BAD OBTETRIC HISTORY

1. The stories that end
badly are sad, sadder
still are the ones that
never began….

2. Definition
The term “bad obstetric history” is
often used to those patients in whom
the obstetrical future is likely to be
modified by the nature of the
previous disaster.

3. WHO definition
BOH implies previous unfavourable
fetal outcome in terms of 2 or more
consecutive spontaneous
abortions,H/o Intrauterine fetal
death,Intrauterine growth
restriction,,Still Birth,early neonatal
death and/or congenital
anomalies.

4.  What can be construed as BOH?
 1st or 2nd trimester miscarriages
 Still births or neonatal deaths
 Pre-term labour
 Fetal anomalies
 If neonatal loss is due to non obsterical reasons like
diarrhoea,fever….they are not included in BOH.

5. VARITIES

6. Bad Obstetric History
May be due to-
1.Still Birth
2. Small Weight Baby
3. Prolonged Labour
4. Intrauterine Death
5. Recurrent Pregnancy Loss

7. 1.STILL BIRTH
 Birth of newborn after period of viability (weighing
1000gm or more) when the baby does not breath
or show any sign of life after delivery.
 They include-Antepartum death
Intrapartum death
Cause-
Birth asphyxia and Trauma
Pregnancy Complications(pre eclampsia, placental
abruption)
Fetal congenital malformations

8. 2.LOW BIRTH WEIGHT BABY
PRETERM LABOUR
(AGA)
 Maternal and Fetal stress
 Infection
 Abnormal placentation
 Bleeding in
Choriodecidual space
 Uterine abnormalities
 Cervical abnormalities
IUGR
(SGA)
 Placental insufficiency
 Chronic medical
conditions
 Fetal chromosomal
abnormalities
Trisomy 18
 Fetal infections

9. EFFECT-
 Asphyxia
 Hypothermia
 Pulmonary syndrome-Pulmonary edema,Intra-
alveolar haemorrhage,Respiratory distress
syndrome
 Cerebral haemorrhage
 Fetal shock
 Heart failure
 Dehydration and acidemia

10. 3.PROLONGED LABOUR
FAULT IN
POWER
Abnormal uterine
contraction-
Uterine inertia
Inco-ordinate
contraction
FAULT IN
PASSAGE
Contracted pelvis
Fetopelvic
disproportion
Cervical dystocia
Pelvic tumour
FAULT IN
PASSANGER
Malposition
( Occipito-Posterior)
Malpresentation
(Face,Brow)
Congenital
anomalies in fetus
(Hydrocephalus)

11. May Cause-
 Fetal Hypoxia
 Intrauterine Infection
 Intracranial stress or Haemorrhage
Labour should be monitored with Partograph.

12. 4.INTRAUTERINE FETAL
DEATH
 Antepartum Death before labour
Intrauterine growth restriction
Hypertensive disorder of Pregnancy
Diabetes mellitus
Chronic Hypertension
Rh incompatibility
Syphilis
Congenital malformations

13. 5.RECURRENT PREGNANCY
LOSS
 Three or more consecutive spontaneous
pregnancy loss

14.  Early pregnancy loss before 12 wk
 Late pregnancy loss after 12 wk
 Pulseless embryo -5 mm or more in CRL
 Gestational Sac->8mm without a yolk sac
 Gestational Sac- >16mm without an embryo

15. Recurrence suggests
a persistent cause
(not just a bad luck)
which must be identified and treated
Ohh….No..

16. Causes of Recurrent
Pregnancy loss
 Genetic/Chromosomal
 Anatomical-Mullerian abnormality,cervical
incomptence
 Endocrinal
 Hypertensive disease
 Rh Isoimmunisation
 Thrombophilia-Antiphospholipid antibody
syndrome
 Unexplained

17. When To Start Investigating?
 Ideally after 3 losses but earlier if high risk pt,
elderly, with medical disorders and known family
history.
 How to Investigate ?
 Investigate commoner and treatable causes first.

