DYSFUNCTIONAL UTERINE

BLEEDING

Oleh :
Adi Setyawan Prianto

gram Pendidikan Konsultan Fertilitas dan Endokrinologi Reprodu

Bagian/SMF Obstetri dan Ginekologi
Fakultas Kedokteran Universitas Diponegoro
SEMARANG
Revised 2010

DEFINITION

Dysfunctional Uterine Bleeding :

The spectrum of abnormal menstrual bleeding patterns that may occur
in anovulatory women who have no medical illness, or pelvic pathology.

Medical treatment based on sound physiologic concepts.

Designed to achieve 2 specific goals :
1. to reverse the abnormalities of endometrial growth and developmen
2. to induce or restore cyclic predictable menses of normal volume an

Leon Speroff et al : Clinical Gynecologic Endocrinology and Infertility 7 e

REGULATION OF THE MENSTRUAL CYCLE

Menstruation is the response of the endometrium to the withdrawal
of progesterone (and estrogen) that occurs with the demise of the
corpus luteum in the absence of pregnancy
(Fig. 1). Involves complex interactions between the endocrine
and immune system are the component blood vessels and the
dynamic population of leukocytes that influx at this time (Fig. 2).

FIG. 2. Distribution of CD56ve uNK ce

endometrium during the secretory p

This shows the close clustering of th
(solid arrow). The spiral vessels are
arrows.
Jabbour et al. Regulation of Menstr

Endocrine Reviews, February 2006, 27(1):

FIG. 1.

Illustration of the alternatives for a progesterone-primed endometrium. The

progesterone induced changes that characterize the endometrium primed for implantation also
bring about progesterone dependency of the tissue. On the demise of the corpus luteum, falling
progesterone levels initiate an inflammatory process that starts in the stromal compartment but
involves leukocyte immigration and metalloproteinase (MMP) activation. Eventual shedding of
the functional layer of the endometrium opens the way for estrogen-dependent regrowth of the
tissue.

18 Endocrine Reviews, February 2006, 27(1):1746 Jabbour et al. Regulation of

Figure 1. Molecular and cellular events occurring after progesterone withdrawal (Critchley et al., 2001).
Coincident events of progesterone withdrawal and hypoxia. Progesterone withdrawal results in an up-regulation o
production of MMPs, a leucocyte influx and expression of stromal KDR in the upper endometrial zones. There is co
an up-regulation of VEGF. VEGF binds to its type 2 receptor, KDR, and there is a paracrine/autocrine action on the
production in the same endometrial upper zone stromal cells. Menstrual sloughing takes place from the superficia
regions of the endometrium. KDR, kinase insert domaincontaining receptor or VEGF receptor 2; PGF2a, prostagla

There are three classic phases of the menstrual cycle:

1. An estrogen-dominated preovulatory phase,
2. a postovulatory and progesterone-dominated secretory phase,
3. And a menstrual phase following progesterone withdrawal that acco
demise of the corpus luteum.

The endometrium is composed of two layers and is a target tissue for st

The upper functional layer is shed at menstruation.
The endometrium regenerates after menstrual shedding from an und

Parameters of normal menstruation

The menstrual cycle is generally defined in the context of its
length, regularity, frequency, and pattern of menstrual blood
loss. Studies have indicated that the mean menstrual cycle
length in the mid-reproductive years is between 28 and 30 d.
The duration of the period of menstruation is commonly 45 d,
with the period of heaviest bleeding reported in the first 2 d of
menses, whereas the volume of blood loss varies between 25
and 35 ml.
by Fraser and Inceboz (287).

The progesterone-dominated latter half of the menstrual cycle is

constituted by an early, mid, and late secretory phase.The
pattern of sex steroid receptor expression in the endometrium
across the secretory phase reflects the fact that the
early secretory phase is regulated by both estrogen and
progesterone.
The mid secretory phase is regulated by progesterone alone as
estrogen receptor (ER) is down-regulated in the glands and
stroma at this time (9); and the late secretory
phase is associated with progesterone withdrawal
and,consequently, menstruation.

FIG. 4. Progesterone withdrawal activates many pathways; prominent among these a

Chemotactic agents,which synergize with vasoactive agents, are also expressed. Ther
which degrade the interstitial matrix of the endometrium, play a major role in the me
uncertain.MMPs can be released from both resident endometrium stromal cells and i

Mechanisms Involved in ONSET and CESSATION of Normal M

ONSET Menstruation :
Basically, menstruation was envisioned as ischaemic necrosis of the end
vasoconstriction spiral arterioles in the basal layer, trigerred by withdra
progesterone.
Initiation of menstruation is an enzymatic autodigestion of
the endometrium with its subsurface capillary plexus, possibly extending
the spiral arteriol system in the basal layer.

