Transcript dub in adolescents history

Menstrual Disorders:
Excessive Vaginal Bleeding, Secondary
Amenorrhea and Primary Amenorrhea
Betsy Pfeffer MD
Assistant Professor Clinical Pediatrics
Columbia University
Morgan Stanley Children’s Hospital of New
York Presbyterian
Normal Menstrual Cycle
Days 1-13
• Hypothalmus-Pituitary
– Increased GnRH, FSH
• Ovary-Follicular Phase
– Estrogen produced by granulosa cells
– Development of primary follicle
– Feedback of E2 (+ to decrease FSH, - to increase LH)
• Uterus-Proliferative Phase
– Increased glandular cells and stroma
Normal Menstrual Cycle
Days 15-28
• Hypothalmus-Pituitary
– Decreased GnRH, FSH, LH
• Ovary
– Primary follicle becomes corpus luteum
– Corpus luteum secretes progesterone x 14 days
• Uterus-Secretory Phase
– Coiling of endometrial glands
– Increased vascularity of stroma
– Increased glycogen in endometrial cells
Normal Menstrual Cycle
• Average age of Menarche is 12.7 (Tanner 4)
– Ovulation occurs in 50% of girls one year post
menarche and in 80% by two years
•
•
•
•
21-40 days long
2-8 days of bleeding
20-80cc blood loss
Once cylic menses established it is still normal to
have an occasional anovulatory cycle
Anovulatory Cycles
• Normal up to gynecologic age of 2-3 years
• Cycles may be long (8-12 weeks)
– If sexually active may be worried about pregnancy
• Cycles often short (2-3 weeks)
Secondary Amenorrhea
• Secondary Amenorrhea
– No period for 12-18 months after menarche
– Absence of three menstrual cycles in the teen who has already
established regular cyclic menses
• Oligomenorrhea
– Uterine bleeding at prolonged intervals (41days –3months) with
normal flow/duration and quantity
• Same differential/evaluation for secondary amenorrhea
and oligomenorrhea
Normal Menses
• Dependant on an intact hypotalamic-pituitaryovarian-uterine axis
• Disruption of this axis at any level can lead to
amenorrhea/oligomenorrhea
Hypothalamic causes of Secondary
Amenorrhea
•
•
•
•
•
•
•
•
•
Pregnancy
Medications
Endocrinopathies
Eating disorders
Tumors/Infiltrative process/Infections
Chronic disease
Exercise
Stress
Idiopathic: abnormal GnRH, Kallman’s syndrome:
hypogonadotropic hypogonadism (low FSH/LH) anosmia
Endocrinopathies
• PCOS: chronic anovulation/hyperandrogenism
• HAIR-AN
Insulin
LH
Estrogen
FSH Normal/Low
Androgen
Theca Cells
Endocrinopaththies
• Thyroid Disease
• Cushings
• Late Onset Congenital Adrenal Hyperplasia
– Primarily 21 hydroxylase deficiency
Pituitary causes of Secondary
Amenorrhea
• Tumor
• Infiltrative
• Nonneoplastic lesions
– Sheehan’s Syndrome: pregnancy related
– Simmonds Disease: non pregnancy related
– Aneurysm
Ovarian and Uterine causes of
Secondary Amenorrhea
• Premature Ovarian Failure
–
–
–
–
Menopause before age 35
Associated with autoantibodies
Increase in thyroid/adrenal disease
Post chemotherapy/radiation
• Asherman’s Syndrome
Secondary Amenorrhea
History
•
•
•
•
•
•
•
•
•
•
•
Menstrual History
Sexual History
Past Medical History/Surgical History
Family History
Headaches
Galactorrhea
Nutritional Status/Dietary History
Androgen excess/Symptoms of Thyroid Disease
Stress
Exercise
Medications
Secondary Amenorrhea
Physical Exam
•
•
•
•
•
•
•
•
Vital Signs/Ht/Wt/BMI
Tanner Stage
Goiter
Signs of androgen excess: hisuitism, cliteromegly, acne,
hair loss
Galactorrhea
Anosmia
Signs of systemic disease
Consider pelvic in sexually active teen
Secondary Amenorrhea
Laboratory Evaluation
•
•
•
•
Rule out pregnancy
FSH/LH
TSH
Consider: Prolactin, DHEAS, Testosterone, 17 –
OHP, Cortisol
Secondary Amenorrhea
Evaluation
• If HCG is negative give progesterone challenge
• + withdrawl bleed
– endometrium has been primed with estrogen
– Suggests anovulation/does not identify the cause
• - withdrawl bleed
– Hypoestrogenemia : CNS lesion, Ovarian failure,
anorexia, Turner’s mosaic
– Endometrial damage: Asherman’s
Secondary Amenorrhea
Treatment
• Treat precipitating cause if it is identified
• If due to anovulation induce uterine bleeding
every 6-8 weeks or place on birth control because
of increased risk of endometrial cancer and
anemia secondary to DUB
• Encourage need for birth control if sexually active
• Refer to specialist when indicated
Etiology of Excessive Vaginal
Bleeding in Teens
• Dysfunctional Uterine Bleeding
-Etiology of >95% excessive vaginal bleeding in
perimenarchal teens w/ normal hemoglobin and
normal physical exam
• Usually due to anovulation
• Diagnosis of exclusion
Dysfunctional Uterine Bleeding
• Irregular, prolonged, excessive, unpatterned
painless bleeding
