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 miscarriagesStill births or neonatal deathsPre-term labourFetal 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


• 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%.


• Increased risk of recurrent miscarriage, hypertension, pre-eclampsia, IUGR, fetal death, preterm birth, abruption, thrombosis

• Risk = Anticardiolipin antibody titre (esp. IgG)• Thrombosis = Lupus anticoagulant


• 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

Inherited thrombophilia defects – recurrent risk of thrombosis

Protein S deficiency

Protein C deficiency

Anti-thrombin III deficiency





15% (12-17%)

25% (22-26%)

35% (32-51%)





Activated protein C resistance (due to Factor V Leiden mutation)

Prothrombin gene mutation

Low prevalence in Asians

& Africans

Inherited thrombophilia defects

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


• 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• Diabetes mellitus• 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)

Lupus Anticoagulant

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

Parental genetic disorders• 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

• 8% reduction in the risk of delivery < 37 weeks

• 14% reduction in the risk of 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

Pre-eclampsia

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


(previous late fetal loss, neonatal death, adverse outcome due to pre-eclampsia, FGR, or abruption)

Management

• Start low dose aspirin

• Warfarin?

• LMWH?


(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.


(women with SLE)

Management


+

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

• Diabetes mellitus• 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



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




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




• multiple gestations, and unknown or normal CL?


Progestrone & PTB






Progestrone & PTB





• prevention of PTB in preterm labor?• prevention of PTB in preterm premature rupture of membranes?

No role

Progestrone & PTB

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.

THANKS….

Bad obstetric history

Health & Medicine

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