Mainly given to address the pain of dysmenorrhea in pelvic introitus or maybe because of dryness in postmenopausal woman
endometriosis - Vaginismus
○ Symptomatic or expanding endometriomas (≥8cm) are removed - Vaginal atrophy
(oophorocystectomy) ○ Severity of the pain?
○ To protect ovarian reserve, asymptomatic and small (<5 cm) ○ Does it happen all the time or intermittent?

👉
endometriomas can be left in place (observe for the meantime) ○ Does it happen in particular sexual position?
● Deep infiltrating endometriosis Infertility
○ Technically impossible to excise ○ Difficulty in getting pregnant in the past 9 years.
○ Medical therapy with hormonal suppression for women with bothersome ■ Are they using any family planning?
urinary or bowel symptoms (1st line) ○ Are they trying to get pregnant?
○ Surgery if with ureteral bowel obstruction or those whose symptoms do ■ Best time to get pregnant: below 35 years old
not improve with medical management. ■ Good eggs are until 37 1⁄2 years old
● Lesions of nonreproductive organs ○ Is she previously diagnosed with anovulatory cycles?
○ Continuous OCP ○ Does she undergo any infertility workups?
○ Ovarian suppression with GnRH agonists – highly effective at ■ Hysterosalpingography
suppressing ovarian hormone production and inhibiting the growth of ■ Ultrasound
endometrial tissue; not advised in young patients ■ Family History of Infertility

IX. CASE Symptomatology is not always associated with the degree of disease. The patient may
45-year-old G0P0 consulted for dysmenorrhea of one-year duration. LMP: 1 week ago. have severe disease, but she may have very mild symptoms. The patient may have very
Regular menses but noted to be heavier than usual with blood clots on the first 3 days. minimal disease, but she may be complaining of severe symptoms.
Married at age 35 with one sexual partner. PPE: BP – 120/80 PR- 84/min RR- 18/min BMI Dra Santiago Case Discussion, 2023.
– 24; slightly pale conjunctiva; Breasts: unremarkable; Abdomen: flabby, soft, non-tender
with no masses palpated; Speculum: cervix- pink, smooth; IE: cervix- firm, long and B. OTHER IMPORTANT INFORMATION IN THE PHYSICAL EXAM
closed; uterus- symmetrically enlarged to 2 months size, retroverted and fixed; adnexa-
bilateral doughy, fixed adnexal masses around 4x5 cm each, with tender nodularities INSPECTION/SPECULUM
noted in the cul-de-sac. ● Check the areas of the cervix and upper vagina.
○ Bluish hemorrhagic looking masses – highly suspicious for
endometriosis.
A. OTHER IMPORTANT INFORMATION IN THE HISTORY ● For multigravida: Check for the episiotomy
● Family history/Genetic Predisposition of endometriosis ○ Masses or bluish hemorrhagic.
○ No known exact genetic predisposition for endometriosis. ○ Tenderness during menstruation.
● History of autoimmune disorders ○ Increases in size.
● Any medications taken to relieve the pain
● Previous infection to rule out PID INTERNAL EXAMINATION
● Bowel and urinary symptoms: for possible bladder and/or rectal involvement. ● Cervix – tender nodulation at the uterosacral ligaments.
○ Difficulty defecating ○ If due to infection: not tender.
○ Presence of dysuria and hematuria ● Fixed or immobile retroverted uterus secondary to adhesions and fibrosis at
● Presence of dyschezia or painful defecation especially during menstruation the lower part.
○ Rule in deep infiltrating endometriosis. ○ Immovable due to endometriosis around the uterosacral ligaments.
● Sexual History ● Enlargement of the uterus.
○ Number of partners (either by wife or husband) ○ Adenomyosis may also cause enlargement of the uterus.
■ Risk for STD ■ “Pelvic endometriosis interna”
○ History of IUD use ■ Endometrial glands and stroma are displaced into myometrium.
○ Use of OCPs ■ There will be inflammatory reactions on the muscles on the
● History of Surgery myometrium since displaced endometrial glands and stroma are
○ May contribute to infertility and dysmenorrhea foreign.
○ Episiotomy and CS, however it is not applicable to the patient since she ■ There will also be hyperplasia and hypertrophy.
is nulligravid. ■ Inflammation + hypertrophy + hyperplasia → enlargement and
■ Aside from the pelvis, endometrial implant may be located at the tenderness of uterus.
other parts of the body. ■ Patient exhibits dysmenorrhea and heavy menstrual bleeding.
○ Uterine surgery like myomectomy – risk of direct implantation - Heavy menstrual bleeding because of an enlarged uterus.
○ Surgeries on cervical area (cone biopsies, cautery, cryosurgeries) that - Enlarged uterus = greater surface area.
may cause cervical stenosis and hematometra ● Ovaries
■ Trauma → healing and fibrosis → stenotic canal. ○ Check for: Adnexal, Ovarian cyst
○ Adhesions (E.g. Appendectomy) ■ (+) Adnexal mass → advanced endometriosis
○ Iatrogenic Theory ○ Most common site of pelvic endometriosis: Peritoneum and Ovaries.
● Vascular/Lymphatic Spread ■ Menstrual Reflux: Opening at the end of fallopian tubes → Spillage
○ Epistaxis during menstruation of endometrial glands and stroma → Attach on the ovaries and

