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NATIONAL LICENSE II 2554




    Sritippayawan S.
PRENATAL DIAGNOSIS
Prenatal diagnosis āļ—āļĩāđˆāļ„āļ§āļĢāļĢāļđāđ‰

ï‚Ļ   Thalassemia

ï‚Ļ   Abnormal fetal karyotype

ï‚Ļ   Other fetal anomalies : NTDs,heart
    diseases,cleft lip/cleft palate
How to approach

ï‚Ļ   History taking : patient history,family
    history,ethnic background

ï‚Ļ   Risk factors: advanced maternal , prior
    affected pregnancy,drugs and toxin exposure
Diagnostic tests

ï‚Ļ   Screening test : maternal serum markers,
    US(NT)

ï‚Ļ   Diagnostic test : US , Amniocentesis ,
    CVS,cordocentesis
DDx
ï‚Ļ   Chromosome anomalies :
    ï‚Ī Autosomal: Trisomy 13,18,21
    ï‚Ī Sex chromosome : 45,X,47,XXY

ï‚Ļ   Genetic disorders :
    ï‚Ī AD
    ï‚Ī AR  : thalassemia
    ï‚Ī X-linked dominant
    ï‚Ī X-linked recessive
    ï‚Ī Multifactorial : NTD ,cleft lip/cleft palate,heart
      disease
Procedures

ï‚Ļ   Invasive procedure :
    ï‚Ī CVS

    ï‚Ī Amniocentesis

    ï‚Ī Cordocentesis
Complication

Complication :

ï‚Ļ   Mother : Placental abruption , Isoimmunization

ï‚Ļ   Fetus : prematurity,stillbirth

Prognosis :
ï‚Ļ   depend on diagnosis
Management

ï‚Ļ   Option of terminate pregnancy,further
    investigation,delivery at tertiary center
ï‚Ļ   Genetic counseling
ï‚Ļ   Pediatric surgery consultation
ï‚Ļ   Rho(D) Immune Globulin for prevent
    isoimmunization
ï‚Ļ   Subsequent management : recurrent rate
Prenatal Diagnosis of thalassemia

ï‚Ļ   Thalassemia
    ï‚Ī Screening    test – interpretation

    ï‚Ī Diagnostic   test – interpretation

    ï‚Ī Who   are couple at risk for severe thalassemia
Prenatal diagnosis of NTD




Who have risk of fetal NTDs?
How to know ?
Prenatal Diagnosis of Down syndrome

 ï‚Ļ   Down syndrome
     ï‚Ī  Who have risk of Abnormal fetal
       karyotype?
     ï‚Ī Screening test : NT,serum markers.US
         ïŪ First
               trimester
         ïŪ Second trimester
     ï‚Ī Diagnostic    test
         ïŪ First
               trimester : CVS
         ïŪ Second trimester : amniocentesis
THALASSEMIA IN
PREGNANCY



  SRITIPPAYAWAN S.
Severe thalassemia in Thailand

ï‚Ļ   Hb Bart ‗s hydrops fetalis
ï‚Ļ   Homozygous beta thalassemia
ï‚Ļ   Beta thalassemia Hb E
Alpha thalassemia diseases
         THALASSEMIA              GENOTYPE


Hb Bart ‗s hydrops fetalis   ïĄ-thal 1 / ïĄ-thal 1)

Hb H disease                 ïĄ-thal 1 / ïĄ-thal 2

Hb H disease with            ïĄ-thal 1 / Hb CS
Hb Constant Spring

Homozygous Hb Constant        Hb CS / Hb CS
Spring
Screening thalassemia

ï‚Ļ   OF test , MCV
ï‚Ļ   DCIP , Hb E screening
āļāļēāļĢāđ€āļ‚āļĩāļĒāļ™genotype Beta thalassemia

ï‚Ļ   Normal

ï‚Ļ   Heterozygous Beta thalassemia (beta trait)

ï‚Ļ   Homozygous Beta thalassemia

ï‚Ļ   Beta thalassemia hemoglobin E
    (Beta thal Hb E)
āļāļēāļĢāđ€āļ‚āļĩāļĒāļ™genotype Beta thalassemia

   āļŠāļąāļāļĨāļąāļāļĐāļ“āđŒ                  āļŦāļĄāļēāļĒāļ–āļķāļ‡
  ïĒ orïĒA or ïĒN        Gene ïĒ globin āļ›āļāļ•āļī
    ïĒT orïĒthal        Gene ïĒ thalassemia

