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Endometriosis

&
Adenomyosis
Najwa Nazri
Ahmad Syahid
Selina Mudzir
Endometriosis
Ectopic endometrial tissue

Presence of normal endometrial mucosa (glands and stroma)

Implanted in abnormal locations (other than the uterine cavity)

Capable of responding to the normal cyclic hormonal fluctuations


(proliferation, secretory activity, and cyclic sloughing of menstrual material)
Table of contents
01 02 03
Incidence and etiology Clinical features Physical examination

04 05 06
Investigation Endometriosis and Management
infertility
01
Incidence
5 to 10% of women of
reproductive age
Found in at least 1/3 of women undergoing diagnostic laparoscopy for
pelvic pain or infertility
Estrogen dependent
02
Etiology
Sampson’s implantation theory

Retrograde menstruation
transports viable endometrial
gland and tissue within the
menstrual fluid

Subsequent implantation on the


fallopian tube, ovary, peritoneal
surface etc

Women with congenital outflow


tract obstruction increase the
risk
Meyer’s coelomic metaplasia

Metaplasia (transformation of one normal type of tissue to another normal type


of tissue)

The endometrium and the peritoneum are derivatives of the same coelomic wall
epithelium

Peritoneal mesothelial totipotent cells has been postulated to retain its


embryologic ability to transform into reproductive tissue (endometrial)

Transformation of coelomic epithelium into endometrial-type glands in


response to as yet unknown stimuli (due to hormonal stimuli, chronic irritation
by retrograde menstrual fluid and inflammatory irritation)
Etiology
Genetic factors Vascular and lymphatic spread

May alter susceptibility of a


Embolization to distant sites has
woman and allow her to develop
been demonstrated and explains
endometriosis
the findings of endometriosis
outside the peritoneal cavity,
Increased incidence in first-
such as lung
degree relatives
Immunological factors

An altered immune response to the displaced endometrial tissue


has been shown to play an important role

Women with this disorder appear to exhibit increased humoral


immune responsiveness and macrophage activation while
showing diminished cell-mediated immunity with decreased T-
cell and natural killer cell responsiveness
03
Clinical features
Clinical features
Infertility

Cyclical intestinal complaint Dysmenorrhea

Deep dyspareunia Chronic pelvic pain


1. Ovary
2. Pouch of Douglas (cul-de-sac)
3. Ligaments of the uterus
4. Fallopian tube
5. Rectovaginal septum
Dysmenorrhea
Lower abdominal and pelvic pain
Dyspareunia
Female reproductive tract
Rupture/torsion endometriosis
Low back pain
Infertility

Cyclical Hematuria/dysuria
Urinary tract
Ureteric obstruction

Dyschezia (pain on defecation)


Gastrointestinal tract Cyclical rectal bleeding
Obstruction

Surgical scars/umbilicus Cyclical pain and bleeding

Cyclical hemoptysis
Lung
Haemopneumothorax
04
Physical
examination
Vaginal examination

Fixed retroverted
Thickening or nodularity uterus
of uterosacral ligament

Adnexal mass Tenderness in the


pouch of Douglas
5.
Endometriosis
Investigation
Investigations

Blood: CA-125 • CA-125 are markedly elevated in cystic ovarian


endometriosis or deeply infiltrating endometriosis
• Slight increase or none, in the luteal phase of
women with minimal or mild endometriosis
Imaging: • Detect gross endometriosis or cyst associated with
• Pelvic ultrasound endometriosis (endometrioma, chocolate cyst)
• Limited value in smaller lesion
• Detect deep infiltrating endometriosis
• MRI • Help in surgical planning
• Assess response to medical therapy
Laparoscopy • Lesions varies, can be red, puckered, black
matchstick or white fibrous lesions.