📑
○ Hemoptysis during menstruation peritoneum (uterosacral ligaments).
Shortness of breath, Chest pain
C. WORKING DIAGNOSIS

👉
ASK THE TRIAD OF SYMPTOMS OF ENDOMETRIOSIS
Dysmenorrhea
○ Complete menstrual history
SALIENT FEATURES:
● Nulligravid
■ MIDAS: menarche and Symptoms. ● Secondary and Progressive Dysmenorrhea
■ Onset ● Advanced age
■ Severity ● Heavy menstrual bleeding
■ Relieving and Precipitating Factors ● Symmetrically enlarged uterus with fixation
■ Duration – does it happen on the start or end of menses. ● Adnexal mass
■ Is it progressive?
- Progressive Dysmenorrhea: One of the characteristics of WORKING DIAGNOSIS
endometriosis ● PRIMARY WORKING DIAGNOSIS: Secondary Dysmenorrhea due to
- Worsening or buildup of tissues inside the endometrium after Adenomyosis
every episode of dysmenorrhea ○ Adenomyosis is prioritized since patient complained of heavy menstrual
bleeding.

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● SECONDARY WORKING DIAGNOSIS: Pelvic Endometriosis with ● NSAIDS
Endometrial Cyst ○ If mild or early stage of pelvic endometriosis, this may be helpful.

📑 ○


Tender nodulation at the uterosacral + involvement of ovaries.
Secondary Dysmenorrhea
Common in older age group

○ Extensive involvement may not respond to NSAIDS.
Amenorrhea
○ The culprit is estrogen.
○ Dysmenorrhea occurred several years after the menarche ■ If there is estrogen and progesterone, the patient will menstruate/
○ Duration of the dysmenorrhea (one year) or chronology of the symptoms ○ To relieve pain, make the patient amenorrheic.
in relation to her age ■ No menstruation = no endometriosis.
○ There is organic pathology which rules out primary dysmenorrhea ■ Most common theory: Reflux menstruation
○ Make patient pseudopregnant by giving:
DIFFERENTIAL DIAGNOSES FOR SECONDARY DYSMENORRHEA: ■ Continuous oral contraceptive pills.
● Myoma ■ Or give progestins.
● Pelvic Infection ○ Make the patient pseudomenopause by giving:
● Pelvic congestion syndrome (ruled out since it will not present with uterus ■ GnRH agonist
enlargement or tender nodularities - Suppress the HPO Axis – no FSH and LH.
● Adenomyosis - Give for 6 months only.
● Congenital Anomaly: Cervical Stenosis → Beyond 6 months → osteoporosis.
○ Especially if the patient complained of dysmenorrhea 6 months after - Decrease the size of ovarian cyst.
menarche. - If patient experience the menopausal signs, little dose (0.3 or
● Intrauterine Devices 0.625) of estrogen may be given.
→ Known as advac treatment
D. DIAGNOSTIC WORK-UP ■ Or give Danazol
■ Levonorgestrel
● Ultrasound - More expensive iodine
○ Ovaries - Very good for adenomyosis because it can cause shrinkage.
■ Ovarian masses can be associated with endometrial cysts.

