Bad obstetric history

Bad Obstetric History (BOH)
What to do about it?
By Dr Yong Soon Leong
Supervisor: Dr Haris N Suharjono

Definition
• The term “bad obstetric history” is often
loosely used to signify that a woman has
had previous disappointments in
childbearing.
Donald, I. (1969): Practical Obstetric Problems, 4th ed., p. 99.
London: Lloyd-Luke Medical Books.

Bad Obstetric History
• What can be construed as BOH?
1st or 2nd trimester miscarriages
Still births or neonatal deaths
Pre-term labour
Fetal anomalies?
How about h/o HIE leading to cerebral palsy?
Shoulder dystocia? Massive PPH? Classical
caesarean section?

What to do about it?
• A detailed obstetric history is important.
• Review the previous medical records and any investigation
results.
• Identify any recurrent or non-recurrent causes of
pregnancy loss and put in place a management plan to
reduce or modify the risks in the current or future
pregnancies.
THE AIM IS TO LEARN FROM THE PAST PREGNANCIES
AND ENSURE A MORE FAVOURABLE OUTCOME IN THE
CURRENT OR FUTURE PREGNANCY...

Detailed History
• Consanguinity
• Previous pregnancy performance
• Drug and environmental exposure
• Family history of thrombotic events, pregnancy losses or
complications
• History of infertility
• Symptoms of metabolic disorders, autoimmune disorders

What causes it?
• There are a multitude of possible causes of
BOH…identify the cause and we are
halfway there!
• One of the biggest obstacle however is the lack of details in previous
pregnancies…APPROPRIATE DOCUMENTATION HELPS!

Recurrent causes
Pre-eclampsia
Acquired / Inherited thrombophilia
Parental genetic disorders
Anatomical factors (uterine / cervix)
Endocrine factors
Infection
Rh isoimmunisation

Pre-eclampsia (PET)
• Pregnancy-induced hypertension with significant proteinuria
(>300mg/24 hours)
• Incidence: 2% of pregnancies, 2% will develop eclampsia
• 15% of chronic hypertension developed PET
• Implications:
• IUGR
• Placental abruptio
• Preterm delivery (iatrogenic)

(NICE clinical guideline 107: Hypertension in pregnancy)

Acquired / Inherited
Thrombophilia
Acquired
• Antiphospholipid
syndrome
Inherited
• Protein C deficiency
• Protein S deficiency
• AT deficiency
• Activated protein C
resistance
• PT gene mutation

Antiphospholipid
Syndrome
• Refers to association between antiphospholipid
antibodies and adverse pregnancy outcome or vascular
thrombosis.
• Adverse pregnancy outcome includes
• ≥ 3 consecutive miscarriage < 10 weeks gestation
• ≥ 1 morphological normal fetus losses after 10th week of
gestation
• ≥ 1 preterm birth before 34th week owing to placental
disease

Antiphospholipid
Syndrome
• 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
• Present in 15% of women with recurrent miscarriage.
• Without treatment, live birth rate is as low as 10%.

Antiphospholipid
Syndrome
• Increased risk of recurrent miscarriage, hypertension, pre-
eclampsia, IUGR, fetal death, preterm birth, abruption,
thrombosis
• Risk = Anticardiolipin antibody titre (esp. IgG)
• Thrombosis = Lupus anticoagulant

Antiphospholipid
Syndrome
• Fetal death can follow IUGR, oligohydramnios, pre-eclampsia.
• Risk of IUGR: > 30%
• Increase risk of non-reassuring fetal heart rate pattern in labour
• Pre-eclampsia is often severe.
• Previous recurrent loss: 10%
• Previous thrombosis / late fetal death: 30% – 50%, PET may develop as
early as 15 weeks.
• Preterm birth risk.
• Previous recurrent loss: 10%
• SLE / previous thrombosis / late fetal death: 30% – 40%,

Inherited thrombophilia
defects
• Protein C & S deficiency
• Anti-thrombin III deficiency
• Activated protein C resistance (due to Factor V Leiden mutation)
• Prothrombin gene mutation
• Hyperhomocysteinaemia
• Mechanism:
• thrombosis of uteroplacental circulation

defects – recurrent risk of thrombosis
Protein S
deficiency
Protein C
deficiency
Anti-thrombin III
deficiency