CESSATION Menstruation:
Similarly, the end of menses was explained by longer and more intense
constriction, combine with coagulation mechanisms activated by vascula
endometrial collaps, aided by rapid reepithelization mediated by est
the emerging new follicular cohort.

The end normal menstruation is

Coagulation mechanisms,
Local vasocontriction, and
Re-epithelization
all contribute to hemostasis.

The enzymatic degradation of the endometrium i.e. the release of intracel

enzymes, proteases from inflitrating inflammatory cells, and the actions o
proteinases.

Progesterone withdrawal also stimulates an inflammatory response in the

The inflammatory inflitrate ( i.e. neutrophils, eosinophils and macrophage
is drawn by chemokines (interleukin 8; IL 8),some of which are
down regulated by progesterone.

Matrix metalloproteinases are family a proteolitic enzymes that degrade c

the extra cellular matrix and basement membrane.

Progressive enzymatic degradation of the endometrium eventually disru

capillary and venous vascular system, causing interstitial hemorrh

surface membrane allow blood to escape into the endometrial cavity.

Desquamation begins in the fundus and gradually extends toward the isth

 The menstrual fluid is composed of an autolysed endometrium rich in infl

red blood cells, and proteolytic enzymes.
PLASMIN, has potent fibrinolityc action that help to prevent clotting of
to facilitate the expulsion of degenerated tissue.

To some extent, the amount of menstrual bleeding is controlled by the lo

between fibrinolysis and clotting
Endometrial stromal cells tissue factor and plasminogen activator inhibi
clotting and help to balance fibrinolytic processes.
Early in menstruation, intravascular platelet plugs, and later thrombi fr
helping to limit blood loss.
Myometrial contractions are not important for control of menstru

STROMAL REGENERATION :

Matrix metalloproteinases present in the menstrual endometrium may b

of the release and activation of growth factors needed for endometrial re
VEGF is an important promoter of endometrial mitosis and can be induc
TGF and IGF-1.
The endometrium is not repaired, but completely remodele

Figure 2. Breakdown and restoration in the endometrium. Tissue is shed as a result of the action of MMP.
Re-epithelialization is very rapid and occurs from theopen mouths of the glands and from the unshed portions of th
Leucocyte products and a variety of other factors derived from the epithelium itself are postulated to play a role in
Subsequent restoration of the underlying stroma includes proliferation of cells associated with blood vessels and en
the laying down of the extracellular matrix. These events are postulated to occur under the influence of increasing
concentrations and are probably locally regulated by a number of growth factors and other regulatory factors (Sala
membrane type 1; ET-1, endothelin 1; BMP-6, bone morphogenetic protein 6; BV, blood vessel; FGFs, fibroblast gro
The ESHRE Capri Workshop Group 424

Endometrial Responses to Steroid Hormones : Physiologic an

Normal menstrual bleeding at the end of an ovulatory cycle results fr

progesterone withdrawal.
Other examples : include the bleeding that follows discontinuiton of bo
progestin in women receiving cyclic postmenopausal hormone therapy
Under these circumstance, bleeding generally is regular, predictable
in volume and duration.
However, estrogen-progesterone withdrawal is not the only pattern
signals that can provoke endometrial bleeding.
Bleeding can also result from :
1. Estrogen withdrawal,
2, Estrogen breakthrough,
3. Progesterone withdrawal, and
4. Progesterone breakthrough.

ESTROGEN WITHDRAWAL BLEEDING :

One clinical sample of estrogen withdrawal bleeding is that bilate

during follicular phase of the cycle.
Other examples include cyclic estrogen only hormone therapy in c
menopausal women and midcycle bleeding that coincides with th
but abrupt fall estrogen levels immediately before ovulation.

ESTROGEN BREAKTHROUGH BLEEDING :

The best examples of estrogen breakthrough bleeding are different patt

observed in women with chronic anovulation.
Relatively low levels of chronic estrogen exposure typically result in inte
or staining that is generally light in volume but may be prolonged.
In contrast, sustained high level estrogen stimulation commonly results
of amenorrhea punctuated by acute episodes of often profuse bleedi

PROGESTERONE WITHDRAWAL BLEEDING :

Progesterone withdrawal bleeding is observed when treatment with exo

or synthetic progestin is discontinued.