                         ïĒ0 – thalassemia OR
     ïĒ0 orïĒ+
                           ïĒ+- thalassemia

        ïĒE                 Gene Hb E
āļāļēāļĢāđ€āļ‚āļĩāļĒāļ™genotype Beta thalassemia

            āļŠāļąāļāļĨāļąāļāļĐāļ“āđŒ                       āļŦāļĄāļēāļĒāļ–āļķāļ‡
              ïĒE/ïĒE                  HbE homozygoys
              ïĒA/ïĒE                 HbE heterozygous
  ïĒA/ïĒ+/0 or ïĒA/ ïĒthal            ïĒ thal heterozygous
    ïĒ+/0/ïĒE or ïĒthal/ïĒE               ïĒ thal /Hb E disease
              ïĒA/ïĒA                       normal
                                      homozygous ïĒ thal
 ïĒthal   /ïĒthal   or   ïĒ+/0/ïĒ+/0
                                          disease
āļāļēāļĢāđ€āļ‚āļĩāļĒāļ™genotype Alpha thalassemia

     āļŠāļąāļāļĨāļąāļāļĐāļ“āđŒ                   āļŦāļĄāļēāļĒāļ–āļķāļ‡
        ï€ ïĄ                Gene ï€ ïĄ globin āļ›āļāļ•āļī

                       Gene ï€ ïĄ globin āļ—āļĩāđˆ 2 āļ•āļēāđāļŦāļ™āđˆāļ‡
      ï€ ïĄï€ ïĄ
                          (ïĄï€ globin haplotype)

- -, or ï€ ïĄ -thal 1        ï€ ïĄ -thal 1 haplotype

-ïĄ   ,or ï€ ïĄ -thal 2       ï€ ïĄ -thal 2 haplotype

       ïĄ cs             Gene Hb constant Spring

      ïĄ csï€ ïĄ          Hb constant Spring haplotype
āđ‚āļˆāļ—āļĒāđŒ āļžāđˆāļ­āđ€āļ›āđ‡āļ™ïĄï€ thal-1 trait (- - / ïĄïĄ)
    āđāļĄāđˆāđ€āļ›āđ‡āļ™ ïĄï€ thal-2 trait (- ïĄ / ïĄïĄ)
    āļĨāļđāļāļ„āļ™āđāļĢāļāđ€āļ›āđ‡āļ™ Hb H disease (- - / - ïĄ)
    āļ–āđ‰āļēāļˆāļ°āļĄāļĩāļĨāļđāļāļ„āļ™āļ•āđˆāļ­āđ„āļ›āļˆāļ°āļĄāļĩāđ‚āļ­āļāļēāļŠāđ€āļ›āđ‡āļ™ Hb H disease āļāļĩāđˆ %
              A. 0%
              B. 25%       
              C. 50%
              D. 75%
              E. 100%
āļāļēāļĢāļ„āļēāļ™āļ§āļ“āļ­āļąāļ•āļĢāļēāđ€āļŠāļĩāđˆāļĒāļ‡āļ‚āļ­āļ‡āļĨāļđāļāļ•āđˆāļ­āļŠāļēāļĄāļĩāļ•āđˆāļ­āļāļēāļĢāļĄāļĩgenotype āļŠāļ™āļīāļ”āļ•āđˆāļēāļ‡āđ†
 āļ‚āļ­āļ‡āļ­āļąāļĨāļŸāļē āļ˜āļēāļĨāļąāļŠāļ‹āļĩāđ€āļĄāļĩāļĒāđāļĨāļ°āļŪāļĩāđ‚āļĄāđ‚āļāļĨāļšāļīāļ™āļœāļīāļ”āļ›āļāļ•āļī
 genotype    genotypeāđāļĄāđˆ
                                        āļ­āļąāļ•āļĢāļēāđ€āļŠāļĩāđˆāļĒāļ‡āļ‚āļ­āļ‡āļĨāļđāļāļ•āđˆāļ­āļāļēāļĢāļĄāļĩgenotypeāļŠāļ™āļīāļ”āļ•āđˆāļēāļ‡āđ†
   āļžāđˆāļ­
 --/-ïĄ        - ïĄ / ïĄïĄ          --/-ïĄ         - - / ïĄïĄ           -ïĄ/-ïĄ            - ïĄ / ïĄïĄ
  Hb H       ïĄ- thal2 trait       Hb H       ïĄ- thal 1 trait homozygous ïĄ        ïĄ - thal2 trait
 disease       (OF   -)       disease(1/4)       (1/4)         - thal2 (1/4)         (1/4)
 (OF +)
              ïĄcsïĄ/ïĄïĄ           - -/ïĄCSïĄ    - - / ïĄïĄ       - ïĄ/ïĄcsïĄ               - ïĄ / ïĄïĄ
              Hb CS trait     Hb H disease ïĄ- thal 1 trait ïĄ - thal2 / Hb        ïĄ - thal2 trait
                (OF - )        with Hb CS      (1/4)       CS(1/4)                   (1/4)
                                   (1/4)
 - - / ïĄïĄ - ïĄ / ïĄïĄ              --/-ïĄ         - - / ïĄïĄ          - ïĄ / ïĄïĄ          ïĄïĄ/ ïĄïĄ
 ïĄ- thal 1 ïĄ - thal2 trait        Hb H       ïĄ- thal 1 trait   ïĄ - thal2 trait   normal (1/4)
    trait     (OF -)          disease(1/4)       (1/4 )            (1/4)
(OF +)
āđ‚āļˆāļ—āļĒāđŒ āļœāļĨāļāļēāļĢāļ•āļĢāļ§āļˆāļ„āļąāļ”āļāļĢāļ­āļ‡āļ˜āļēāļĨāļąāļŠāļ‹āļĩāđ€āļĄāļĩāļĒāđƒāļ™āļ„āļđāđˆāļŠāļĄāļĢāļŠ āļžāļšāļ§āđˆāļē
āđāļĄāđˆ : OFT +,DCIP -,%HbA2 = 2.8    Not exclude ïĄ-thal1trait)

