1) First trimester fetal death refers to death of the fetus before 12 weeks of gestation, often called a miscarriage. About 80% of spontaneous pregnancy losses occur in the first trimester. 2) Chromosomal abnormalities account for about 50% of first trimester losses, with the most common being trisomy 16, monosomy X, and translocations. Other causes include diabetes, thyroid disorders, infections, and luteal phase defects. 3) Diagnosis involves history, ultrasound to check for cardiac activity, and beta-hcg levels. Management depends on stability of the woman and includes expectant, medical, or surgical options. Recurrent losses should be further evaluated and treated.

1. DR. Archana Rathore

2. DEFINATION
First-trimester fetal death: Death of the
fetus in the first 12 weeks of gestation
 Many prefer miscarriage to refer to
spontaneous fetal loss before viability.
 Use of sonography and measurement of
serum human chorionic gonadotropin levels
allow identification of extremely early
pregnancies whose failure to be termed as
early pregnancy loss or early pregnancy
failure.

3. incidence
Of all pregnancies diagnosed from β-HCG
measurements 31% are lost.
 Preclinical or silent-22% (2/3rd)
 Clinical-12% (1/3rd)
About 80% of spontaneous pregnancy
losses occur in the first trimester; the
incidence decreases with each
gestational week.
Most of these occur <8 weeks.

4. classification
Can be classified as
 Anembryonic gestation
 Preclinical (2/3rd)
Biochemical pregnancy loss
 Clinical(1/3rd)
Natural course of 1st trimester IUD
 Missed abortion
 Incomplete abortion
 Complete abortion
 Inevitable abortion
 Septic abortion

5. Missed abortion
 Presence of definitive
embryo without cardiac
activity
 Expelled spontaneously in
about 4 weeks
 Now readily diagnosed by
USG
CRL ≤ 6 mm: viability
uncertain, rescan in 7-10
days
CRL > 10 mm: delayed
miscarriage
 50% due to chromosomal
abnormality

6. Anembryonic gestation (blighted ovum)
 An intrauterine sac
without fetal tissue
present at more than
7.5 weeks of gestation
 USG criteria
MSD ≤20 mm: viability
uncertain, rescan in 7-10
days
MSD >20 mm: blighted
ovum
 Accounts for ½ of
pregnancy loss

7. causes
 Chromosomal abnormalities
 Luteal phase defects
 Thyroid disorders
 Diabetes mellitus
 Asherman syndrome
 Infections
 Others
 Contraceptives
 Smoking
 Alcohol
 Radiation
 Trauma
 Drugs

8. Chromosomal abnormality
Autosomal trisomy
 50% of all chromosomal anomalies
 M.C. is trisomy 16
Polyploidy
 Normosaic triploid/ tetraploidy
Results in partial mole
Tetraploidy non viable
 Diploid/triploid mosaicism
Sex chromosome polysomy
 Frequency increased in ICSI

9. Monosomy X
 Single most common
chromosomal cause (15-
20%)
 Maternal age not
contributory
 80% of Monosomy X
abort rest are live born
with turner’s syndrome.

10. Autosomal Monosomy
Translocations
Inversions
Mendelian or polygenic factors
 30-50% of 1st trimester pregnancy loss
showing no chromosomal abnormalities
 Abortus have isolated structural defects
 Confined placental mosaicism- mosaicism
restricted to placenta
 Uniparental disomy- due to trisomic
rescue

11. Luteal phase defects
Defn.- Lag of >2 days in histologic
development of Endometrium to day of
menstrual cycle.
Mechanism
 Inadequate progesterone secretion due to
deficient action of corpus luteum
 Endometrium not responsive to progesterone
 Estrogen primed endometrium unfavorable for
implantation
 Early & recurrent pregnancy loss

12. Causes
 Hypothalamo-pituitary-ovarian axis
Decreased FSH
Abnormal pattern of LH secretion
Decreased LH & FSH surge at ovulation
 Hyperprolactenemia
 Hypothyroidism
 Ovarian
PCOS
Ruptured corpus luteum
 Uterine
Fibroid
Uterine septa
Endometriosis

13. Diabetes mellitus
Risk increases with loss of metabolic
control measured by HbA1c
Also with increased insulin resistance or
serum insulin levels
If diabetes is controlled in 1st 21 days of
conception & maintained throughout
pregnancy, abortion risk become
equivalent to non diabetic controls but
risk of congenital malformation remains
unchanged.

14. Influence of hyperglycemia
 Implantation-inhibits trophoectoderm
differentiation
 Embryogenesis- increases oxidative stress
affecting expression of critical genes
essential for embryogenesis
 Miscarriage- increases premature
programmed cell death of key progenitor
cells of blastocyst
 Organogenesis- activates the diacylglycerol-
protein kinase C cascade increasing
congenital defects

15. Thyroid disorders
Hypothyroidism
 Thyroid peroxidase negative
Hyperthyroidism
 TSH 2.5-4 mIU/ml (3.6%)
<2.5 mIU/ml (6.1%)
Autoimmune thyroidits:
 Thyroid antibodies
Antibody to thyroid peroxidase
Antibody to thyroglobulin

