Bad obstetric history

1. BOH

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

3. 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, 4 th ed., p. 99. London: Lloyd-Luke Medical Books .

4. Bad Obstetric History What can be construed as BOH? 1 st or 2 nd 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?

5. 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...

6. 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

7. 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!

8. Recurrent causes

9. 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)

10. (NICE clinical guideline 107: Hypertension in pregnancy)

11. Acquired / Inherited Thrombophilia

12. 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 10 th week of gestation ≥ 1 preterm birth before 34 th week owing to placental disease

13. Antiphospholipid Syndrome Mechanism of disease Inhibition of T ROPHOBLASTIC function and differentiation Activation of complement pathways at the maternal-fetal interface resulting in a local I NFLAMMATORY response Thrombosis of utero- P LACENTAL vasculature in later pregnancy Present in 15% of women with recurrent miscarriage. Without treatment, live birth rate is as low as 10%.

14. 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

15. 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%,

16. 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

17. Inherited thrombophilia defects – recurrent risk of thrombosis

18. Inherited thrombophilia defects – recurrent risk of thrombosis 15% (12-17%) 25% (22-26%) 35% (32-51%)

19. Inherited thrombophilia defects – recurrent risk of thrombosis Low prevalence in Asians & Africans

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

21. 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

22. Parental genetic disorders

23. 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

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

25. 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

26. Investigations

27. 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

28. Pre- eclampsia - prediction 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

29. Pre- eclampsia - prediction 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?

30. Investigations

31. Lupus Anticoagulant

32. 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

33. Investigations

34. Investigations

35. 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

36. Management

37. Management (NICE clinical guideline 107: Hypertension in pregnancy)

38. Management Why 75mg? Can it be higher dose? The more the better? The less the safer?

39. Management

40. Management

41. Management

42. 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)

43. 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 .

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

45. Management Antiphospholipid Syndrome + Pre- eclampsia

46. Management

47. Management

48. Management

49. Management

50. Management

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

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

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

54. 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?

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

56. Progestrone & PTB singleton gestations with no prior PTB, with unknown CL? singleton gestations, with no prior PTB, but short CL? 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

57. 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 ? 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.

58. 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? 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

59. 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? No evidence of effectiveness

60. 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? No evidence of effectiveness

61. 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? No role

62. Progestrone & PTB

63. 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.

64. 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

65. 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.

66. Thanks….