 Permanent cessation of menstruation resulting

from loss of ovarian follicular activity.

 It can only be determined after 12 months'
spontaneous amenorrhoea.
 Permanent cessation of menstruation resulting
from loss of ovarian follicular activity.
 It can only be determined after 12 months'
spontaneous amenorrhoea.
occurs after bilateral oophorectomy with or
without hysterectomy.
Premature menopause may also be radiation-
or chemotherapy-induced, or occur after
hysterectomy with ovarian conservation.
 A premature menopause is one that occurs
before the age of 40 years.
 Primary premature menopause may occur at
any age and present as amenorrhoea. Not all
women have acute symptoms. FSH levels are
elevated. Spontaneous fertility may recur.
 INCIDENCE — Vaginal bleeding occurs in
approximately 4 to 11 percent of
postmenopausal women .
 The incidence of bleeding appears to correlate
with time since menopause, with the likelihood
of bleeding decreasing over time.
 Atrophic – vaginitis,cervicitis,endometritis
 Traumatic – Pessary
 Exogenous hormonal therapy
 Benign – Cervical Polyp, Endometrial Polyp
 Malignant –
Vaginal,Cervical,Endometrial(Endometrial
Hyperplasia),Ovarian(Hormone Secreting
tumours)
 Post irradiation
 Consider bleeding from adjacent organs
 Once menopause occurs, estrogen and progesterone
are no longer produced by the ovaries; nor are they
produced in any appreciable amounts by the liver
and fat.
 The endometrium regresses to some degree, and no
further bleeding should occur. When bleeding does
resume, it must be investigated.
Evaluation is called for when :
1. Any menopausal woman not taking HRT
develops uterine bleeding after more than 1 year
of amenorrhea.
2. Any postmenopausal woman on HRT for 6
months or more with persistent uterine bleeding.
3. Any previously amenorrhoeic woman on HRT
who begins bleeding without apparent cause.
 History

 Examination

 Investigations
 Information that is important in the history includes
the following:
 ●When did the bleeding start?
 ●Were there precipitating factors, such as trauma?
 Associated vaginal discharge?
 ●What is the nature of the bleeding (temporal
pattern, duration, postcoital, quantity)?
 ●Are there any associated symptoms such as
pain, fever, or changes in bladder or bowel
function?
 ●What is the medical history and are any
medications being taken (eg, hormones,
anticoagulants)?
 ●Are any soy-containing herbal or dietary
supplements being taken?
 ●Is there a family history of breast, colon, and
endometrial cancer?
 Assess risk factors for endometrial carcinoma

(Nulliparity,Diabetes,Hypertension,Obesity etc.
 General – Pallor, Loss of
weight(BMI),Lymphadenopathy
 Abdominal – Lumps,Ascites
 Vulva- Bleeding, Ulcers
 Speculum – Atrophic changes, Cervical
lesions,vaginal lesions,uterine size,adnexal
masses
Vaginal ultrasonography.
Saline Sonography.
Endometrial biopsy.
Office biopsy
Dilatation and Curettage
Hysteroscopic guided biopsy
Vaginal Ultrasound
 Transvaginal Ultrasound Scan
endometrial endometrial
thickness is > 4mm thickness is < 4mm

If low risk If high risk Endometrial sampling

office endometrial D/C biopsy OR But symptoms

biopsy and SIS hysteroscopy persist

In women with continued bleeding after a negative initial evaluation, further testing
with hysteroscopically directed biopsy is essential,
 The introduction of intrauterine fluid (saline-
infusion sonography) during transvaginal
ultrasound is one of the most significant
advances in ultrasonography of the past
decade.
 CYST

POLYP

With polyps the endometrial-myometrial

interface is preserved well-defined, homogeneous,
isoechoic to the endometrium
 The Thickened endometrium may
be a Submucosal leiomyomas