āļžāđˆāļ­ : OFT -,DCIP +,%HbA2 = 22       Hb E trait



     1. āļˆāļ‡āđāļ›āļĨāļœāļĨ
     2. āđ€āļ›āđ‡āļ™āļ„āļđāđˆāđ€āļŠāļĩāđˆāļĒāļ‡āļ˜āļēāļĨāļąāļŠāļ‹āļĩāđ€āļĄāļĩāļĒāļŠāļ™āļīāļ”āļĢāļļāļ™āđāļĢāļ‡āļŦāļĢāļ·āļ­āđ„āļĄāđˆ
āļ–āđ‰āļēāđ€āļĨāļ·āļ­āļ”āđ€āļāđˆāļēāđ€āļāļīāļ™ 3 āļ§āļąāļ™ āļ­āļēāļˆāđƒāļŦāđ‰āļœāļĨāļĨāļšāļĨāļ§āļ‡āđ„āļ”āđ‰
    OF                āļ—āļąāđ‰āļ‡āļ—āļĩāđˆāļˆāļĢāļīāļ‡ āđ† āđāļĨāđ‰āļ§āđ€āļ›āđ‡āļ™āļžāļēāļŦāļ°

ï‚Ļ   OF positive                  ï‚Ļ   OF negative
    ï‚Ī ïĄ - thal   trait (~100%)       ï‚Ī Hb E trait (30-
    ï‚ĪïĒ   - thal trait (~100%)          40%)
    ï‚Ī Hb   E trait (60-70%)          ï‚Ī āđ„āļĄāđˆāđ„āļ”āđ‰āđ€āļ›āđ‡āļ™āļžāļēāļŦāļ°āļ˜āļēāļĨāļąāļŠāļ‹āļĩāđ€āļĄāļĩāļĒ



DCIP
āļœāļĨāļšāļ§āļ : Hb E, Hb H
āļœāļĨāļ•āļĢāļ§āļˆāļ„āļąāļ”āļāļĢāļ­āļ‡āļ—āļĩāđˆāđ€āļ›āđ‡āļ™āļšāļ§āļ(āļœāļīāļ”āļ›āļāļ•āļī)

        MCV < 80 fL or OF positive
                And / or
             DCIP positive



             Work up : confirm test
                      āļ•āļēāļĄāļŠāļēāļĄāļĩāļĄāļēāļ•āļĢāļ§āļˆ
Hb A 2

      Result           HbA2
     Normal            <4%
  ïĄ thal - 1 trait     < 4%
   ïĒ thal trait       4-8%
    Hb E trait       10 – 30 %
ïĒ thal/HbE disease   30-60 %
Homozygous Hb E       > 60 %
āđ‚āļˆāļ—āļĒāđŒ āļ„āļđāđˆāđ€āļŠāļĩāđˆāļĒāļ‡āļ˜āļēāļĨāļąāļŠāļ‹āļĩāđ€āļĄāļĩāļĒāļŠāļ™āļīāļ”āđ„āļŦāļ™

     OFT     HbE           PCR                  HbE
No   MCV     DCIP
                    % A2   ïĄ-1
                                 ïĄ-1     ïĒ

                                  ?      ?        ?
āļ.   + ve

                                  X     X
āļŠ.   - ve                                         ?