18. History
 Menstrual history
 Past Obstetric History-
 Gestational age at time of pregnancy loss
1st trimester-Genetic,Endocrinal
2nd trimester-Anatomical,Cervical incomptence
 Mode of delivery
 Delivery conducted by whom?
 H/o instrumental delivery
 H/o Still birth-
H/o meconium stained liquor
H/o loss of fetal movement
Type – Fresh/ Macerated

19.  H/o Preterm labour-
H/o spontaneous or induced abortion or preterm
delivery
Pregnancy following assisted reproductive
technique
Recurrent UTI
H/o leaking p/v
H/o genital tract infection
Indicated preterm delivery
H/o medical illness

20.  Prolonged labour-
• contracted pelvis-
H/o fracture,T.B. of pelvic joints or spine
H/o difficult delivery and fundal pressure
H/o early neonatal death or late neurological stigmata
following difficult labour
Maternal injuries-perineal tear,vesico-vaginal or recto-
vaginal fistula
• Congenital anomaly of uterus-
Recurrent malpresentation

21.  H/o Rh isoimmunization
 H/o multiple induced abortions-Curettage-> ASHERMAN
SYNDROME
 H/O medical illness-Hypertension,DM,Thyroid d/s,Heart
d/s,Chronic renal d/s
 H/o congenital malformation in baby

22. One of the biggest obstacle however is the
lack of details in previous pregnancies…
APPROPRIATE DOCUMENTATION HELPS!

23. Examination
 Physical examination-
Stature
Deformities of pelvic bone,hip joint,spine
Anaemia,Hypertension,Edema,Jaundice,Thyroid d/s
 Abdominal examination-
Pendulous abdomen sp. In primigravida-Inlet contraction
Obstetric examination-Fundal height,engagement of head
before onset of labour
 Vaginal examination-helps to diagnose cervical incomptene
infections

24. Investigations for
Recurrent Miscarriages
1 Complete blood count
2 Thyroid function test
3 Glycosylated Hb
4 Hormone profile
5 Lupus anticoagulant
6 Anticardiolipin antibodies
7 Rubella status
8 Thrombophilia screen
9 Pelvic ultrasound
10 Hysterosalpingography
11 Karyotyping

25. A.Hypertensive disorder
Hypertensive disorder of pregnancy
 Gestational Hypertension
 Pre eclampsia
 Eclampsia
Chronic Hypertension

26. Diagnosis
 Regular antenatal checkup
 Regular BP monitoring
 Excessive weight gain and Edema
 Urine protein estimation if BP is 140/90 mmhg or
more
Proteinuria –
 300mg/L or more in 24 hr urine collection
 1+ or more by qualitative estimation
Significant –Protein/Creatinine-≥0.3
 Other signs and symptoms-Headache,Epigastric
or right upper quadrant pain,visual symptoms

27. Prediction of Pre
Eclampsia
 Roll over test-Increase in BP ≥20mmHg from lateral
to supine posture
 Urine Calcium ≤12mg/dl in 24 hr collection
Calcium/Creatinine <0.06
 Angiotensin Stress test
 Plasma Fibronectin-↑
 Uterine artery Doppler-BEST

28. Pre-
eclampsia

29. Management
Pre-
eclampsia
(aspirin)
(NICE clinical guideline 107:
Hypertension in pregnancy)

30. • Halve the risk of pre-
eclampsia and
reduce serious
morbidity and death
in women at high risk
and with low dietary
intake
• High dose-2 gm/day
• Starting since 16wk GA
Pre-
eclampsia
(calcium)

31. B.Endocrine factors
1)Diabetes mellitus
 Recurrent spontaneous abortions
 Preterm labour
 Infections-Chorioamnionitis
 Pre eclampsia
 Polyhydroamnios
 Fetal Macrosomia
 Congenital malformations-
 Sudden IUFD
Each category of BOH can be caused by DM

32. Screening for Gestational
DM
 50 gm oral glucose is given without regard to time
of day or last meal,b/w 24-28 wk of
pregnancy.venous plasma glucose is measured
1 hr later.
 If ≥140mg /dl – Do Glucose Tolerance Test
 if ≥200mg/dl- Diabetic

33. Upper limit of Normal for 3 hr
Glucose Tolerance Test during
pregnancy after 100 gm glucose
load
Fasting 95mg/dl
1 hr 180mg/dl
2hr 155mg/dl
3hr 140mg/dl

34. Criteria for diagnosis with 75gm oral
glucose
TIME NORMAL IMPAIRED
GLUCOSE
TOLERANCE
DIABETES
MELLITUS
FASTING <100mg/dl 100 to
<126mg/dl
≥126mg/dl
2 HR POST
PRANDIAL
<140mg/dl 140 to
<200mg/dl
≥200mg/dl

35. Objective of treatment
Time Plasma glucose(mg/dl)
Fasting <95
PrePrandial <110
1hr PostPrandial <140
2hr PostPrandial <120

36.  Oral hypoglycemic drug-
Glyburide-increase release of insulin
decrease insulin resistance
 Insulin

37. Delivery
Low risk
GDM(adequate
control with diet
alone)
 Spontaneous labour
 Reaches 40 wk-
Induction
 EFW>4000gm-C.S.
High risk GDM(pt on
Glyburide and/or
Insulin)
 Induction at 38 wk
 >4000gm-C.S.