It usually occurs only when endometrium has first been primed with endo
exogenous estrogen.

The amount and duration of bleeding can vary widely and generally corel
the level and duration previous estrogen stimulated endometrial prolifer

In women receiving cyclic hormone therapy with exogenous estrogen and

bleeding follows withdrawal of progesterone, even if estrogen treatment
Progestin withdrawal bleeding can be delayed, but only
if estrogen levels are increased 10-20 fold.

PROGESTERONE BREAKTHROUGH BLEEDING :

Progesterone breakthrough bleeding occurs when the ratio of progeste

is unfavorably high.

Clinical examples of progesterone breakthrough bleeding are the bleed

women using the progestin-only contraceptive mini-pill or other long
only conraceptive methodes (progestin implants, depot medroxypro

Also women using combination estrogen-progestin oral contracep

net effect of oral contraceptives on the endometrium is profoundly prog

Abnormal Uterine Bleeding with Combination OCPs

TABLE 4
Treatment Options for Abnormal Uterine Bleeding in Women Using Hormonal Contraception

Treatment

Dosage

Nonsteroidal anti-inflammatory drug such as ibuprofen

(e.g., Advil, Motrin)

800 mg three times daily for 1 to 2 weeks or until

bleeding stops

Supplemental estrogen
Conjugated equine estrogens (Premarin)

0.625 to 1.25 mg per day for 1 to 2 weeks

Ethinyl estradiol (Estinyl)

20 mcg per day for 1 to 2 weeks

Estradiol (Estrase)

0.5 to 1 mg per day for 1 to 2 weeks

Abnormal Uterine Bleeding with Progestin-Only Co

Presumed Dysfunctional Uterine Bleeding

in Women of Childbearing Age:
Evaluation Based on Risk Factors
for Endometrial Cancer

ANOVULATORY BLEEDING

Anovulatory bleeding can represent :

1. Estrogen withdrawal bleeding : reflecting the transient fall in estro
from regression of the most recent follicular cohort.
2. Estrogen breakthrough bleeding :due to focal breakdown of an ov
structurally fragile endometrium under continous estrogen stimulatio
Tend to occur in women with :
1.Polycystic ovarian syndrome.
2. Obese women.
3. Postmenarcheal adolescent
4. Perimenopausal women
To older women who is deeply concerned that she may have CANCER.

Session II
DYSFUNCTIONAL UTERINE
BLEEDING LECTURE
11 Oktober 2010 Revised

ANOVULATORY BLEEDING
Regression of most follicular cohort

Transient fall estrogen level

Estrogen withdrawal
bleeding

ANOVULATORY BLEEDIN

1. Focal breakdown
Estrogen breakthrough
2. Structurally fragile endometriumbleeding

Under continous estrogen stimulation

Clinical examples :
1.Polycystic ovary syndrome
2. Obese women.
3. Postmenarcheal adolesce
4. Perimenopausal women

Always in the follicular phase of the ovarian cycle.

In the proliferative phase of the endometrial cycle.

Characterizes
Anovulatory Woman

There is no luteal or secretory phase, because there is no cycl

The only ovarian steroid signal the endometrium receives is e

Estrogen level constanly fluctuate, rising and falling as each g

of cohort follicles and later into atresia.

DIFFERENTIAL DIAGNOSIS

1.

2.

3.

4.
5.
6
.

Accident or complication 1. Threatened or incomplete abortion

of pregnancy
2. Ectopic pregnancy.

1. Uterine neoplasia
Possibility of underlying pathology2. Cervical and endometrial polyps
3. Adenomyosis.

Thyroid disorders

1. Hypothyroidism
2. Hyperthyroidism.

1. A hystory of postpartum hamorrhage or

Coagulopathy 2. Excessive bleeding with surgery,
3. Dental procedurs,or trauma
1. Glucocorticoids, tamoxifen, and anticoagulants.
Medications 2. Herbs have estrogenic activity.
Affects ovarian blood supply,
Post tubal ligation syndromeincreased after sterilization by electrocautery.

DIAGNOSTIC EVALUATION OF ABNORMAL BLEEDING

True anovulatory bleeding

1. Without additional laboratory evaluation
2.Infrequent, irregular, unpredictable menstrual bleeding

Anatomical lesion

Regular monthly periods that heavy and prolon

Laboatory test :

1.Serum progesterone > 3 ng/mL : ovulation.