📑
■ For younger patients (45 y/o included), look for normal looking SURGICAL OPTION FOR PAIN RELIEF
ovarian tissue. Prior surgery, check Hgb levels because the patient presented with slightly
- To consider conservative treatment. pale conjunctiva.
○ Uterus ● Consevative Surgery: Leave the ovaries.
■ Visualize the retroverted uterus in relation with the bladder ● Radical Surgery
■ Adenomyosis ○ Remove the ovaries.
- Posterior myometrium is thicker than anterior myometrium. ○ For our patient: TAH BSO – remove everything.
- Overall, myometrium is thicker than normal. ■ Chance of being pregnant at 45 is very small.

📑 ○ Endometrial cyst: Ground-glass appearance.


Hysterosalpingography
○ Fallopian tubes are not patent, indicative of fallopian tube obstruction


Patient has no uterus → no menstruation → no reflux.
Patient should be advised there she will have surgical menopause.
■ To relief symptoms of menopause:
secondary to endometriosis. - Give the combination drug first
● Laparoscopy – Gold standard. - At first, do not give estrogen alone because microimplants

📑
○ Diagnostic and therapeutic. may flare-up.
○ Probably not appropriate for our patient. If the patient is not amenable for the surgery, a non-pharmacologic treatment.
○ Endometrial Implants/Pelvic Endometriosis ○ TENS (Transcutaneous Electrical Nerve Stimulation) may be given.
■ Blebs/burns ■ Will only relieve the patient of the pain but will not treat the cause

📑YOUNGER
■ Can be yellow, white, red, brownish or bluish-black lesions.
– Yellow, white, red – active lesions PATIENT
– Brownish or bluish-black lesions – older lesions; less painful. ● Be more conservative and give GNRH agonists first.
✓NOTE: According to Dra. Trinidad’s SGD, white lesions are ● OCPs may be given for a while to decrease the stimulation of the
active lesions. However, according to the Book and Dra. Castro’s endometriosis that are present already
lecture, white lesions are older lesions. ● Then do laparoscopy later on to remove the endometriotic parts only
● Husband – sperm analysis ○ Give ovulants afterwards if pregnancy is desired.
● Tumor Marker (eg: CA-125)
○ May be elevated but not useful since it is not highly specific to pelvic
X. REFERENCES
endometriosis.
○ Other diseases may elevate this tumor marker such as: ● Lobo, R. A., Gershenshon, D. M., Lentz, G. M., & Valea, F. A. (2017). Comprehensive
Gynecology. Philadelphia: Elsevier.
■ Myoma, Liver disease, Colon Cancer, Ovarian Cancer, etc. ● Batch 2024 - D3 Dr. Anne Catherine Castro Endometriosis. [Case Discussion]. Manila,
● History taking, Physical Exam, Imaging studies are enough. Philippines: Faculty of Medicine and Surgery, University of Santo Tomas,
E. TREATMENT OPTIONS ● Batch 2024 - D1 Dr. Anne Marie Trinidad Endometriosis. [Case Discussion]. Manila,
Philippines: Faculty of Medicine and Surgery, University of Santo Tomas,
GOALS OF TREATMENT ● Batch 2023 - GYN.1.10.ENDOMETRIOSIS Trans
● Pain Relief
● Prevent Progression: Prevent infertility, chronic pelvic pain, and complications.

PAIN RELIEF

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XI. APPENDIX

Figure 17. American Society for Reproductive Medicine revised Classification of


Endometriosis

Figure 16. Recommended dosage for different NSAIDs in the treatment of


dysmenorrhea

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