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Nancy E Fay MD FACOG
Division of Reproductive Medicine
Definition-AUB
 Any bleeding that is not regular cyclic menstrual flow
 Intermenstrual spotting
 Post coital bleeding
 Excessively heavy bleeding
 Unpredictable bleeding
PALM-COIEN Classification
 PALM-Structural causes






Polyp (AUB-P)
Adenomyosis (AUB-A)
Leiomyoma (AUB-L)
Sub mucosal
Intramural
Malignancy/hyperplasia(AUB-M)
PALM-COEIN Classification
 COEIN: Nonstructural causes





Coagulopathy (AUB-C)
Ovulatory dysfunction (AUB-O)
Endometrial (AUB-E)
Iatrogenic (AUB-I)
Not yet classified (AUB-N)
Physiology of
the menstrual
cycle
Proliferative or follicular
phase
Endometrium
Height starts <5
mm to <15 mm
Mitotic growth
of tubular glands
response to rising
estrogen
Follicular
phase
*Primordial follicles
develop
INDEPENDENT of FSH
Estradiol promotes FSH
receptors
Ends with LH surgeand
meiosis of dominant
follicle
Secretory or luteal phase
 Endometrium

Stromal height fixed, becomes edematous

Glands tortuous, sub nuclear vacuoles

Arteries spiral

Endometrium stratified into basalis 25%,
spongiosa 50% and outer compacta 25%

Endometrial biopsy to date endometrium; luteal
insufficiency. Timed progesterone alternative
Secretory or luteal phase
 Ovary

LH surge causes reduction division of oocyte

Growth of granulosa cells in size, #’s and
metabolic activity

Day 8 capillary growth and progesterone peak

If no HCG to stimulate, follicular atresia begins

*Progesterone suppresses new follicular growth
Luteal or
secretory
phase
Menstrual phase
 Steroid withdrawal causes lysosomal instability
releasing prostaglandin synthetase, proteases and
collagenases
 High thromboxane A2 results in vasospasm and
ischemic necrosis of the endometrium at the level of
basalis layer
 Endometrial healing by rising estrogen from new
follicles with estradiol mediated growth
Adolescent development
 Average development






Breast bud 9.8 yrs
Pubic hair 10.5 yrs
Maximal growth velocity 11.4 yrs
Menarche at 12.8 yrs
Adult pubic hair by 13.4 yrs
Adult breast by 14.6 yrs
Adolescent development
 55% of cycles first year are anovulatory
 Usually at least 15 months from menarche to achieve 10
cycles
 Normal fertile adults have 1-2 anovulatory and 10-12
cycles per year
 Adolescent menstrual pattern ends 2-3 yrs after
menarche
Tanner
Stages
Adolescent AUB, persistent
 10% with menorrhagia will have coagulopathy
 Most common are ITP, Von Willebrand’s,
Glanzmann's, Thalassemia major and Fanconi’s
anemia
 Tests: INR, PTT, bleeding time, platelet count and
VonWillebrand’s screen
Other terms
 Polymenorrhea; frequent cycles <18 days
 Metrorrhagia; intermittent intermenstrual bleeding
 Menorrhagia; regular but excessively heavy flow
 Menometrorrhagia; irregular, frequent, heavy and
light bleeding
 Hypomenorrhea; light flow at regular intervals
 Oligomenorrhea; irregular, infrequent cycles >45 days
apart, ovulatory or anovulatory
Average menses
 Estrogen + progesterone withdrawal
 5 day flow (2-8 normal)
 Volume loss 30 cc (>80 cc abnormal)
 Average cycle range 21-35 days
Menstrual
cycle
Mature follicle 2-2.5
cm size
Corpus luteum
complex cyst 1-3 cm
size
Endometrial height
range 3-14 mm
Causes of anovulation (AUB-O)
 Physiologic: adolescence, perimenopause, lactation
and pregnancy
 Pathologic