With myomas the endometrial-

myometrial interface is distorted broad-based, hypoechoic,
The Thickened endometrium may
be an endometrial hyperplasia
Endometrium thickness = A-B

A
B

diffuse thickening of the echogenic

endometrial stripe without focal
abnormality
Endometrial cancer is typically a diffuse process,
but early cases can appear as a polypoid mass
Endometrial biopsy
 Endometrial biopsy is required if:
 ●The endometrial lining is thicker than 4 mm
 ●The endometrium shows diffuse or focal
increased echogenicity (heterogeneity)
 ●The endometrium is not adequately visualized
 ●The woman has persistent bleeding.
 HYSTEROSCOPY

OUTPATIENT INPATIENT
Hysteroscopic visualization has several
advantages:
 Immediate evaluation,
 visualization of the endometrium and
endocervix,
 the ability to detect minute focal endometrial
pathology and to perform directed endometrial
biopsies.
 Once malignancy excluded – Reassure
 Premalignant Changes –Hyperplasia with or
without atypia,?Proliferative
endometrium(Abnormal for a Postmenopausal
Woman)- Treat
 Benign – Polyps etc. – Treat by removal
 Atrophic Changes – Local Oestrogen therapy
 Traumatic – Eg Pessary(remove the cause
 Types (represent a continuum of changes
based on duration and level of estrogen
excess):
1. Simple (cystic) Hyperplasia
2. Complex Hyperplasia without
atypia
3. Complex Hyperplasia with atypia:
20 to 25% risk of carcinoma
 Causes irregular uterine bleeding
Simple (cystic) hyperplasia
 Lower-grade
hyperplasias of the
endometrium show:
 architectural glandular
changes (branching &
budding)
 with cystic glandular
dilatation (synonymous
with anovulatory
changes).
 No increase in glands
or nuclear changes
 Complex hyperplasia
Nuclei all with atypia
look the  Atypical
same hyperplasias exhibit :
around
this gland
 increased
gland/stroma ratio
(gland crowding)
 *epithelial
stratification (arrows).

 Complex hyperplasia
without atypia:
 increased
gland/stroma ratio,
but not nuclear
changes.
Complex hyperplasia with atypia

Can see nucleoli

ENDOMETRIAL CARCINOMA
 Most frequent cancer of the female genital tract
in USA (formerly cervical CA prior to PAP
smear)
 Second Commonest cancer of the female
genital tract in the developing world

 55 to 65 yrs (uncommon <40years; however

with increasing obesity rate has caused an
increase in the younger population getting
endometrial carcinoma)
 The majority of women with endometrial
cancer are diagnosed at an early stage:
 confined to primary site (67 percent);
 spread to regional organs and lymph nodes (21
percent); and
 distant metastases (8 percent) .
 conditions typically associated with chronic elevations
of endogenous estrogen levels or increased estrogen
action at the level of the endometrium. These include
 Obesity.
 history of chronic anovulation – PCOS
 Nulliparity
 diabetes mellitus/Hypertension
 estrogen-secreting tumors.
 exogenous estrogen unopposed by progesterone .
 tamoxifen use.
 a family history of colorectal, ovarian, or endometrial
cancer.
 Early menarche
 Late menopause
 Lynch syndrome — Women with Lynch syndrome
(hereditary nonpolyposis colorectal cancer) have a high
risk of developing endometrial cancer and are likely to
develop the disease at a young age. Women with
Lynch syndrome are also at an elevated risk of colon
and ovarian cancer, along with other malignancies.
Lynch syndrome is an autosomal dominant disorder.
 BRCA — Carriers of mutations in the BRCA genes
are at a high risk of breast and ovarian cancer. Some
data suggest that BRCA1 mutations are associated with
endometrial carcinoma.
Clinical Presentation:

 Postmenopausal Bleeding
 irregular bleeding in a premenopausal
patient
 Abnormal cervical cytology finding –
Endometrial cells
Atypical glandular cells
Adenocarcinoma
 Incidental finding on imaging
 Incidental finding at hysterectomy
 Endometrioid carcinoma — Endometrioid
histology is the most common type of EC,
accounting for 75 to 80 percent of cases .These
tumors are stimulated by estrogen, are
typically are preceded by endometrial
hyperplasia present at an early stage, and have
a good prognosis.
 Mucinous carcinoma — Mucinous EC, by
World Health Organization (WHO) definition,
is composed of >50 percent mucinous cells, and
the remainder of the tumor shows
endometrioid morphology .These are type 1
tumors, which are graded using the FIGO
system. These tumors are typically low grade
with a good prognosis.
 Serous carcinoma — Serous carcinoma is the
second most common type of EC but only
accounts for about 10 percent of cases.
 Most serous endometrial carcinomas have a
worse prognosis, as there is frequently
clinically occult extra uterine disease present at
the time of diagnosis
 Clear cell carcinoma — Clear cell EC is an
uncommon histologic type (<5 percent) of EC.
Like serous carcinoma, this tumor is typically
high grade and often presents at an advanced
stage.
 Clear cell EC has several different architectural
patterns: papillary, glandular, tubulocystic, and
diffuse, composed of cells with abundant clear
cytoplasm
 Mixed cell tumors — Mixed carcinoma with
both endometrioid and high-grade
nonendometrioid patterns (usually serous)
may occur. The minimum amount of the
second component has been set at 5 percent, as
even this small amount of a serous component
leads to a poorer prognosis [11].
 Carcinosarcoma (malignant mixed müllerian
tumor) — Carcinosarcomas are rare
endometrial carcinomas (<5 percent) that
contain both a malignant epithelial component
(carcinoma) and a malignant stromal
component (sarcoma) (picture 5). They often
form a large polyp, completely filling the
endometrial cavity.
 HISTOPATHOLOGY — Adenocarcinoma of
the endometrium is the most common site and
type of uterine cancer. Among endometrial
carcinomas, there are two histologic categories,
which differ in incidence, responsiveness to
estrogens, and clinical behavior.
 ●Type I tumors include tumors of
endometrioid histology that are grade 1 or 2;
these comprise approximately 80 percent of
endometrial carcinomas. These tumors
typically have a favorable prognosis, are
estrogen-responsive, and may be preceded by
an intraepithelial neoplasm (atypical and/or
complex endometrial hyperplasia).
 ●Type II tumors account for 10 to 20 percent of
endometrial carcinomas. They include grade 3
endometrioid tumors as well as tumors of non-
endometrioid histology: serous, clear cell,
mucinous, squamous, transitional cell,
mesonephric, and undifferentiated.
 Stage of disease
 Myometrial invasion
 Lymph node involvement
 Capillary like space involvement
 Histology
 Peritoneal cytology
 Steroid receptor status
 Stage I disease

Total Abdominal Hysterectomy + Bilateral

Salpingo-oophorectomy
+ Brachytherapy to vaginal vault
+ or – Teletherapy to pelvis
The status of both the pelvic and paraaortic
lymph nodes should be assessed
intraoperatively in all patients
 Stage II disease

Total Abdominal Hysterectomy + Bilateral

Salpingo-oophorectomy
+ Pelvic Lymphadenectomy
+ Brachytherapy to vaginal vault
+ Teletherapy to pelvis
 Stage III disease

 Radiotherapy (Brachytherapy + Teletherapy)

 Surgery TAH+BSO
 Stage IV Disease

 Total Abdominal Hysterectomy + Bilateral

Salpingo-oophorectomy
+ high dose progesterone
+ Radiotherapy
 Chemotherapy has a limited role in advanced
disease

Adriamycin
Cisplatin
Carboplatin
Hexamethylmelamine
 5-year survival rate:
Stage I:80% - 90%
Stage II: 70% - 80%
Stage III and IV: 20%- 60%