• Anovulatory cycle
• Endometrial in origin
• No structural or organic pathology
Differential Diagnosis of Excessive
Vaginal Bleeding
• Complications of Pregnancy
– ectopic, threatened abortion, hydatiform mole
• Infections
– cervicitis, PID
• Endocrine Disorders
– hypothyroidism, PCOS, late onset CAH, cushings,
androgen producing tumor, prolactinoma
Differential Diagnosis of Excessive
Vaginal Bleeding
• Blood Dyscrasias
– ITP, VWD, Glanzman’s disease, SLE, leukemia liver/renal
failure, inherited clotting deficiencies, vit K deficiency
• Ovarian Masses
– hormonally active cysts, tumor, polyps
• Trauma/foreign body
• Medications
– contraception
DUB in Adolescents
• History often unreliable
• Hormonal therapy almost always works
• Curettage rarely necessary
DUB in Adolescents
•
•
•
•
•
•
•
•
•
•
History
Gynecological Age
Menstrual History
Sexual Activity
Method of Contraception
Presence of Pain
Nausea/breast tenderness
Dizziness
Symptoms of endocrinopathies
Other Bleeding History
Medications
DUB in Adolescents
physical exam
•
•
•
•
•
Vital signs
Pallor
Bruising/Petechiae
Murmur/Tachycardia
Evaluation for endocrinopathies-hirsuitism,
acne,cliteromegaly, goiter, visual fields,
acanthosis, galactorrea
• Pelvic exam if sexually active
Lab Evaluation
•
•
•
•
HCG
CBC: hemoglobin and platlets
GC/Chlamydia
LH/FSH, TSH, 17- OHP, Prolactin, Testosterone,
DHEAS
• If Hemoglobin less than 10
– PT/PTT, Von Willebrand’s Ag, Ristocetin Cofactor, Factor
X111 and 1X, Platlet aggregation studies
– Referral to Hematology
Mild DUB in Adolescents
hemoglobin >11
•
•
•
•
•
•
Reassure
Iron supplementation
Menstrual calendar
Phone follow-up in one week
Follow-up 3 months unless continues bleeding
Contraception if sexually active
Moderate DUB in Adolescents
Hemoglobin 9-11
• Low dose monophasic OCP
–
–
–
–
2-4 tabs a day until bleeding stops
Then once a day
Allow withdrawal bleed when Hemoglobin >11
Cycle for at least 6 months
• Iron when on one OCP/day
• Progesterone only pills: Aygestin better than Provera
• Close follow-up
Severe DUB in Adolescents
Hemoglobin < 9 and/or Massive Hemmorhage
•
•
•
•
•
•
•
Hospitalize
Fluid resuscitation
Blood transfusion rarely needed
Premarin 25mg IV q 4-6 hours (max 4 doses)
Monophasic OCP q6h then tapered to qd
Iron
Continue OCP 6 months
Etiology of Acute Menorrhagia
Requiring Hospital Admission
Other
7%
Primary Coagulation
Disorder-19%
DUB-75%
DUB in Adolescents
Goals
•
•
•
•
•
Correct hemodynamic imbalance
Prevent uncontrolled bleeding loss
Correct anemia
Replace iron storees
Encourage contraception for the sexually
active teen
Primary Amenorrhea
• Primary Amenorrhea
–
–
–
–
No uterine bleeding by age 16
No secondary sex characteristics by age 14
SMR5 for one year and no uterine bleeding
No uterine bleeding four years after breast
development
Etiology of Primary Amenorrhea
• Primary amenorrhea w/o breast development but
w/ normal genitalia
–
–
–
–
Turner’s Syndrome/Mosaicism
Structurally abnormal X chromosome
Gonadal dysgenesis
17 alpha hydroxylase deficiency (normal
stature,hypertension, hypokalemia, sexually infantile)
– Hypothalamic failure due to inadequate GnRH
Etiology of Primary Amenorrhea
• Primary amenorrhea w/ breast development (SMR
4) but absent uterus
– Testicular Feminization
– Congenital absence of the uterus (Rokitansky
Syndrome). Associated with renal and skeletal
anomolies
Etiology of Primary Amenorrhea
• Primary amenorrhea w/o breast development and
w/o uterus
– RARE
– Usually male karyotype w/ elevated gonadotropin
levels and low testosterone. Produce enough MIF to
inhibit develpoment of female internal genital
structures (17,20-lyase deficiency, agonadism, 17
alpha hydroxylase deficiency w/ 46XY karyotype)
Etiology of Primary Amenorrhea
• Primary amenorrhea w/breast development
(SMR4) and w/ uterus
– Same evaluation as for secondary amenorrhea
– Imperforate Hymen
– Turner’s Mosaic
Primary Amonorrhea
Physical exam
• Blood Pressure/Height/Weight
• Tanner stage
• Signs of gonal dysgenesis: Webbed neck, low set ears,
broad shieldlike chest, short fourth metacarpal
• Pelvic exam
– Imperforate hymen
– Transverse vaginal septum
– Absent uterus
Primary Amenorrhea
Evaluation
•
•
•
•
FSH/LH
Testosterone
Karyotype
Pelvic Ultrasound
Primary Amenorrhea
Treatment
• Turner’s Syndrome
– growth hormone first
– estrogen replacement later
• Rokitansky Syndrome
– vaginoplasty
• Testicular Feminization
– remove gonads
– Estrogen replacement
– Vaginoplasty
• Enzyme Defects
– hormone replacement
– remove gonads if Y chromosome is present