2. TSH
3. BIOPSI :
Biopsi (-) : endometrial thickness < 5 mm.
Biopsi (+), if the clinical history suggests long-term unopposed estrogen expo
and endometrial thickness > 12 mm

PROGESTIN THERAPY

Androgen

Androgen
Aromatase

Aromatase

17-hydroxysteroid
dehidrogenase
Estradiol
Estrone
Sulfotransferase
Estradiol
sulfate

Sulfotransferase

Sulfatase

Estrone
sulfate

1. Progestin stimulate 17-hydroxysteroid dehidrogenase and sulfotransfe

Progestins are
powerful antiestrogens 2. Estrogen receptor replenishment.
3. Suppress estrogen mediated transcription of oncogens.

The ANTIMITOTIC
growth-limiting effects
on endometrium

Prevention and reversal hyperplasia.

Arrest of growth secretory phase
(pregnancy and oral contraceptive combination.)

Continued Progestin Therapy ..

Oligomenorrheic anovulatory women

With episodic abnormal bleeding

Self-limited progesterone
withdrawal bleeding

Medroxyprogesterone acetate
(5-10 mg daily for 2 weeks every month)
When menses (-)
Possibility of a more profound
ovulatory dysfunction due to

grossly low estrogen le

2.

Anovulatory with
metrorrhagia/polymenorrhea
Progestin treatment for 14 days

3.

Failed progestin treatment

Induce stabilizing predecidual changes in

a vascular and fragile endometrium
and withdrawal medical curettag

Diagnostic evaluation

ORAL CONTRACEPTIVE THERAPY

Prolonged episodes of
heavy anovulatory bleeding

Diagnostic evaluation
Transvaginal ultrasound examination

Low dose monophasic combination oral contracep

(one pill twice daily)
Bleedings stop expected within 24 48 hours.
Continue for at least
5-7 days even when bleeding

If oral contraceptive cannot be used

Uniformly increased endometrial thickness

Minimize the risk of unsuccessful treatment

With continued heavy blood loss.

Higher doses progestin therapy

(medroxyprogesterone acetate 20 mg , or
Norethindrone acetate 5 mg daily)

ESTROGEN THERAPY

Initial treatment strategy

Intermitten vaginal spotting
Estrogen levels are insufficient to stimulste the g
fondation of actions of progesterone
Diagnostic evaluation
Frankly low levels of estrogen stimulation
(estrogen breakthrough bleeding)

Transvaginal ultrasound
1. Defining endometrial thickness
2. Anatomic abnormality of the uterine cavity.

Endometrium is attenuated and

bleeding is acute and heavy

A very thin and denuded endometrium

1,25 mg conjugated estrogens

Tappering tp once daily dose for 7-10 days
bleeding is controlled

Followed by treatment with progestin

To stabilize the estrogen-stimulated
endometrial growth

Continued Estrogen Therapy..

1. Women with low-dose combination edtrogen-progestin contraceptives

2. Depot progestin contraceptives.

Insufficient endogenous estrogen to balance progestin effects

Progestin attenuates the endometrium

Estrogen Therapy
Logical and best choice
Inducing pseudoathropy

The light spotting,

Episodic
staining, or
bleeding may occur progesterone breakthrough bleeding

ENDOMETRIAL HYPERTPLASIA AND NEOPLASIA

Endometrial hyperplasia without atypia

1. Regress spontaneously
2. After curettage
3. With progestin therapy

Cyclic progestin therapy

(medroxyprogesterone acetate 10 mg daily for 14 day
Oral contraceptives.

In contrast,
Quite resistant curettage or prolongred high dose progestational therapy
Risk 10 30 % progression to adenocarcinoma

Hyperplasia with atypia

Best treated surgically.

ENDOMETRIAL ABLATION
Persistent bleeding despite treatment
Lower risk
Fewer complication
More rapid recovery

Both frustating and concerning

Endometrial ablation

HysterectomyMore satisfied
with the outcome

Hysteroscopic technique
Non- hysteroscopy technique
A bipolar vaporizing electrode
Hydrothermal technique
Circulates heated water (87 5 C) inside in ballon
Using electrodes on the outer surface
And radiofrequency-induced thermal destruction
Result

better, if:

1 Performed during the early follicular phase

2. After endometrium is first attenuated for 4-6
by progestin, danazol, GnRHa

 By definition, the anovulatory woman is always in the follicular phase o

and in the proliferative phase of the endometrial cycle.
There is no luteal or secretory phase because there is no cycle.
The only ovarian steroid signal the endometrium receives is estrogen.
Epithel repair is focal, in the areas of breakdown, not universal;
The results is a constantly changing patchwork of small repairs, instead
and well structured remodeling.