Protein S
deficiency
Protein C
deficiency
Anti-thrombin III
deficiency
15% (12-17%)
25% (22-26%)
35% (32-51%)

Protein S deficiency
Protein C deficiency
Anti-thrombin III deficiency
Activated protein C resistance (due to
Factor V Leiden mutation)
Prothrombin gene mutation
Low
prevalence
in Asians
& Africans

defects
• Adverse pregnancy outcome:
• Pre-eclampsia
• IUGR
• Placental abruption
• Recurrent early miscarriage
• Late fetal demise
• Intrauterine death and stillbirth

Parental genetic
disorders
• One of the parents carries a balanced structural
chromosomal anomaly
• Most commonly a balanced reciprocal or Robertsonian
translocation
• Possible outcome:
• Miscarriage
• Live birth with multiple congenital malformation and/or
mental disability due to unbalanced chromosomal
rearrangement

Anatomical factors
• Uterus
• Congenital uterine malformation
• Arcuate uteri tend to miscarry in second trimester
• Septate uteri more likely to miscarry in first trimester
• Term delivery rate of only 50%
• Acquired: submucosal fibroid, uterine synechiae
• Cervical incompetence
• History of second trimester miscarriage preceded by SROM
or painless cervical dilatation

Endocrine factors
• Diabetes mellitus
• Thyroid disease (anti-thyroid antibody)
• PCOS (due to insulin resistance, hyper-insulinaemia,
hyper-androgenaemia)

Infections
• Bacterial vaginosis
• BV in the first trimester is a risk factor for second trimester
miscarriage and preterm delivery.
• Treatment with oral clindamycin reduces complication rate.
• ? TORCHES
• Not recommended as these diseases do not persist in genital
tract and, patients often symptomatic and were treated
earlier.
• Thus, less likely to cause repeated pregnancy loss

Investigations
Pre-eclampsia
Anatomical factors (uterine / cervix)
Endocrine factors
Infection
Rh isoimmunisation

Pre-eclampsia - prediction
• Identify risk factors at booking
• Extremes of age
• Genetic (increased incidence if mother & sisters affected)
• Primigravida
• Previous history if pre-eclampsia
• Multigravida with new partner
• Obesity
• Essential hypertension
• Pre-existing renal disease
• Antiphospholipid syndrome
• Inherited thrombophilia

Pre-eclampsia IUGR
Previous PET Sensitivity: 100%
Specificity: 60-66%
Sensitivity: 85%
Specificity: 70-77%
Kidney Disease Sensitivity: 50%
Specificity: 75-79%
Sensitivity: 83%
Specificity: 80-84%
Mixed high-risk factors Sensitivity: 78-97%
Specificity: 42-71%
Sensitivity: 84%
Specificity: 39%
*Mixed high risk factors: previous pre-eclampsia, previous stillbirth, previous placental abruption, previous
IUGR, chronic hypertension, diabetes, autoimmune disease, kidney disease, recurrent miscarriage
Uterine artery dopplers at 20-24 weeks

Is uterine artery Doppler velocimetry of
value in the clinical management of women
at high risk of pre-eclampsia / IUGR?
- Still a controversial issue whether to screen in
the first trimester, 20 weeks, 24 weeks?

Investigations
• APS screening (2 positive tests ≥ 6 weeks apart either lupus
anticoagulant / anticardiolipin antibody in a median / high titre over
40 g/l / ml/l or above 99th percentile)
• Lupus anticoagulant:
• Activated partial thrombin time (APTT) vs Dilute Russell
viper venom time (dRVVT)….the latter is more sensitive and
specific
• Thrombophilia screening (Factor V Leiden, Factor II (prothrombin)
gene mutation , Protein S)

Thrombophilia screening
• A history of recurrent, atypical, or unprovoked (not
associated with COC, pregnancy, trauma, or surgery)
thromboembolism
• A family history of thromboembolism
• Universal screening of women with BOH for inherited
thrombophilia? Not recommended, only screen those with
risk factors