Hyperandrogenic

Hypothalamic

Thyroid disease

Primary pituitary

Premature ovarian failure

Medications/herbal supplements
History the most important
 Qualify and quantify bleeding: type of protection,
frequency of change saturation, clotting
 Establish current complaint and find out what ‘normal’
menses usually are like OFF any hormonal
contraceptives (many women don’t think of hormonal
contraceptives as a medication)
 Other symptoms such as cramping, dyspareunia
 Evaluate use of medications prescriptive as well as
OTC and herbal supplements
Pregnancy
ALWAYS
check HCG
Polycystic ovary syndrome
 Affects 1 in 9 women
 Most common cause of anovulation
 Diagnosis, Oligo or anovulation with one of:

Evidence of androgen excess

Polycystic ovary
 Begins in teen years or early twenties
 Multifactorial inheritance associated with insulin
resistance and metabolic syndrome. Family history of
type II DM
PCOS
 Need to treat proactively with OCP’s, cyclic
progesterone to decrease their risk of endometrial
cancer from unopposed estrogen
 For fertility purposes, use of insulin sensitizers
(metformin) may decrease insulin resistance enough
to allow ovulation along with low carb diet and
exercise. Ideal body weight the goal. Otherwise
ovulation induction needed to conceive.
 Milder cases of PCOS ovulatory, low progesterone, and
have a higher risk of miscarriage
PCOS
Associated with
thyroid
dysfunction.
Hirsutism treated
with
spironolactone
and OCP’s
Endometrial
biopsy? When
needed?
Hypothalamic dysfunction
 Hyper or hypothyroidism

Age factor in screening >35 hypo
 Hyperprolactinemia

Amenorrhea or hypomenorrhea 2/3

Galactorrhea present in 1/3

Infertility with normal menses

Need repeat >48 hrs apart to confirm

Level >50 need to consider MRI of sella
Hypothalamic dysfunction
 CNS suppression, low FSH and LH
 Stress most common cause
 Anorexia
 Athletic
 Lower suppression higher estradiol, more suppression
hypoestrogenic
 Rare congenital absence of LH or mutation in
gonadotropins or GnRH (the latter primary
amenorrhea)
Coagulation disorder
 Most common causes are ITP, VonWillebrand’s,
Glanzman’s, Thallasemia major or Fanconi’s anemia
 Test for bleeding time, INR, PTT, platelet count and
VonWillebrand’s screen
 Remember if severely anemic testing skewed
 In adolescents 10% will have coagulopathy
 Usually ovulatory cycles with severe menorrhagia
 Tranexamic acid may be of benefit for some
Chromosome disorders
 Suspect if initial normal cycles then irregular or
amenorrhea and evidence of diminished reserve
 <25 y/o Turner mosaic more likely
 Later 20’s to early mid 30’s diminished reserve
associated with Fragile X pre-mutation or on the older
end BRCA 1 mutation
 If mutation and some reserve left consider ART
options: gamete freezing, IVF with PGD
 Otherwise fertility with donor eggs and use of HRT or
OCP’s as replacement therapy till 50
Anatomic
causes of
AUB
Endometrial
polyp
Sub mucus
fibroid
Ovarian
masses
Endomctrioma
Hormone
secreting
tumors
PID
Malignancies
 Endometrial cancer

What age should you biopsy to rule out?
 Endometrial hyperplasia

Simple

Complex adenomatous

Atypical complex
 Ovarian
Treatment of AUB
 Anatomic causes treat and usually bleeding controlled.
If not likely hormone issue
 Thyroid dysfunction treatment will resolve AUB once
normal functions after 2 months
 Hyperprolactinemia treat with cabergoline or
bromocriptine. When prolactin normal, normal
menses in 2 cycles
 If unable to treat cause then cyclic progestins or
hormonal contraceptives best treatment.
Treatment of hemorrhage
 Usually at extremes of menstrual ages
 Rule out pregnancy, trauma, coagulopathy; replace
blood products as needed
 Endometrial biopsy depending on age and history
 High dose IV conjugated estrogen 25 mg Q4-6 hrs till
bleeding slows then switch to oral estrogen and
progestin. Give for 3 weeks then withdrawal.
Antiemetics
 Oral high dose E+P an option if stable
 Cycle with hormonal contraceptives 2 months