Endometriosis /Adenomyosis

Definition
Prevalence
Sites
Mechanism of origin of endometriosis
Clinical features
Investigations
Treatment
Definition
Define as presence of functioning endometrium
( glands and stroma) in sites other than uterine
mucosa

1st describe by von Rokitansky (1860)

Prevalence
Ranges 3-10%
Occur in 7% of reproductive age group in US
10-25%of female undergoing
laparatomy by gynae
40-60% seen in dysmenorrhoea
20-40% of infertile women
Contd…
Infertile women are 7-10 times more likely to have
endometriosis than fertile
6.9% occurrence rate in 1st degree relatives
Sites
Abdominal
 Ovary
 Pelvic peritoneum including uterovesical pouch and pouch of

Douglas
 Outer coat of uterus

 Round ligament , uterosacral ligament recto vagina septum

 Fallopian tubes

 Intestine

 Bladder and ureter

Contd…
Extra abdominal
Vagina
and vulva
Abdominal wall

Remote
Lung and pleura
Deep tissue of arms and thigh
Mechanism for origin
of endometriosis
Reflux and direct implantation theory
Coelomic metaplasia theory
Induction theory
Vascular dissemination theory
Autoimmune disease
Genetic factor
Promotional factor
Clinical features
Patient profile
Age-30-35yrs( can occur in any time)
Parity- Nulliparous
primary and secondary infertility
voluntary postponement of
conception
until late age
Socioeconomic factor
Family history
Outflow obstruction
Symptoms
25% of patient have no symptoms accidentally
diagnosed during laparoscopy
Symptom not related to extent of lesion
Symptoms related to site of lesion and its ability to
respond to hormones
Signs
Clinical triad
Subfertility(20-40%)
Possible mechanism
-mechanical interference
-alteration in peritoneal fluid
-abnormal systemic immune
system response
-ovulatory dysfunction
-implantation failure
-early spontaneous abortion
Contd..
Dysmenorrhoea (25-67%)
Dyspareunia / chronic pelvic pain (29%)
Beside these,
Abnormal menstruation
Tumor formation
Extra pelvic symptoms
GIT
Urinary
Pulmonary
Intermittent Pyrexia
Clinical examination
Abdominal examination
Per speculum examination
Pelvic examination
Rectal examination
 American fertility society scoring system of
endometriosis
Endometriosis <1cm 1- >3cm
---------------------- -------- 3cm--- -------
1 ------- 4
Superficial
Peritoneum 2
Deep 2 6
4
Rt superficial 1 2 4
Rt deep 4 16 20
ovary
Lt superficial 1 2 4
Lt deep 4 16 20
 Contd..
Partial Complete

Posterior cul de 4 40
sac obliteration
Contd
Adhesion <1/3enclose 1/3-1/2 >2/3enclose
------------ -------------------- ----------- --------------------
Rt filmy - - ----
Ovary Rt dense 1 2 4
4 8 16
Lt filmy
Lt dense 1 2 4
4 8 16
Rt filmy 1 1 4
Rt dense 4* 8* 16
Tube
Lt filmy 1 2 4
Lt dense 4* 8* 16
Contd

* if fimbriated end of fallopian tube is completely

enclosed change point to 16
Stage 11-5 (minimal)
Stage 26-15(mild)
Stage 316-40(moderate)
Stage 440( severe)
Investigations

Imaging
 USG(TVS /TRS)
 HSG

 CT SCAN

 MRI

Confirmatory
 LAPRATOMY / LAPROSCOPY
CA125
Treatment
Medical treatment
Surgical treatment
Combined
Contd..

Therapy initiated for

 Correction of pain
 Improve the fertility
 For persistence pelvic mass
 To prevent recurrence

Treatment depend on
 Age
 Clinical history and finding
 extend if lesion Desire of fertility
 Result of previous therapy
Medical treatment

NSAIDS or Prostaglandin inhibiting drug

OCP
Progestogens
Anti gonadotropin
Gonadotropin releasing hormone agonist
Progesterone antagonist
Aromatase inhibitors
Selective estrogen receptor modulators
Contd..
OCP
Used in mild case
Those who do not want to get pregnant

Mechanism of action (pseudo pregnant state)

Absence of follicular activity and ovulation
Suppress the menstruation
Conversion of ectopic endometrium in decidua
which undergoes necrosis and involution
Dose
Low dose 30-35mg of ethinyl estradiol
Continuously for 6-12 month

Start 2tab daily and dose increase 1-2 tab

till amenorrhea
High dose OCP

not used now

Contd
Dose
Low dose 30-35mg of ethinyl estradiol
Continuously for 6-12 month

Start 2tab daily and dose increase 1-2 tab

till amenorrhea
High dose OCP

not used now

Contd..
Progestogens (pseudo pregnant state)
Suppress ovarian steroid genesis and promote
secretary changes in endometrium ->
decidualisation -> atrophy
the growth promoting effect of estrogen

(nuclear estrogen receptor)-> increase17B

hydroxysteroid dehydrogenase which
convert estradiol into estrone
Prevent reflux menstruation
Contd..

