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Bad obstetric history
- 3. Bad Obstetric History(BOH) What to do about it? By Dr Yong Soon Leong Supervisor: Dr Haris N Suharjono
- 4. 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.
- 5. 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?
- 6. What to doabout 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...
- 7. 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
- 8. 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!
- 9. Recurrent causes Pre-eclampsia Acquired /Inherited thrombophilia Parental genetic disorders Anatomical factors (uterine / cervix) Endocrine factors Infection Rh isoimmunisation
- 10. Pre-eclampsia (PET) • Pregnancy-inducedhypertension 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)
- 11. (NICE clinical guideline107: Hypertension in pregnancy)
- 12. Acquired / Inherited Thrombophilia Acquired •Antiphospholipid syndrome Inherited • Protein C deficiency • Protein S deficiency • AT deficiency • Activated protein C resistance • PT gene mutation
- 13. Antiphospholipid Syndrome • Refers toassociation 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
- 14. Antiphospholipid Syndrome • Mechanism ofdisease • 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%.
- 15. Antiphospholipid Syndrome • Increased riskof recurrent miscarriage, hypertension, pre- eclampsia, IUGR, fetal death, preterm birth, abruption, thrombosis • Risk = Anticardiolipin antibody titre (esp. IgG) • Thrombosis = Lupus anticoagulant
- 16. Antiphospholipid Syndrome • Fetal deathcan 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%,
- 17. Inherited thrombophilia defects • ProteinC & 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
- 18. Inherited thrombophilia defects –recurrent risk of thrombosis Protein S deficiency Protein C deficiency Anti-thrombin III deficiency
- 19. 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%)
- 20. Inherited thrombophilia defects –recurrent risk of thrombosis 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
- 21. Inherited thrombophilia defects • Adversepregnancy outcome: • Pre-eclampsia • IUGR • Placental abruption • Recurrent early miscarriage • Late fetal demise • Intrauterine death and stillbirth
- 22. Parental genetic disorders • Oneof 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
- 23.
- 24. 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
- 25. Endocrine factors • Diabetesmellitus • Thyroid disease (anti-thyroid antibody) • PCOS (due to insulin resistance, hyper-insulinaemia, hyper-androgenaemia)
- 26. 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
- 27. Investigations Pre-eclampsia Acquired / Inheritedthrombophilia Parental genetic disorders Anatomical factors (uterine / cervix) Endocrine factors Infection Rh isoimmunisation
- 28. 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
- 29. Pre-eclampsia - prediction Pre-eclampsiaIUGR 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
- 30. Pre-eclampsia - prediction Isuterine 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?
- 31. Investigations Acquired / Inheritedthrombophilia • 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)
- 32.
- 33. Thrombophilia screening • Ahistory 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
- 34. 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
- 35. 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
- 36. POSTCONCEPTION EVALUATION • Confirm intrauterinepregnancy, 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
- 37. Management • 15% reductionin 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)
- 38. Management Pre-eclampsia (aspirin) (NICE clinical guideline107: Hypertension in pregnancy)
- 39. Management Pre-eclampsia (aspirin) Why 75mg? Can itbe higher dose? The more the better? The less the safer?
- 40. Management • Halve therisk of pre- eclampsia and reduce serious morbidity and death in women at high risk and with low dietary intake Pre-eclampsia (calcium)
- 41. Management • magnesium • folicacid • antioxidants (vitamins C and E) • fish or algal oils • garlic • restricting salt intake Pre-eclampsia (no role)
- 42.
- 43. Management • Low doseaspirin + 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)
- 44. Management • Start lowdose 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.
- 45. Management • Hydroxychloroquine may providesome protection from thrombosis and should be continued in pregnancy. Antiphospholipid Syndrome (women with SLE)
- 46.
- 47. Management • Prompt referralto 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
- 48. Management • Congenital uterinemalformations • 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)
- 49. 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)
- 50. Management • Insufficient evidenceto prevent miscarriage • Pregestrone supplementation • hCG supplementation • Suppression of high LH in PCOS • Metformin supplementation • Diabetes mellitus • Ensure glycaemic control Endocrine factors
- 51. Management • Insufficient evidenceto 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
- 52. Preterm Birth (PTB) •Incidence of 5-10% of pregnancies • 1/3: Preterm labour with intact membrane • 1/3: PPROM • 1/3: Iatrogenic
- 53. Preterm Birth (PTB) •Previous preterm labour is strongest predictor for recurrence. • 15% : 1 previous PTB • 30% : 2 previous PTBs • 45% : 3 previous PTBs
- 54. Progestrone & PTB •Suppress immunity to prevent rejection of fetal cells • Promotes uterine quiscence
- 55. 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?
- 56. Progestrone & PTB •Singleton gestations with no prior PTB, with unknown CL? No evidence of effectiveness
- 57. 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
- 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? 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.
- 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? 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
- 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? 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? No evidence of effectiveness
- 62. 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
- 63.
- 64. General management • Stopsmoking/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.
- 65. Unexplained cause • GOODprognosis 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
- 66. Conclusion • Managing BOHshould 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.
- 67.
Editor's Notes
- #31 - Will uterine artery dopplers change the clinical management in patients who are already high risk of pre-eclampsia?Uterine artery Doppler velocimetry is a poor predictor of pre-eclampsia as it has limited test accuracy.Those studies involved only small numbers of sample size and the sample are often mixed groups of patients.
- #40 There were studies comparing 60mg, 75mg, 100mg, 150mg. 60mg showed marginal statistical significant, 75mg showed statistical significant. 100mg or more was inconclusive (some studies proved higher dose is more effective but some studies did not yield statistical significant result due to underpowered study). Furthermore, current reassurance about safety of aspirin in pregnancy only applies to lower doses.