38.  Capillary blood glucose is measured every 2-4 hr
during labour
 If above normal-Regular insulin or low dose i/v
insulin to maintain blood glucose 100-120mg/dl

39. 2)Thyroid disease
Poorly controlled Hypothyroidism and
Hyperthyroidism
Abortion
Placental abruption
Preeclampsia
Stillbirth
Prematurity
IUGR

40. Diagnosis
 Sign and Symptoms
 Clinical examination
 Estimation of
TSH,FT3,FT4
s.TSH should be repeated at interval of 6-8 week.
Antithyroglobulin,Antimicrosomal antibodies,Thyroid
stimulating immunoglobulin
 USG of fetal thyroid gland – if mother is taking
antithyroid drugs
 Cord blood should be taken for TSH and FT4-
neonatal hyperthyroidism.

41. Treatment
 Hyperthyroidism-
Propylthiouracil(300-450 mg daily po)
Carbimazole(10-40mg daily PO)
S/E-Fetal goiter,hypothyroidism
 Hypothyroidism-
Levo-thyroxine(0.1 mg/day)

42. c.Acquired / Inherited
Thrombophilia
Acquired
 Antiphospholipid
syndrome
Inherited
 Protein C deficiency
 Protein S deficiency
 AT deficiency
 Activated protein C
resistance
 PT gene mutation

43. Antiphospholipid antibody
syndrome (APLA)
 Antiphospholipid syndrome (Hughes syndrome) is a
disorder of immune system ,characterised by
excessive clotting of blood ,thrombocytopenia & /or
adverse pregnancy outcomes
 an acquired autoimmune thrombophilia

44.  Mechanism of disease
 Inhibition of TROPHOBLASTIC function and
differentiation
 Activation of complement pathways at the
maternal-fetal interface resulting in a local
INFLAMMATORY response
 Thrombosis of utero-PLACENTAL vasculature
in later pregnancy

45. Presentation
 Recurrent pregnancy loss
 Unexplained second or third trimester loss
 Early onset severe preeclampsia
 Arterial or venous thrombosis
 Unexplained fetal growth restriction
 Prolonged coagulation studies
 Autoimmune diseases
 Cardiac valvular diseases
 Neurological disorders
 Thrombocytopenia

46. Sapporo Criteria
At least 1 clinical and 1 lab criteria)
At least one clinical criteria and one laboratory criteriaClinical Laboratory
Thrombosis ≥1 documented episodes of:
 Arterial
 Venous and/or
 Small vessel thrombosis
ACA ACA of IgG and/or IgM
isotype in medium/high titre
(> 40 IU) or >99th percentile
Pregnancy
morbidity
(WILSON
CRITERIA)
≥1 unexplained fetal deaths of ≥ 10
weeks POA
(morphologically normal fetus)
LA Detected
≥1 premature births of ≤ 34th week
POA d/t:
Severe PE or
Placental insufficiency (IUGR)
(morphologically normal neonate)
Anti-
beta2-
glycopr
otein
>99th percentile
≥3 unexplained consecutive
spontaneous abortions < 10 week POA
* On 2 or more occasions
At least 6 weeks apart

48. Treatment of APLA
Syndrome
 Prophylactic Heparinization-
 UFH- 1st TM-5000U SC twice daily
2nd TM-7500U SC twice daily
3rd TM-10000U SC twice daily
 LMWH- 40 mg SC twice daily
 Low dose ASPIRIN-75 mg PO daily

50. D.Infections
 Bacterial vaginosis-MC cause of vaginal
discharge
 Ureaplasma urealyticum
 Mycoplasma hominis
 TORCH infection
 UTI

52. Bacterial Vaginosis
Vaginal infection involving loss of normal lactobacilli
and an overgrowth of anaerobes,such as
Gardenella vaginalis,Bacteroides,Mycoplasma
hominis and Peptostreptococci.
Effects-
Chorioamnionitis
Preterm premature rupture of membrane
Preterm labour
Low birth weight

53.  Syphilis-
Ascending pattern
More recent the maternal infection,more severe
the congenital disease

54. DIAGNOSIS
 Clinical examination
 Blood Counts
 VDRL
 HIV
 Urine-
Routine,Microscopy
 Urine-Culture,Senstivity
 Vaginal-
Culture,Senstivity
TREATMENT
 Antibiotics

