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POSTMENOPAUSAL

BLEEDING

By Dr OU ONWUAGBU

Common gynaecological complaint in elderly females


About 10% OPD patients
Amount of bleeding is not significant- pink spot, brown dot, frank
bleeding, clots
Potentially dangerous- malignancy until proven otherwise. Workup is
needed.
In practice, any bleeding after age 55 irrespective of dx of
menopause or any abn bleeding after age 40 in premenopausal.

Physiology
Menopause
Post menopausal bleeding (detail)

PHYSIOLOGY
Hypothalamic anterior Pituitary- Ovarian axis
Cyclic activity controlled by hypothalamus which regulates menstrual function
by means of hormones from the anterior pituitary gland and therefore the
ovaries.
Before puberty, hypothalamus and pituitary are relatively inactive and hence
hormonal secretion is minimal leading to no menstrual function and breast
development.
2-3yrs prepubertal, unknown trigger causes the hypothalamus to produce
GnRH
GnRH acts on anterior pituitary and causes it to produce and secret FSH and LH
FSH and LH act on the ovary to produce oestrogen and progesterone
NB higher cortical centres can influence the hypothalamus

HYPOTHALAMUS AND
PITUITARY
GnRH produced from arcuate nucleus in the hypothalamus
Transported via median eminence and released into the vascular
bed of the portal system into anterior pituitary leading to pulsatile
release of FSH and LH
FSH release of oestrogen from ovary
LH transformation of oestrogen secreting cells into progesterone
secreting cells; also, oocyte maturation and ovulation

OVARY
In the foetus at 20 weeks of intrauterine life there are approx.
20million primordial follicles
At birth 1 million
Puberty 300 thousand
Reproductive age 1000 follicles each month; only 400 of these will
ovulate
Postmenopausal 500; small fibrotic ovaries

OVARY CNTD FOLLICULAR


PHASE
Under the influence of FSH only 3-11 primordial follicles develop per ovary but only one
usually matures.
Primary follicle- increased number of granulosa cells
Pre antral follicle- growth is accelerated and oestrogen is produced
Antral follicle- increase in follicular fluid leading to a cavity formation
Dominant follicle- only one forms
Pre ovulatory follicle- continued production of oestrogen till it peaks leading to positive
feed back on LH secretion causing the LH surge which subsequently leads to
progesterone production
Ovulation- 10-12 hrs. after LH surge; continued rise in progesterone levels causing
negative feed back on LH secretion thereby termination the surge.
Thinning of follicular wall+ changes in collagen structure+ proteolytic enzyme action+
PGE &PGF (contraction of ovarian smooth muscle)= Ovulation/ release of the oocyte.

OVARY CONTD LUTEAL


PHASE
Peak in oestrogen and progesterone 8-9 days after ovulation
Progesterone suppresses new follicular growth + give negative
feedback to the pituitary leading the decreased production of FSH
and LH causing further decline in follicular growth.

ENDOMETRIUM
Cyclical proliferation and shedding
In two phases
Proliferative phase- coincides with the follicular phase and ends
with the LH peak. Duration varies from 7-21 days with an average
of 14 days
Secretory phase- coincides with luteal phase. Lasting about 14 days

ENDOMETRIUM
PROLIFERATIVE PHASE
Begins at the end of menstrual period, when bleeding has stopped
Consists of basal layer + necrotic glandular and stromal tissue
Rising oestrogen levels lead to a build up and repair of the
endometrium to a thin surface epithelium with narrow glands which
are far apart and a compact stroma
With further proliferation there is enlargement of the glands and
increase in the number of stromal cells
Prior to ovulation the glands become even larger, thicker and
tortuous.

ENDOMETRIUM CONTD
SECRETORY PHASE
Progesteronic effects on the epithelium causes the glands become
more tortuous and stromal cells become clearer (stromal oedema)
With dropping levels of oestrogen and progesterone endometrial
growth slows down and stromal dehydration occurs.
Leucocyte infiltration of the stroma causes focal areas of
haemorrhage under the epithelium.
Haemorrhage continues and the endometrium becomes necrotic
leading to disintegration of the surface epithelium and therefore
shedding

ENDOMETRIUM CONTD
MENSTRUATION
The superficial and intermediate layers are desquamated and shed
but the basal layer remains intact
Stromal and glandular debris + leucocytes and blood coagulate but
is subsequently broken down by fibrinolysis
Normal menses lasts about 5days with blood loss of about 50ml.
Blood is usually dark without clots.
PGE2 causes vasodilation of uterine vasculature predisposing to
more menstrual blood loss
PGF2alpha causes vasoconstriction leading to decreased bleeding
E2: F2alpha influences the amount of menstrual blood loss

