The stories that end badly are sad, sadder still are the ones that never began….

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.

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.

What can be construed as BOH? 1st or 2nd 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.

VARITIES

Bad Obstetric History

May be due to-

1.Still Birth

2. Small Weight Baby

3. Prolonged Labour

4. Intrauterine Death

5. Recurrent Pregnancy Loss

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

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

EFFECT-

Asphyxia

Hypothermia

Pulmonary syndrome-Pulmonary edema,Intra-alveolar haemorrhage,Respiratory distress syndrome

Cerebral haemorrhage

Fetal shock

Heart failure

Dehydration and acidemia

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)

May Cause-

Fetal Hypoxia

Intrauterine Infection

Intracranial stress or Haemorrhage

Labour should be monitored with Partograph.

4.INTRAUTERINE FETAL DEATH

Antepartum Death before labour

Intrauterine growth restriction

Hypertensive disorder of Pregnancy

Diabetes mellitus

Chronic Hypertension

Rh incompatibility

Syphilis

Congenital malformations

5.RECURRENT PREGNANCY LOSS

Three or more consecutive spontaneous pregnancy loss

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

Recurrence suggests

a persistent cause (not just a bad luck)

which must be identified and treated

Ohh….No..

Causes of Recurrent Pregnancy loss

Genetic/Chromosomal

Anatomical-Mullerian abnormality,cervical

incomptence

Endocrinal

Hypertensive disease

Rh Isoimmunisation

Thrombophilia-Antiphospholipid antibody

syndrome

Unexplained

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.

History Menstrual history

Past Obstetric History-

Gestational age at time of pregnancy loss

1st trimester-Genetic,Endocrinal

2nd 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

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

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

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

One of the biggest obstacle however is the lack of details in previous pregnancies…

APPROPRIATE DOCUMENTATION HELPS!

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

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

A.Hypertensive disorder

Hypertensive disorder of pregnancy

Gestational Hypertension

Pre eclampsia

Eclampsia

Chronic Hypertension

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

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

Pre-eclampsia

Management

Pre-eclampsia(aspirin)

(NICE clinical guideline 107: Hypertension in pregnancy)

• 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)

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

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

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

Criteria for diagnosis with 75gm oral glucose

TIME NORMAL IMPAIRED GLUCOSE TOLERANCE

DIABETES MELLITUS

FASTING <100mg/dl 100 to <126mg/dl

≥126mg/dl

2 HR POST PRANDIAL

<140mg/dl 140 to <200mg/dl

≥200mg/dl

Objective of treatment

Time Plasma glucose(mg/dl)

Fasting <95

PrePrandial <110

1hr PostPrandial <140

2hr PostPrandial <120

Oral hypoglycemic drug-

Glyburide-increase release of insulin

decrease insulin resistance

Insulin

DeliveryLow 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.

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

2)Thyroid disease Poorly controlled Hypothyroidism and

Hyperthyroidism

Abortion

Placental abruption

Preeclampsia

Stillbirth

Prematurity

IUGR

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.

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)

c.Acquired / Inherited Thrombophilia

Acquired Antiphospholipid

syndrome

Inherited Protein C deficiency

Protein S deficiency

AT deficiency

Activated protein C resistance

PT gene mutation

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

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

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

Sapporo CriteriaAt 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 >99th percentile

Pregnancy morbidity(WILSON CRITERIA)

≥1 unexplained fetal deaths of ≥ 10 weeks POA(morphologically normal fetus)

LA Detected

≥1 premature births of ≤ 34th week POA d/t:

Severe PE or Placental insufficiency (IUGR)

(morphologically normal neonate)

Anti-beta2-glycoprotein

>99th percentile

≥3 unexplained consecutive spontaneous abortions < 10 week POA

* On 2 or more occasionsAt least 6 weeks apart

http://circ.ahajournals.org/content/vol112/issue3/images/large/23FF1.jpeg

Treatment of APLA Syndrome

Prophylactic Heparinization-

UFH- 1st TM-5000U SC twice daily

2nd TM-7500U SC twice daily

3rd TM-10000U SC twice daily

LMWH- 40 mg SC twice daily

Low dose ASPIRIN-75 mg PO daily

D.Infections

Bacterial vaginosis-MC cause of vaginal discharge

Ureaplasma urealyticum Mycoplasma hominis TORCH infection UTI

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

Syphilis-

Ascending pattern

More recent the maternal infection,more severe the congenital disease

DIAGNOSIS Clinical examination

Blood Counts

VDRL

HIV

Urine-Routine,Microscopy

Urine-Culture,Senstivity

Vaginal-Culture,Senstivity

TREATMENT Antibiotics

Diagnostic criteria for diagnosis of Bacterial Vaginosis

A. Homogenous vaginal discharge

B. 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

Treatment

Oral Metronidazole 400 mg TDS* 5 -7DAYS

Oral clindamycin 300 mg BD* 7 days

Lactobacilli vaginal pessary/gel/suppository

E.Anatomical factors

15 to 16% of women with RPL have uterine abnormalities.

2nd trimester pregnancy loss and preterm delivery

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

MULLARIAN ANOMALIESCLASS ANOMALY

1 Segmental,mullerian agenesis-HypoplasiaA. VaginalB. CervicalC. FundalD. TubalE. Combined

II UnicornuateA. CommunicatingB. NoncommunicatingC. No cavityD. No horn

III Didelphys

1V BicornuateA. Complete(division down to internal os)B. Partial

V SeptateA. CompleteB. Partial

VI Arcuate

VII Diethylstillbestrol related

Early Pregnancy Loss-

Septate Uterus

Bicornuate Uterus

D/t inadequate blood supply to conceptus

Preterm Labour-

Didelphus

Unicornuate

Occuring later with each successive pregnancy

Diagnosis History

USG

Hysteroscopy

Laproscopy

MRI

Treatment Hysteroscopic resection

of uterine septum

FibroidSubmucous

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

Diagnosis Sign and symptoms

Examination

USG

Hysteroscopy

Treatment Myomectomy

Hysteroscopic resection of submucous fibroid

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.

Asherman syndrome

Normal uterus Intrauterine synechiae

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.

Cervical incompetence

Painless cervical dilatation

Inability of cervix to retain a pregnancy in the absence of uterine contractions.

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

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

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.

F.Genetic Causes

50% of 1st trimester losses.

Type-Chromosome NO.(Aneuploidy)

Structure

Aneuploidy• Trisomy(50%)

Trisomy 16 (most common)

• Monosomy(20%)

• Triploidy(15%)

• Tetraploidy(5%)

Structure• Translocation

Reciprocal

Robertsonian

• Inversion

Click icon to add picture

Now we know.. What we don’t know…

Thank you