Investigations
• Cytogenetic analysis on POC of 3rd & subsequent consecutive
miscarriage
• Parental peripheral blood karyotyping if POC reports unbalanced
strucutural chromosomal anomaly
Anatomical factors (uterine)
• Initial 2D pelvic US ± HSG as screening, combined hysteroscopy +
laparascopy ± 3D US for definitive diagnosis
Anatominal factors (cervix)
• The following investigations are not recommended
• Hysterography
• Cervical resistance index
• Insertion of cervical dilators

Investigations
Endocrine factors)
• Diabetes (HbA1c, Random blood glucose)
• Thyrotoxicosis (thyroid function test, antithyroid antibodies
especially thyroid peroxidase antibodies)
Infection
• Screen for BV: Amsel criteria, take smear at the posterior fornix to
detect BV (please do not take HVS)
Rh Isoimmunisation
• Maternal and paternal blood group and rhesus
• Kleihauer test

POSTCONCEPTION
EVALUATION
• Confirm intrauterine pregnancy, viability
• CVS / Amniocentesis if indicated
• Serial TVS to monitor cervix if incompetence suspected
• Detailed anomaly scan at 20 weeks
• MOGTT at 24-28 weeks and repeated at 32 weeks if negative
• Smear to detect bacterial vaginosis before 20 weeks of
gestation
• Serial scan for fetal growth
• Karyotyping analysis of POC if she aborts / post-mortem
• Monitor cases of Rh isoimmunisation

Management
• 15% reduction in the risk of
PET
delivery < 37 weeks
death (stillbirth,
neonatal/infant death)
• No overall difference in the
risk of PIH, placental
abruption and SGA
Pre-eclampsia
(aspirin)

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

Management
Pre-eclampsia
(aspirin)
Why 75mg?
Can it be higher dose?
The more the better?
The less the safer?

Management
• Halve the risk of pre-
eclampsia and reduce
serious morbidity and
death in women at high
risk and with low dietary
intake
Pre-eclampsia
(calcium)

Management
• magnesium
• folic acid
• antioxidants (vitamins C
and E)
• fish or algal oils
• garlic
• restricting salt intake
Pre-eclampsia
(no role)

Management
• Low dose aspirin + heparin
• Reduce pregnancy loss by 54%
• No difference of efficacy and safety
between unfractionated heparin & LMWH
• LMWH: less risk of thrombocytopenia /
oestopenia
Antiphospholipid
Syndrome
(previous late fetal loss,
neonatal death, adverse
outcome due to pre-
eclampsia, FGR, or
abruption)

Management
• Start low dose aspirin
• Warfarin?
• LMWH?
Antiphospholipid
Syndrome
(prior thrombosis)
LMWH is preferred. But, if risk of thrombosis is not
reduced by LMWH itself, warfarin can be continued but
avoid during 6-12 weeks of gestation by replacing with
LMWH temporarily. This is to avoid risk of fetal warfarin
embryopathy.

Management
• Hydroxychloroquine may
provide some protection from
thrombosis and should be
continued in pregnancy.
Antiphospholipid
Syndrome
(women with SLE)

Management
Antiphospholipid
Syndrome
+
Pre-eclampsia

Management
• Prompt referral to a clinical
geneticist
• Genetic counseling
• Continue to conceive with /
without prenatal diagnosis test,
gamete donation, adoption
• PIGD with IVF
• 50 – 70% chance of a healthy live
birth in future untreated pregnancy
via natural conception, compared
with PIGD + IVF (30%)
Parental genetic
factors

Management
• Congenital uterine malformations
• Insufficient evidence to assess
the effect of uterine septum
resection to prevent further
miscariage
• Open uterine surgery: infertility,
scar rupture during pregnancy
• Uterine fibroid
• Hysteroscopic resection of
submucous fibroids, intrauterine
adhesion
Anatominal
Factors
(Uterine)