THE MENOPAUSE
Permanent end of menstruation and fertility
12 (6) months after the LNMP
Between age 40 and 55, average age 51yr
Early menopause before age 40, late menopause (no real def)
More accurately, cessation of primary ovarian function- ripening
and release of ova and release of hormones
Climacteric stage AKA Perimenopause- transition years leading to
the menopause characterised by fluctuation hormone levels and
prolongation of menstrual cycles

POSTMENOPAUSAL
BLEEDING!!!
Ruling out malignancy is main concern
Cervical cancer
Endometrial cancer
Ovarian cancer
Vulva or vagina cancer
Referral to oncology after thorough work up

History
Heavier more frequent bleeding- indicates some malignancy
Foul smelling pervaginal discharge or postcoital bleeding- possible
ca cervix
Nulliparous, diabetic, hypertensive, obesity- possible endometrial
ca
Hormonal therapy- HRT or contraceptives, especially oestrogens

On examination
C A J C O L D- anaemia, lymphadenopathy, oedema (ascites), dehydration
Blood pressure, HGT, BMI
Chest- pleural effusions (clinically and on CXR, also cannon ball lesions)
Abdomen- masses, organomegaly (uterus and ovaries), ascites
Vulva and vagina (need good lighting)- bleeding, masses, lesions trauma
Cervix- (speculum)bleeding spontaneously or on contact or through the os,
mass or tissue.
Uterus and adnexa- bimanual exam. NB the obese patient
Rectum- some masses are easily palpable, rule out PR bleeding

On the cervix- where there is no overt pathology, a pap smear


should be done

Endometrial sampling is compulsory to get histological diagnosis


and rule out malignancy
DD+C (diagnostic dilatation and curettage)- previously considered
the gold standard. Endocervical and endometrial curettage is done
and sent off as two separate specimen usually done under general
anaesthesia

Out patients endometrial sampling.


Thin pipette which curettes and aspirates endometrial tissue. 80%
accurate, minimal discomfort, OPD procedure, quick

Transvaginal ultrasound to assess endometrial thickness.


Acceptable value for postmenopausal patients is less than 5mm (47mm).

Hysteroscopy
Direct visualisation of the endometrium.
Done in theatre under general of regional anaesthesia.
Focal lesions can be identified and biopsied.
The current gold standard.
Preferred when DD+C or OPD sampling have little or no yield.

None of the methods for endometrial sampling is ideal.


Each has its advantages and disadvantages.
Method chosen depends on the patients profile

OTHER CAUSES
Atrophic vaginitis- in 20% cases, a diagnosis of exclusion, treated with topical oestrogen.
Bleeding associated with hormone replacement- in 15-20% of cases, especially oestrogen administration.
Treatment depends on the patients overall need for the oestrogens. Either HRT is stopped or progesterone
is added.
Endometrial hyperplasia- 7.5% of cases, unopposed oestrogen. Commonly secondary to obesity but can be
due to oestrogen producing tumour or HRT. Treated with progesterone therapy and weight loss and/or
hysterectomy if there is atypia or poor response to medical therapy
Endometrial polyps- found in 20% of postmenopausal patients and usually asymptomatic. Causes 7.5% of
postmenopausal bleeding. Once diagnosed, should be removed by avulsion or electrosurgical resection via
hysteroscopy. Hysterectomy is indicated if there is malignancy or persistence.
Cervical polyps- should be removed
Trauma- usually post coital and due to the atrophic vulvar and vaginal mucosa. Treated with topical
oestrogen cream. Rape should be excluded.
Foreign body in vagina, forgotten IUCD
PMBUO- no cause found despite thorough investigation. Regular follow up is required. If bleeding recurs,
investigations need to be repeated and if still no cause or bleeding is persistent, hysterectomy may be
needed.

NON GYNAECOLOGICAL
CAUSES
Urethral caruncle
Cystitis
Haematuria- bladder polyp, neoplasia
Anorectal causes- fissures, haemorrhoids, neoplasia
Systemic disease- bleeding disorders, anti coagulation therapy

SUMMARY
>55yrs with or without diagnosis of menopause
>40 yrs. premenopausal with abnormal menses
Any amount of type of bleeding
First priority- rule out malignancy

THANK YOU
References.
Clinical gynaecology by Odendaal et al
Reference images google search.