• Advantage: concurrent surgical diathermy and/or


excision of the endometriotic lesion and staging of
the disease.
Endometriosis on Transvaginal Ultrasound

Findings include:
• Cystic lesion with ground glass
appearance
• May be single or multiple
• Little or no blood flow on color
Doppler
• ‘kissing’ ovaries sign:
Ovaries that are adherent to one
another posterior to the uterus & is
seen in bilateral endometriomas.
Laparoscopic findings

Red lesion on peritoneum White fibrous lesion Black ‘matchstick lesion’

• Preferred method for diagnosis is surgical visual inspection of


pelvic organs with histologic confirmation.
• Varied appearance allows less-obvious lesions to be overlooked
Diagnosis & assessment

• Consider referral for an ultrasound or gynecology


opinion if:
‒ They have severe, persistent/recurrent
symptoms of endometriosis
‒ They have pelvic signs of endometriosis
‒ Initial management is not effective

NICE UK, endometriosis pathway


6.
Endometriosis
& Infertility
Structure Possible mechanisms
Ovarian function • Luteolysis caused by prostaglandin F2
• Oocyte maturation defects
• Endocrinopathies
• Luteinized unruptured follicle syndrome
• Altered prolactin release
• Anovulation
Tubal function • Impaired fimbrial oocyte pick-up
• Altered tubal mobility
Coital function • Dyspareunia & coital dysfunction – reduced frequency
Sperm function • Antibodies causing inactivation
• Macrophage phagocytosis of spermatozoa
Early pregnancy failure • Prostaglandin induced
• Immune reaction
• Luteal phase deficiency
7.
Endometriosis
management
Management
• Coexisting additional disease like irritable bowel
disease/constipation should also be treated to
improve overall success rate
• Endometriosis is known to be a recurrent
disorder throughout the whole reproductive life
& is impossible to guarantee complete cure
• Treatment should be tailored according to the
patient age, symptoms, extent of disease & her
desire for future childbearing
• In most patient, disease has little proggresion
Medical Therapy

Analgesics Only work as symptomatic ↓ severity of dysmenorrhea & pelvic pain


(NSAID) treatment

Avoid additional usage of Worsened coexisting irritable bowel


opiates/codeine symptoms → exacerbate pelvic pain

Combined Used as diagnostic & therapeutic Taken continuously for 6 month →


oral purposes amenorrhoeic
contraceptive
agents Outcome Cyclical pelvic pain Diagnosed as mild Continue therapy
(COC agents) disappear & no gross /moderate until pregnancy is
endometriosis on USG endometriosis intended
Symptoms persist Likely to be coexisting Treat coexisting
irritable bowel disease condition
/constipation
Progestogens Used for patient with Induce amenorrhea
contraindication to COC agents

• Medroxyprogesterone Effective in long-term therapy effect, particularly


acetate (MPA) after surgical treatment
• Levonorgestrel intrauterine
systems (LNG-IUS)

Gonadotrophin Induce hypogonadotrophic Taken continuously for 6 month to induce


-releasing hypogonadism amenorrhea, side effect include post-
hormone (pseudo menopause) menopausal symptoms
agonist
Forms available: Long-term use (>6 month)
(GnRH-a)
• Multiple, daily administered →drug induced osteoporosis
intranasal spray
• Slow-release formulation
(last ≥ 6)
Administer hormone Recurrence upon
replacement therapy to therapy cessation is
prevent effect of rapid
estrogen deficiency
Other agent Ovarian suppressive agents: • Not commonly used now although effective
• Danazol due to side effects such as androgen effects
• Gestrinone • GnRH-a is as effective as danazol in
relieving symptoms, differ only in side effect
Side effects: • Weight gain
• Greasy skin
• Acne
• Alteration in lipid profile or liver function
Surgical Therapy

1. Conservative surgery / fertility-sparing surgery

• Laparoscopic surgery + techniques such as diathermy, laser vaporization or


excision
• Example: Laparoscopic ovarian cystectomy for endometriomas
• Recurrent risk : 30%
• Concurrent long-term medical therapy is usually useful
2. Definitive surgery (Hysterectomy & bilateral salpingo-oophorectomy)

• Indication:
‒ Severe symptoms
‒ Progressive disease
‒ In women who have completed family