Management
• Cervical incompetence
• Cervical survelliance if
history of one second
trimester miscarriage with
suspected cervical weakness
• US-indicated cerclage if
cervical length ≤ 25 mm by
TVS before 24 weeks of
gestation.
• Progestrone therapy
Anatominal
Factors
(Cervix)

Management
• Insufficient evidence to prevent
miscarriage
• Pregestrone supplementation
• hCG supplementation
• Suppression of high LH in
PCOS
• Metformin supplementation
• Ensure glycaemic control
Endocrine
factors

Management
• Insufficient evidence to evaluate the effect
of heparin to prevent a miscarriage in
recurrent 1st trimester miscarriage.
• Heparin therapy may improve the live birth
rate in women with previous 2nd-trimester
miscarriage
Inherited
Thrombophilia
• Appropriate antibiotics for specific
organism identified.
• No role for empirical antibiotics.
Infection

Preterm Birth (PTB)
• Incidence of 5-10% of pregnancies
• 1/3: Preterm labour with intact membrane
• 1/3: PPROM
• 1/3: Iatrogenic

Preterm Birth (PTB)
• Previous preterm labour is strongest predictor for
recurrence.
• 15% : 1 previous PTB
• 30% : 2 previous PTBs
• 45% : 3 previous PTBs

Progestrone & PTB
• Suppress immunity to
prevent rejection of
fetal cells
• Promotes uterine
quiscence

Progestrone & PTB
• singleton gestations with no prior PTB, with unknown CL?
• singleton gestations, with no prior PTB, but short CL?
• singleton gestations with prior PTB, and unknown or
normal CL?
• singleton gestations with prior PTB, and short CL?
• multiple gestations, and unknown or normal CL?
• multiple gestations, and short CL?
• prevention of PTB in preterm labor?
• prevention of PTB in preterm premature rupture of
membranes?

Progestrone & PTB
• Singleton gestations with no prior PTB, with unknown CL?
No evidence of effectiveness

Progestrone & PTB
17-alpha-hydroxyprogestrone Vaginal progestrone
- No difference compared to
placebo
- Less effective than cerclage in
reducing PTB
- Reduction in PTB and
composite perinatal morbidity &
mortality.
- Can be offerred if CL ≤ 20mm
at ≤ 24 weeks

Progestrone & PTB
normal CL?
17-alpha-
hydroxyprogestrone
Vaginal progestrone Oral progestrone
Which is the winner?
Progestrone administration is beneficial. Limitted data comparing the
different preparations of progestrone. There is present strongest evidence
of effectiveness for 17P. Recommendation: IM 17P 250mg weekly at 16-
20 weeks till 36 weeks.

Progestrone & PTB
normal CL?
17-alpha-hydroxyprogestrone Vaginal progestrone
Insufficient evidence to assess efficacy of different preparation of
progestrone therapy if CL < 25mm at < 24 weeks.
Recommendation: IM 17P weekly till 36 weeks + cerclage

Progestrone & PTB
normal CL?

Progestrone & PTB
normal CL?
• prevention of PTB in preterm labor?
• prevention of PTB in preterm premature rupture of
membranes?
No role

General management
• Stop smoking/drugs, avoid alcohol
• Preconception: folic acid supplementation, good glycaemic
control in overt diabetes
• Psychological support
• ? Role of induction of labour at 38-39 weeks
• Can be offered after counseling with the couple in term of
weighing the small risk of stillbirth at term and the risk of IOL.

Unexplained cause
• GOOD prognosis for future pregnancy (75%) outcome without
pharmacological intervention but with supportive care alone.
• REASSURANCE plays an important role
• Appropriate f/up in antenatal specialist clinic needed as part of
providing reassurance and adequate monitoring
• Prognosis worsens with increasing maternal age and number of
previous miscarriages.
• Role of Aspirin ± Heparin???
• Not recommended

Conclusion
• Managing BOH should be individualised.
• Detailed history taking is required to identify targeted risk
factors.
• Proper documentation of the workout investigation result
will ease the subsequent antenatal care.
• Use the correct weapon to shoot the correct target.
• Hopefully, we can yield a fruitful pregnancy outcome.

Bad obstetric history

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