BAD OBTETRIC HISTORY

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? 1 st or 2 nd 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 1 st trimester- Genetic,Endocrinal 2 nd 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. Management (NICE clinical guideline 107: Hypertension in pregnancy)

29. 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

30. 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

31. 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

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

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

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

35. 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.

36. 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

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

38. 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.

39. 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)

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

41. 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

42. 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

43. 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

44. Sapporo Criteria At least 1 clinical and 1 lab criteria) At least one clinical criteria and one laboratory criteria Clinical 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 >99 th percentile Pregnancy morbidity ( WILSON CRITERIA ) ≥1 unexplained fetal deaths of ≥ 10 weeks POA (morphologically normal fetus ) LA Detected ≥1 premature births of ≤ 34 th week POA d/t: Severe PE or Placental insufficiency (IUGR) (morphologically normal neonate) Anti-beta2-glycoprotein >99 th percentile ≥3 unexplained consecutive spontaneous abortions < 10 week POA * On 2 or more occasions At least 6 weeks apart

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

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

47. 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

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

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

50. Diagnostic criteria for diagnosis of Bacterial Vaginosis Homogenous vaginal discharge 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

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

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

53. 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

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

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

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

57. 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

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

59. 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.

60. Asherman syndrome Normal uterus Intrauterine synechiae

61. 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.

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

63. 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

64. 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

65. 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.

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

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

68. Now we know.. What we don ’ t know…

69. Thank you