Normal endometrium. (2) Sagittal transvaginal US scan of the uterus shows the menstrual-phase endometrium (a
(normal thickness, 1-4 mm).
(3) Transverse transvaginal US scan shows the proliferative-phase endometrium (arrows) (normal thickness, 4-6
(4) Sagittal transvaginal US scan obtained during the periovulatory phase (day 15) shows the trilaminar endometr
with a thickness of approximately 11 mm (arrows).
(5) Sagittal transvaginal US scan shows the secretory-phase endometrium (cursors) (normal thickness, 8-16 mm)

Figures 8, 9. (8) Polyp in a 47-year-old woman with excessive bleeding. (a) Sagittal transvaginal US s
the endometrium with a thickness of 15 mm.
(b) Sagittal sonohysterogram shows a single polyp (arrowheads) with a catheter. The endometrium is no
(9) Polyps in a 56-year-old woman. (a) Sagittal transvaginal US scan shows the endometrium with a thick
(b) Sagittal sonohysterogram shows three polyps (P) with an otherwise thin (1-2-mm) endometrium.

Endometrial carcinoma in a 51-year-old woman with a 4-week history of bleeding.

(a) Sagittal transvaginal US scan shows the endometrium with a thickness of 23 mm.
(b) Sagittal sonohysterogram shows diffuse thickening secondary to hyperplasia.

DIAGNOSTIC EVALUATION OF ABNORMAL BLEEDING

MENSTRUAL HISTORY:

Detail information regarding :

1. Intermenstrual intervals ( number of days, regularit).
2. Volume.(heavy, light, or variable).
3. Duration. (normal or prolonged, consistent or variable)
4. The onset abnormal menses.(perimenarcheal, sudden, gradual)
5. temporal associations (postcoital, postpartum, postpill, weight gain or l
6. Associated symptoms (premenstrual molimina, dysmenorrhea,dyspareu
hirsutism)
7. Underlying systemic illnesses (renal, hepatic, hematopoeitic, thyroid)
8. Medications.(hormonal, anticoagulants)

 Regular monthly periods that are heavy or prolonged are more likely
anatomical lesion or bleeding disorder than to anovulation.
A sensitive pregnancy test can quickly exclude any realistic possibility
related to an accident or complication of pregnancy.

A well-timed serum progesterone determination during what shou

of the cycle can help to document ovulation or anovulation.

A serum thyroid-stimulating hormone (TSH) level can quickly exlude a

thyroid disorders.

In adolescents, suspicion of bleeding disorders is sufficient indication f

coagulation study.

Endometrial hyperplasia and cancer are more commonly detecte

in younger women, but duration of exposure to unopposed estrogen
the more critical risk factor.

ULTRASOUND :

A very thin endometrial stripe (< 5 mm), suggests an attenuated or den

best treated first with estrogen rather than progestin or estrogen-proges

In perimenopausal and postmenopausal women when the endometrial t

is < 4-5 mm, endometrial biopsy is considered unnecessary, because the
endometrial hyperplasia or cancer is remote.

The biopsy is indicated when the clinical hystory suggests long-term

unopposed estrogen exposure even when the endometrial thickness
normal (5-12 mm).

EVALUATION TO STRONG EVIDENCE FOR ANATOMIC CAUSE :

1. Regular monthly cycles with increasing volume or duration of bleeding

2. Regular monthly cycles complicated by intermenstrual bleeding in t
vaginal or cervical lesion.
3. Abnormal bleeding despite objective evidence of ovulation from measu
serum progesterone (>3 ng.ml) or from endometrial biopsy (secre
4. Failed empirical medical management.

PROGESTIN THERAPY

In most circumstances, progestin therapy will control anovulatory bleeding

pathology has been excluded.
In women who do not ovulate, cyclic progestin therapy restores the norm
endometrial steroid hormone stimulation-estrogen,
follow
estrogen plus progesterone,
followed by withdrawal.

Mechanisms of progestin action in regimen progestin therap

Progestin stimulate 17-hydroxysteroid dehydrogenase and sulfotranferas

the enzymes that work in concert to convert estradiol to estrone sulfate

(rapidly clear from the body).
Progestin antagonize estrogen action by inhibiting estrogens induction
Progestin also supress estrogen-mediated transcription of oncogen.
Together, these action explain ANTIMITOTIC (prevention and reversal o
arrest growth of secretory phase of the cycle).

Continued,.