                                       āļŠāļēāļĒ % A2
ïĒthal/HbE?    Further investigation    āļŦāļāļīāļ‡ Hb E /DCIP
PRENATAL DIAGNOSIS OF NTDS
Neural tube defect(NTD)
ï‚Ļ   NTDs result from failure of the neural tube to close
    normally between the 3rd and 4th weeks after
    conception (the 5th and 6th weeks of gestation).
ï‚Ļ   Type of NTD :
    ï‚Ī Spine (Spina bifida, meningomyelocele or
      myelomeningocele ) , cranium(Anencephaly
      ,exencephaly, Encephalocele )
      ïŪ Open   NTDs : often involve spine and cranium
      ïŪ Closed  NTDs are usually localized and confined to
        the spine
NTDs & AFP

ï‚Ļ   AFP : glycoprotein is synthesized by

    ï‚Ī Fetal   yolk sac

    ï‚Ī Fetal   GI tract and liver

ï‚Ļ   AFP in fetal serum and AF ïƒą until GA 13 wk. then
    ïƒē and

ï‚Ļ   AFPïƒą in maternal serum after 12 wk., peaks
    between GA 28 -32 weeks and then ïƒē
NTDs & AFP

          NTDs , ventral wall defects



        permit AFP to leak into the AF,
               maternal serum



       ïƒąAFP in maternal serum and AF



   Women who carry fetuses with NTDs have
     :MSAFP at GA 16 – 18 wk. > 2.5 MoM
Risk factors of NTDs
ï‚Ļ   95 % of NTDs occur in the absence of risk factor or family
    history
ï‚Ļ   NTDs : genetic causes and multifactorial disorders

ï‚Ļ   Recurrence rate

    ï‚Ī   4 % : couple has previous child with NTD

    ï‚Ī   5 % : either parent was born with NTD

    ï‚Ī   10% : couple has 2 affected children

ï‚Ļ   Etiology in some population : mutation MTHFR ï‚Ū impaired
    homocysteine and folate metabolism
Risk Factors for Neural-Tube Defects
Family history of neural-tube defects

Exposure to certain environmental agents

 Diabetes (hyperglycemia)

 Hyperthermia

 Drugs and medications

Genetic syndrome with known recurrence risk
Some racial or ethnic groups and/or living in high-risk
geographical regions
Production of anti- folate receptor antibodies
Some Risk Factors for NTDs
Genetic cause
â€ĒFamily history—multifactorial inheritance
â€ĒMTHFR mutation—677CT
â€ĒSyndromes with autosomal recessive inheritance : Meckel-Gruber Roberts Joubert
Jarcho-Levin HARDE—hydrocephalus–agyria–retinal dysplasia–encephalocele
â€ĒAneuploidy Trisomy 13 Trisomy 18 Triploidy
Exposure to certain environmental agents
â€ĒDiabetes—hyperglycemia
â€ĒHyperthermia Hot tub or sauna Fever (controversial)
â€ĒMedications Valproic acid Carbamazepine Coumadin Aminopterin Thalidomide
Efavirenz
Geographical region—ethnicity, diet, other factor
â€ĒUnited Kingdom ,India,China,Egypt,Mexico,Southern Appalachian United States
Prenatal diagnosis of NTD

ï‚Ļ   Screening test : maternal serum AFP at 2nd
    trimester
    ï‚Ī GA   15 – 20 wk.

    ï‚Ī Upper   normal limit of maternal serum AFP = 2.0-
      2.5 MoM( Abnormal if > 2.0 – 2.5 MoM)

ï‚Ļ   Diagnosis test : ultrasound
Screening test : MSAFP at 2nd trimester

 ï‚Ļ   ïƒą MSAFP  risk for NTD and other
     disorders
 ï‚Ļ   ïƒē MSAFP  risk for Down syndrome
Factors influence of the maternal serum AFP level


ï‚Ļ   Maternal weight : reflect the volume of
    distribution
ï‚Ļ   GA : maternal serum AFP 15 % /wk. during
    the 2nd trimester
ï‚Ļ   Race or ethnicity : African American women
    have 10 %  serum AFP (but low risk NTDs)
ï‚Ļ   DM : serum AFP may be ï‚Ŋ than non DM
    women
ï‚Ļ   Twins : ï‚Ū use higher screening threshold
     (â‰Ĩ 3.5 MoM)
Unexplained  Abnormal MSAFP often forcast
a poor pregnancy outcome