55. Diagnostic criteria for diagnosis of
Bacterial Vaginosis
A. Homogenous vaginal discharge
B. Asymptomatic-
AMSEL CRITERIA (at least 2 of the following)
1.Presence of clue cells
2.Whiff test
3.Vaginal pH>4.5
4.Absence of normal vaginal lactobacilli
5.DNA Probe test
6.PCR quantification

56. Treatment
 Oral Metronidazole 400 mg TDS* 5 -7DAYS
 Oral clindamycin 300 mg BD* 7 days
 Lactobacilli vaginal pessary/gel/suppository

57. E.Anatomical factors
 15 to 16% of women with RPL have
uterine abnormalities.
 2nd trimester pregnancy loss and preterm
delivery

58. Anatomical factors
Congenital
• Mullerian Abnormalites
(septa, bicornuate,
didelphus)
• DES exposure (T shaped
uterus, +/- cervical
changes)
• Incompetent cervix
Acquired
• Fibroids.
• Endometrial polyps,
• Intrauterine adhesions
• Incompetent cervix

59. MULLARIAN ANOMALIES
CLASS ANOMALY
1 Segmental,mullerian agenesis-Hypoplasia
A. Vaginal
B. Cervical
C. Fundal
D. Tubal
E. Combined
II Unicornuate
A. Communicating
B. Noncommunicating
C. No cavity
D. No horn
III Didelphys
1V Bicornuate
A. Complete(division down to internal os)
B. Partial
V Septate
A. Complete
B. Partial
VI Arcuate
VII Diethylstillbestrol related

61. Early Pregnancy Loss-
Septate Uterus
Bicornuate Uterus
D/t inadequate blood supply to conceptus
Preterm Labour-
Didelphus
Unicornuate
Occuring later with each successive pregnancy

62. Diagnosis
 History
 USG
 Hysteroscopy
 Laproscopy
 MRI
Treatment
 Hysteroscopic resection
of uterine septum

63. Fibroid
Submucous
The mechanism –
•congestion and dilatation of
endometrial venous plexus
•Atrophy and ulceration of
endometrium over submucous
fibriods
•Distortion of uterine cavity
•Poor endometrial
receptivity..
•Degeneration with increasing
cytokine production.
•Reduced space for growing fetus

64. Diagnosis
 Sign and symptoms
 Examination
 USG
 Hysteroscopy
Treatment
 Myomectomy
 Hysteroscopic resection
of submucous fibroid

65. Asherman syndrome
 Band like structure b/w walls of uterus,causing
minimal to almost complete obliteration of uterine
cavity.
 Bands are made of fibrous tissue,myometrium and
endometrium which is usually atrophic.

66. Asherman syndrome
Normal uterus Intrauterine
synechiae

67. Diagnosis
 History
 Hysteroscopy
Treatment
 Lysis of intrauterine
adhesion
 Placement of
Intrauterine device to
avoid contact b/w
sectioned ends of
adhesions
 t/t with estrogen to
stimulate endometrial
growth.

68. Cervical
incompetence
Painless cervical dilatation
 Inability of cervix to retain a
pregnancy in the absence
of uterine contractions.

69. Causes of cervical
incompetence
Congenital
 Mullerian tube defects
 Diethylstilboestrol
exposure in utero
 Abnormal collagen
tissue(Ehlers-Danlos
syndrome,Marfan’s
syndrome)
Acquired
 Forceful mechanical
cervical dilatation
 Cervical lacerations
 Cervical cone or LEEP
procedure

70. Diagnosis
 Non pregnant female-
 History of second trimester losses
 No6-8 Hegar dilator can be passed easily
withoout causing discomfort and absence of
internal os snap on its withdrawl.
 Pregnant female-
 cervical length by transvaginal USG is
<25mm.
 Funneling of internal os >1cm
 Funneling of amniotic sac into endocervical
canal.
 Dynamic changes-T-> Y-> U
 Acute presentation

71. Treatment
 Encirclage operation-MC DONALD operation
 Time of Oper-14 wk of pregnancy
or
at least 2 wk earlier than lowest
period of previous wastage,as early as 10 wk.

72. F.Genetic Causes
 50% of 1st trimester losses.
 Type-Chromosome NO.(Aneuploidy)
Structure

73. Aneuploidy
• Trisomy(50%)
Trisomy 16
(most common)
• Monosomy(20%)
• Triploidy(15%)
• Tetraploidy(5%)
Structure
• Translocation
Reciprocal
Robertsonian
• Inversion

76. Now we know.. What
we don’t know…