Self-limited progesterone withdrawal bleeding can be induced by cyclic t

an orally active progestin like :
MEDROXYPROGESTERONE ACETATE
( 5-10 mg daily for 2 weeks every month ).
The interval therapy can be fixed to the calendaer beginning on the first
to the onset of menses.

In women who likely still ovulate (albeit infrequently) or want to avoid pr

an estrogen-progestin contraceptive is a better choice.

In anovulatory women with metrorrhagia or polymenorrhea :

progestin tretment for 14 days can induce stabilizing predecidual chang
in a vascular and fragile endometrium and, after withdrawal, so called

medical curettage
Failed progestin treatment requires further diagnostic evaluation ????

ORAL CONTRACEPTIVE THERAPY :

Prolonged episodes of heavy anovulatory bleeding and transvaginal

examination can confirm the diagnostic of uniformly increased endometr
usually are treated best with combined estrogen-progestin therapy in th
of combined oral contraceptive.

To respite from heavy bleeding that only recently stopped, oral contrace
continued (one pill per day) until the package of pills is completed.
In women wih normal uteri, oral contraceptive reduce menstrual flow
from that in natural cycles.

Episodic breakthrough bleeding is relatively common and can be tre

Mechanisms of action are :

For the short term, the decidual changes induced by treatment, provide so
and stop further random breakdown of an overgrown, vascular, and fragile
substantial amount of tissue remains to be shed upon estrogen-progestin w

ESTROGEN THERAPY

Endometrium is typically extremely thin with frankly low levels of estrogen

frequently intermittent vaginal spotting (estrogen breakthrough bleedin
treatment with progestin, commonly failed and may further aggravate the p
A similar situation can develop after prolonged episodes of heavy bleeding
In either case, estrogen therapy is most effective as initial treatment
Under such circumstances, transvaginal ultrasound can help guide the
by defining the endometrial thickness and revealing any abnormalit

Estrogen therapy is also the logical and best choice for management of
episodic progesterone breakthrough bleeding, that commonly occured
receiving low-dose combination estrogen-progestin contraceptive, or depo
Progestin inducing pseudo atrophy.
Symptom is similar likely ; light spotting, staining or bleeding that similar
estrogen breakthrough bleeding with very low levels of circulating estroge

Continued, ..
In all such cases, a short interval of added estrogen :
Conjugated estrogen 1,25 mg , or micronized estradiol 2,0 mg
daily for 7 10 days)
If treatment failed, so..what ??????
Further evaluation can exclude possibilty of a previously
unrecognized endometrial polyp,
or sub mucous myoma

DILATATION AND CURETTAGE

Dilatation and curettage is the most expeditious and effective way to sto
uterine bleeding.
Mechanisms of effects of curretage is not entirely clearbut
Surgical denudation of basal layer of endometrium is presumed to acute
normal processes involved in cessation of normal menstrual bleeding, lik
1. Local clotting mechanism
2. Vasoconstriction of basal arterioles
3. Rapid reepithelization.

NON SPECIFIC TREATMENTS FOR ABNORMAL MENSTRUAL BLEE

A spesific cause for heavy or prolongrd menstrual bleeding in ovulatory w

be identified; may be local defects in endometrial hemostasis are pre

1. Nonsteroidal Antiinfflamatory Drugs (NSAIDs) :

The concentration of PGE2 and PGF 2 increase progresively in human e

during the menstrual cycle.
NSAIDs inhibit PG synthesis and decrease menstrual blood loss.
NSAIDs might be considered the first line therapy for ovulatory women w
heavy menstrual bleeding and no demontrabel pathology.
NSAIDs have the added advantage of providing relief from dysmenorrhe

2. The Levonorgestrel IUD :

The LNG-IUD has a reservoir containing 52 mg LNG.

Menstrual blood loss can be reduced by 75 95 %
LNG-IUD is more effective than cyclic administration of norethindrone
LNG_IUD is an atractive option for chronic ilness (renal failure).

ENDOMETRIAL ABLATION
Indication :
Persistent bleeding when medical treatment are rejected, unsuccessful,

Hysteroscopic and non- hysteroscopic techniques

Blind techniques for ablation are technically easier to perform, take less
are more likely to require only local anesthesia, and achived similar resul
equipment problems are more common.

There are legitimate concerns that

endometrial carcinomas might be advertantly treated by endometrial
or procedure might obliterate portions of the uterine cavity
Endometrial ablation is not recommended for women at high risk for end

Microwave Endometrial Ablation (MEA)