NOTES FOR UNDERGRADUATES AND POSTGRADUTES IN GYNE

1. DR.PRIYA SAXENA

2.  DEFINITION:
 Defined as the occurrence of three or more consecutive spontaneous
abortions before 20 weeks of gestation ( 24 weeks in UK, 28 weeks in
India)

3.  Genetic factors
 Anatomic factors
 Endocrine factors
 Infectious
 Immunological
 Other factors

4.  Genetic factors:
 Chromosomal: most common balanced translocation
 Single gene defects
 Multifactorial
 Anatomical factors:
 Congenital
o Incomplete mullerian fusion or septum resorption
o DES exposure
o Uterine artery anomalies
o Cervical incompetence

5.  Acquired
o Cervical incompetence
o Synechia
o Leiomyoma
o Adenomyosis
 Endocrinal factors:
 Luteal phase insufficiency
 PCOS
 Other androgen disorder
 Diabetes mellitus
 Thyroid disorder
 Prolactin disorder

6.  Infectious factor:
 Bacteria
 Virus
 Parasites
 Zoonotic
 Fungal
 Immunologic factors:
 Cellular mechanism
o Suppressor cell or factor deficiency
o Alteration in major histocompalibility antigen expression
o Hormonal-progesterone,estrogen,androgen alteration
o Tryptophan metabolism

7.  Humoral mechanism:
o Antiphospholipid antibody
o Antithyroid antibody
o Antisperm antibody
 Thrombotic factors:
 Heritable thrombophilias
o Single gene defects
o Antibody mediated thromboses
 Other factors:
 Altered uterine receptivity
 Environmental
o Toxins
o Illicit drugs
o Cigarette and caffeine

8.  Placental abnormality(circumvallate,marginate)
 Maternal medical illness(cardiac,renal,hematologic)
 Male factors
 Exercise
 Dyssynchronous fertilization

9.  History:
 Pattern, trimester and characteristic of prior pregnancy loss
 History of subinfertility or infertility
 Menstrual history
 Prior or current gynecologic or obstetric infection
 Signs or symptoms of thyroid, prolactin, hyperandrogenic disorder
 Personal or familial thrombotic history
 Features associated with APLA
 Other autoimmune disorders
 Medications
 Environmental exposure, illicit drugs
 Family history of RPL, obstetric complication or any syndrome
associated with fetal loss
 Previous diagnostic tests and treatment

10.  General physical examination:
 Obesity
 Hirsutism/acanthosis
 Thyroid examination
 Breast examination/galactorrhea
 Pelvic examination:
o Anatomy
o Infection
o Trauma
o Estrogenization
o masculinization

11.  Laboratory:
 Parenteral peripheral blood karyotype
 Chromosome testing on products of conception
 HSG, TVS, sonohysterography, hysteroscopy/laparoscopy if indicated
 TSH level, serum prolactin level if indicated
 Anticardiolipin antibody levels
 Lupus anticoagulant
 CBC with platelets
 Factor 5 leiden, homocysteine level, Protein S activity
 Protein C activity, antithrombin level if personal or family history of
venous thromboembolic events

12. CAUSE TREATMENT
GENETIC CAUSES:
Recurrent aneuploidy Not available
Parental balanced translocation genetic counselling
ENDOCRINE CAUSES
Thyroid dysfunction Treat hypo or hyperthyroidism
Diabetes Treat diabetes with insulin
Inadequate luteal phase Natural micronized
progesterone,clomiphene,low dose
FSH
PCOD Laparoscopic diathermy to ovaries in
selected resistant cases

13. CAUSE TREATMENT
ANATOMICAL CAUSES
Fibroids(rare cause) myomectomy in selected cases
Uterine anomalies Resection of septum
hysteroscopically or on laparotomy
Asherman’s syndrome synechiolysis
Cervical insufficiency or
incompetence
Cervical cerclage
IMMUNOLOGICAL CAUSES
Anti-phospholipid antibody
syndrome
Low dose aspirin 75mg daily and
injection heparin 5000 units s/c twice
daily or LMWH 40mg im daily from
the time of appearance of fetal heart
activity upto 34 weeks.Benefit of
immunotherapy is not yet proven

14. THANK YOU