Detecting Bad Smells in Source Code using Change History Information
BAD OBTETRIC HISTORY
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The stories that end badly are sad, sadder still are the ones that never began….
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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.
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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.
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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.
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VARITIES
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Bad Obstetric History
May be due to-
1.Still Birth
2. Small Weight Baby
3. Prolonged Labour
4. Intrauterine Death
5. Recurrent Pregnancy Loss
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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
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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
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EFFECT-
Asphyxia
Hypothermia
Pulmonary syndrome-Pulmonary edema,Intra-alveolar haemorrhage,Respiratory distress syndrome
Cerebral haemorrhage
Fetal shock
Heart failure
Dehydration and acidemia
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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)
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May Cause-
Fetal Hypoxia
Intrauterine Infection
Intracranial stress or Haemorrhage
Labour should be monitored with Partograph.
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4.INTRAUTERINE FETAL DEATH
Antepartum Death before labour
Intrauterine growth restriction
Hypertensive disorder of Pregnancy
Diabetes mellitus
Chronic Hypertension
Rh incompatibility
Syphilis
Congenital malformations
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5.RECURRENT PREGNANCY LOSS
Three or more consecutive spontaneous pregnancy loss
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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
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Recurrence suggests
a persistent cause (not just a bad luck)
which must be identified and treated
Ohh….No..
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Causes of Recurrent Pregnancy loss
Genetic/Chromosomal
Anatomical-Mullerian abnormality,cervical
incomptence
Endocrinal
Hypertensive disease
Rh Isoimmunisation
Thrombophilia-Antiphospholipid antibody
syndrome
Unexplained
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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.
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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
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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
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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
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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
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One of the biggest obstacle however is the lack of details in previous pregnancies…
APPROPRIATE DOCUMENTATION HELPS!
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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
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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
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A.Hypertensive disorder
Hypertensive disorder of pregnancy
Gestational Hypertension
Pre eclampsia
Eclampsia
Chronic Hypertension
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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
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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
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Pre-eclampsia
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Management
Pre-eclampsia(aspirin)
(NICE clinical guideline 107: Hypertension in pregnancy)
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• 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)
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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
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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
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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
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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
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Objective of treatment
Time Plasma glucose(mg/dl)
Fasting <95
PrePrandial <110
1hr PostPrandial <140
2hr PostPrandial <120
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Oral hypoglycemic drug-
Glyburide-increase release of insulin
decrease insulin resistance
Insulin
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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.
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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
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2)Thyroid disease Poorly controlled Hypothyroidism and
Hyperthyroidism
Abortion
Placental abruption
Preeclampsia
Stillbirth
Prematurity
IUGR
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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.
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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)
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c.Acquired / Inherited Thrombophilia
Acquired Antiphospholipid
syndrome
Inherited Protein C deficiency
Protein S deficiency
AT deficiency
Activated protein C resistance
PT gene mutation
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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
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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
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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
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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
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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
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D.Infections
Bacterial vaginosis-MC cause of vaginal discharge
Ureaplasma urealyticum Mycoplasma hominis TORCH infection UTI
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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
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Syphilis-
Ascending pattern
More recent the maternal infection,more severe the congenital disease
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DIAGNOSIS Clinical examination
Blood Counts
VDRL
HIV
Urine-Routine,Microscopy
Urine-Culture,Senstivity
Vaginal-Culture,Senstivity
TREATMENT Antibiotics
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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
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Treatment
Oral Metronidazole 400 mg TDS* 5 -7DAYS
Oral clindamycin 300 mg BD* 7 days
Lactobacilli vaginal pessary/gel/suppository
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E.Anatomical factors
15 to 16% of women with RPL have uterine abnormalities.
2nd trimester pregnancy loss and preterm delivery
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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
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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
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Early Pregnancy Loss-
Septate Uterus
Bicornuate Uterus
D/t inadequate blood supply to conceptus
Preterm Labour-
Didelphus
Unicornuate
Occuring later with each successive pregnancy
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Diagnosis History
USG
Hysteroscopy
Laproscopy
MRI
Treatment Hysteroscopic resection
of uterine septum
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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
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Diagnosis Sign and symptoms
Examination
USG
Hysteroscopy
Treatment Myomectomy
Hysteroscopic resection of submucous fibroid
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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.
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Asherman syndrome
Normal uterus Intrauterine synechiae
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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.
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Cervical incompetence
Painless cervical dilatation
Inability of cervix to retain a pregnancy in the absence of uterine contractions.
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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
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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
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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.
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F.Genetic Causes
50% of 1st trimester losses.
Type-Chromosome NO.(Aneuploidy)
Structure
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Aneuploidy• Trisomy(50%)
Trisomy 16 (most common)
• Monosomy(20%)
• Triploidy(15%)
• Tetraploidy(5%)
Structure• Translocation
Reciprocal
Robertsonian
• Inversion
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Now we know.. What we don’t know…
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Thank you