• Initiating combined hormone replacement therapy (HRT) may be postponed


for up to 6 month following surgery, especially when active disease was found
during surgery, to prevent activation of any residual disease
Adenomyosis

Presence of ectopic nests of endometrial glands and stroma within the


myometrium, surrounded by reactive smooth muscle hyperplasia
Pathophysiology
• Absence of any discrete transitional layer
• Mechanical disruption – multiparity, history of uterine trauma (uterine curettage
or caesarean section), hyperperistalsis of uterus
• Elevated levels of oestrogen, oestradiol, aromatase enzymes
• May be indistinguishable from a leiomyoma and both may coexist but as it
growth takes time, it tends to occur later in reproductive years

mechanically disrupt the myometrial junctional zone by the action of the trophoblast on the
myometrium, favoring infiltration of endometrial cells into the myometrium. As pregnancy
progresses, mechanical weakening of the myometrium may occur as the uterus becomes
distended, with further resultant infiltration of the endometria basalis. Finally, the tremendous
hormonal fluctuations which occur throughout pregnancy may facilitate development of
adenomyotic foci
Aetiology
• Strongly associated with
• middle age (40-50) - increased prevalence of risk factors by that age range
and the duration of adenomyotic development. Nowadays, 20s to 30s.
• multiparous status - mechanically disrupt the myometrial junctional zone by
the action of the trophoblast on the myometrium, favoring infiltration of
endometrial cells into the myometrium.
• history of gynaecologic surgery – due to trauma to the uterus which may
cause weaknesses within myometrium, allowing invasion of the adjacent
endometrium
Clinical features
• Most patients with adenomyosis are asymptomatic
• Dysmenorrhea - Progressively increasing pain associated with menstruation.
Pain increases throughout menstruation, reaching its peaks towards the latter
stage.
• Metrorrhagia - Menstrual irregularities, such as premenstrual staining and
spotting
• Menorrhagia - increased flow, or more frequent periods.
• May also complain of chronic pelvic pain and dyspareunia.
Physical examination
• Diffusely enlarged, tender, “boggy” uterus is suggestive of adenomyosis.
• Asymmetrical like fibroid uterus but softer than a fibroid.

A full physical exam should be performed. This should include inspection of the perineum, vagina, cervix, and
bimanual exam of the uterus and adnexa. The uterine size, shape, mobility and tenderness should be
evaluated. A diffusely enlarged, tender, “boggy” uterus is suggestive of adenomyosis. Alternatively, severe
endometriosis often presents as a fixed, tender uterus, with palpable nodules within the posterior cul-de-sac
and/or lining the uterosacral ligaments and rectovaginal septum
Investigation
• Ultrasound
• haemorrhage-filled, distended endometrial glands
• Sometimes this may give an irregular nodular development within the
uterus, very similar to that of uterine fibroids.

Uterine enlargement
– Globular enlargement Uterine wall
(up to 12 cm) and no thickening –
explained by any especially if the
presence of adenomyosis is focal,
leiomyomata with there would be
obscure asymmetry between
endometrial/myometrial anterior and posterior
border
Increased vascularity – might
Venetian blind– or “rain
also involved increased number
shower” appearance linear
or tortuous vessels penetrating
striations, parallel shadowing)
myometrium
Adenomyosis vs Fibroids

Capsulated
No increased in vascularity
No distinct capsule
Adenomyosis vs Fibroids

No increased in vascularity
Increased in vascularity
• MRI
• More definitive investigation of choice
• Provides excellent images of myometrium,
endometrium and areas of adenomyosis

Note the bright reflections of the central


endometrium and flecks of ectopic endometrium in
the underlying myometrium.t
Management
• If the woman has no symptoms and the adenomyoma is not large, no treatment
is needed and most important factors in deciding management is the patient’s
desire for future fertility
• Any treatment that induces amenorrhea will relieve the pain and excessive
bleeding
• On ceasing the medical treatment, symptoms will rapidly return in most of
patients
• Hysterectomy is the only definitive treatment
• Uterine artery embolization is being used increasingly as an alternative or
women wishing to preserve their ertility

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