16. Asherman syndrome
Intrauterine adhesions- loss of endometrial
surface area resulting in either failure of
implantation or expulsion of products of
conception on further growth
Causes
 Uterine curettage
 Intrauterine surgery, e.g. myomectomy
 Endometriosis
 PID- tuberculosis, schistosomiasis
 Infections related to intrauterine devices

17. Clinical presentation
 hypo or amenorrhea
 infertility
 repeated miscarriages
Diagnosis
 Hysteroscopy
 Hysterosalpingography (HSG)
 Sonosalpingography
Treatment: hysteroscopic resection

19. infections
Viral
 Parvovirus B19
 Cytomegalovirus
 Variola
 Varicella
Bacterial
 Ureaplasma
 Chlamydia
Parasitic
 Toxoplasma
 Malaria
Infections causing
fever
 Salmonella
 Shigella
 E.coli

20. diagnosis
Presenting complaints
 Amenorrhea
 Bleeding PV
 Passage of clots
 Passage of tissues
 Pain in abdomen
 Discharge PV
 Fever, chills, rigors

21. Past history
 Previous pregnancy loss
& their timing
 Uterine surgery
 Any febrile illness
 Stillbirths
 Malformed babies
 Big size baby
 Infertility
Menstrual history
 Regularity of cycles
 Any shortening of
cycles

22. Personal history
 Age
 Hypertension, diabetes mellitus, thyroid
disorders
 Contraceptive use
 Drug intake
 Alcohol & smoking
 Exposure to radiation
Family history
 Diabetes mellitus
 Genetic disease

23. Examination
 Pallor
 Temperature
 Pulse
 Blood pressure
 Tachypnea /dyspnea
 Body mass index
 Neck swelling
 Galactorrhea
 P/A
Abdominal distension
Abdominal tenderness
Enlarged irregular
shaped uterus
 P/S
 Status of os
 Bleeding
 Discharge
 POC’s in vagina
 P/V
 Uterine size
 Status of os
 Bleeding
 POC’s in cervical canal
 Adnexal mass
 Adnexal tenderness
 Uterine tenderness

24. Investigations
 Hemoglobin
 Blood group & Rh typing
 Peripheral smear for TLC, DLC
 Platelet count
 BT, CT, CRT
 Sickling
 Coagulation profile
PT
aPTT
Fibrinogen level
 Blood culture
 Intrauterine products culture

25. Confirmation
 USG- normal findings
5 wks- empty GS- MSD 10mm
5.5 wks- GS with yolk sac
6 wks- heart beat- embryo 3 mm- MSD 16 mm
6.5 wks-CRL 6mm
7 wks-CRL 10 mm
8 wks- CRL 16 mm- amniotic sac- fetal body
movements
 β-HCG
1500(3000) U/ml- TVS(TAS) shows GS
2X in 48 hrs- normal intrauterine pregnancy
Fall- miscarriage
Low value or <2X rise- extrauterine pregnancy
High value- twin pregnancy or H. mole

26. Criteria for predicting non viability
 Sac size (Nyberg criteria)
 >20(8-TVS) mm without yolk sac
 >25(16-TVS) mm without embryo
 Failure of sac/embryo to grow at expected
rate (1.1 mm/day)
 Embryo of 10 mm without cardiac activity
 Loss of cardiac activity previously present
 Failure of rise in β-HCG levels at expected
rate (2X in 48 hrs)
 Yolk sac >6 mm with abnormal morphology

27. Specific Investigations
Thyroid
 Sr. TSH levels
 Sr. fT4 levels
Diabetes
 Blood sugar levels
 HbA1c levels
 Sr. insulin levels
Infections
 IgM, IgG antibodies
 HRP-2

28. Chromosomal abnormalities
 Products of conception
Histopathology
Culture
Karyotyping- FISH, array CGH, 24 chromosome
SNP
 Placenta- karyotyping
 Parents- karyotyping

29. management
Hemodynamically
stable
• Patient’s choice
• Expectant
• Medical
• Surgical
Hemodynamically
unstable
• Stabilize vitals
• Arrange for
blood
• surgical
Septic abortion
• Broad spectrum
i.v. antibiotics
• surgical
expectant
• Wait and watch
• Up to 7 days
• No intervention
medical
• Misoprost
induction
surgical
• Manual vacuum
aspiration
• Electric vacuum
aspiration
• Dilatation &
evacuation

31. Prenatal counseling
 Early registration
 Repeat abortion
 Congenital malformation
 Diet control
 Regular follow up
 Assisted reproductive techniques
 Folic acid administration 3 month before
conception
 Investigations and management accordingly

32. Prenatal investigations
 HbA1c
 TSH
 Chorionic villous biopsy
 Trophoectoderm biopsy
 Preimplantation genomic diagnosis (PGD)
 Luteal phase defects
Basal body temperature (BBT) chart
Follicular size USG
Sr. Progesterone level
• At D21 <10 ng/ml
• 3 measurements within D5-D9 after ovulation-
total <30 ng/ml, pooled concn. <9 ng/ml
Luteal phase endometrial biopsy
Sr. prolactin level

33. Management
 Control of diabetes
 Control of thyroid disorders
 LPD
GnRH agonists
Clomiphene citrate
Progesterone support
• Oral
• Intramuscular
• Vaginal suppositories
• Vaginal gel
Bromocriptine