Different regime
 Medroxy progesterone 150mg I M every 3mth
 Medroxy progesterone acetate(30-35 mg x 4-6mth)
 Megestrol acetate40mg /day
 Dydrogesterone 20-30mg /day
 Lynogesternol 10mg /day


Levonergerol releasing IUD for 12 month
Rate of recurrence
 After 11 month 18%
 After 2yr 42%
Contd..
Anti gonadotropin
 Danazol
 Gestrinone

Danazol
 High androgenic and low estrogenic
 Derived from 17alpha ethinyl testosterone
Contd…

Dose
 400mg daily and increased dose if necessary to achieve
amenorrhea
Recurrence of symptoms
 50% In 4-12 month at discontinuation
Side effect
 Hypo estrogenic
 Androgenic
 Metabolic
Contd..
Gestrinone
 19 testosterone derivatives
Mechanism of action
 Androgenic effect: increase testosterone and decrease SHBG
 Anti estrogenic effect :reduce serum estradiol
 Anti gonadotropin: decrease LH and FSH

Doses
 2.5 mg twice a week
Contd…
Gonadotropin releasing hormone agonist
Mechanism of action (Pseudo menopause)
 Bind with pituitary GnRH receptor release LH and FSH
(longer T1/2 than endogenous )continuous exposure of
GnRH receptor irreversible down regulation  decrease
FSH and LH decrease ovarian steroid genesis
Contd.
Doses
 Regulated according to estradiol level( need 30-40pg/ml)
Different preparation
 Leuprolide 500mg/day , 3.75mg monthly sc /im
 Goserelin 3.6mg monthly sc

 Buserelin 300mcgm daily intrasnasal

 Triptorelin 3.75mg monthly

 Naferelin
Contd
Recurrence rate
 57% after discontinuation
Add back therapy
To prevent vasomotor symptoms and hypo estrogenic

state by GnRH agonist

Progestogens only (norethisterone 1.2mg , nor
ethindione acetate 5mg )
Tibolone 2.5mg /day

Estrogen and Progestogens ( conjugated estrogen

0.625mg and Medroxy progesterone acetate5mg)

Estradiol2mg + nor ethisterone acetate 1mg)
Contd..
Progesterone antagonist
Antiproliferative effect on endometrium
without risk of hypoestrogenism
Drugs

Mifepristone

Onapristone

Doses

25-100mg /day
Contd..
Aromatase inhibitors

Fadrozole
hydrochloride
Anastrazole

Selective estrogen receptor modulators

Raloxifen
 Surgical treatment
Conservative treatment
Radical treatment
Contd..
Indication
 Correction of pain
 Correction of infertility

 Other symptom of patient with extensive pelvic

endometriosis
 When hormonal manipulation failed
Contd..
Therapeutic planning depend on
 Age
 Desire for fertility

 Desire for pain relief

 Duration and intensity of symptoms

 Extent of disease

 Previous treatment undertaken

Contd..
Goal of surgery
Excise or coagulate all visible endometriotic lesion and
associate adhension
Procedure
 Laparoscopy
 Laparatomy
Contd..
Laproscopy

Considered in all cases
unless there is difficulty in establishing

the appropriate tissue plane

Access necessary for atraumatic

manipulation of involved organ

Contd..
Laparatomy
Extensive dense pelvic adhesion
Endometrioses >5 cm in diameter

Deep involvement of rectovaginal septum

with fibrotic extension into the perirectal

fossa
Invasion in bowel moscularis

Endometriotic infiltration in uterine vessel

and ureter
Contd..
Ovarian endometriosis
Superficial
 Vaporized

Small lesion <3cm

 Aspirated, irrigated and inspected for ovarian
cystoscopy for intracystic lesion and interior wall
vaporized
Large lesion >3cm
 Aspiratedfollowed by incision
 Cystectomy
Contd..
Incision scar
 Excision and repair
Thorax
 Pleural ablasion
Contd
Radical surgery
 Oophorectomy
 Total hysterectomy
Contd..
Indication
 Advanced stage disease
 >40yrs

 Fertility not required

 ADENOMYOSIS
Condition where islands of endometrium found in
wall of uterus
Myometrial lesion has general characterstics of
endometriosis
C/S: striated ,whorled appearance but no capsule
Produces diffuse enlargement of uterus
Mechanism of origin: downward growth of basal layer
of endometrium
Parous women around 40 yrs of age
Clinical features
Menorrhagia : 75%
-enlargement of uterine cavity
-increased blood supply
-impaired contractility
Dysmenorrhoea -30%
Icreased frequency of micturition
Pelvic discomfort
Uterus- 12-14 wks
Clinical
Symmetric examination
enlargement
Firm-more than fibroid
Tender to touch
mobile
Diagnosis :
 Incidental finding
 15% diagnosed preoperatively
 Investigations :
1. Transvaginal USG:
-ill defined hypoechoic area
-heterogenous myometrial echotexture
-small anechoic lakes
-indistinct endometrial –myometrial junction
-subendometrial halo thickening
2. Myometrial biopsy:
-TVS under USG guidance
-transabdominal during laparotomy
3. Hysterography :
ill defined area of contrast intravasation extending
perpendicular from uterine cavity into myometrium
4. Hysteroscopy: myometrial distortion
5. CA125 –raised
6. MRI eith gadolinium contrast-sensitivity of 90%
management
 Medical – ( little role)
progesterone / GnRH agonist

 Surgical: mainstay of t/t

1. Hysterectomy ( in parous and aged women)
2. Localised adenomyosis: Adenomyomectomy
resection particularly in younger women