   ïŪLow   birth weight
   ïŪOligohydramnios

   ïŪPlacental   abruption
   ïŪFetal   death
Maternal serum
                     AFP (MoM) adjusted
markers screening
                      for maternal age ,
 (triple screening                           AFP â‰Ĩ2.0MoM
                      BW,ethinicity,GA,
test at GA 15 -20
                          twins,DM
      weeks




                                             US evaluate to
                        AFPâ‰Ĩ2.5 MoM        exclude twins , fetal
        US
                       (Abnormal result)        death and
                                             recalculate AFP
āđ‚āļˆāļ—āļĒāđŒ āļŠāļ•āļĢāļĩāļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ•āļĢāļ§āļˆ AFP   āļžāļšāļ§āđˆāļēāđ€āļ—āđˆāļēāļāļąāļš 3.0 MoM
āļˆāļ°āļžāļšāđ„āļ”āđ‰āđƒāļ™āđ‚āļĢāļ„āđƒāļ”

   a. Cystic fibrosis
   b. Down syndrome
   c. Polycystic kidney disease
   d. Neural tube defect
   e. Nephroblastoma
āđ‚āļˆāļ—āļĒāđŒ    āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 18 āļ›āļĩ G2P1 GA 5 weeks
āļ›āļĢāļ°āļ§āļąāļ•āļīāļšāļļāļ•āļĢāļ„āļ™āđāļĢāļ āđ€āļ›āđ‡āļ™ spina bifida
āļˆāļ°āđƒāļŦāđ‰āļ„āļēāđāļ™āļ°āļ™āļēāļ­āļ°āđ„āļĢāđ€āļžāļ·āđˆāļ­āļ›āđ‰āļ­āļ‡āļāļąāļ™āļāļēāļĢāđ€āļāļīāļ”āļ āļēāļ§āļ°āļ”āļąāļ‡āļāļĨāđˆāļēāļ§āļ‹āđ‰āļē
    a.   Iron
    b.   Zinc
    c.   Folic acid
    d.   B6
    e.   Thiamine
āđ‚āļˆāļ—āļĒāđŒ    āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 31āļ›āļĩ āļ›āļĢāļ°āļ§āļąāļ•āļīāļšāļļāļ•āļĢāļ„āļ™āđāļĢāļ āđ„āļĄāđˆāļĄāļĩ
āļāļĢāļ°āđ‚āļŦāļĨāļāļĻāļĩāļĢāļĐāļ° āļĄāļēāļ•āļĢāļ§āļˆāļāļēāļĢāļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒ
āļ„āļ§āļĢāđƒāļŦāđ‰āļāļēāļĢāļ”āļđāđāļĨāļĢāļąāļāļĐāļēāļ­āļĒāđˆāļēāļ‡āđ„āļĢ

a.   āđƒāļŦāđ‰āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ•āđˆāļ­āđ„āļ›āđ„āļ”āđ‰
b.   āļ™āļēāļŠāļēāļĄāļĩ āļ āļĢāļĢāļĒāļēāļĄāļēāļ•āļĢāļ§āļˆāļ„āļ§āļēāļĄāļœāļīāļ”āļ›āļāļ•āļīāļ‚āļ­āļ‡āđ‚āļ„āļĢāđ‚āļĄāđ‚āļ‹āļĄ
c.   āđƒāļŦāđ‰āļāļīāļ™Folic acidāđ€āļŠāļĢāļīāļĄ
d.   āđƒāļŦāđ‰āļāļīāļ™āļ˜āļēāļ•āļļāđ€āļŦāļĨāđ‡āļāđ€āļŠāļĢāļīāļĄ
e.   āđƒāļŦāđ‰āļāļīāļ™āđāļ„āļĨāđ€āļ‹āļĩāļĒāļĄāđ€āļŠāļĢāļīāļĄ
Prevention of neural tube defects

ï‚Ļ   Periconceptional folic acid supplementation reduces the
    incidence of neural tube defects by 50 - 70 %

ï‚Ļ   Women who have risk for NTDs :

    ï‚Ī women     with a previously affected child

    ï‚Ī Women     who take anticonvulsant drugs

    ï‚Ī family   history of NTD

    ï‚Ī insulin-requiring   diabetes
Prevention of neural tube defects

ï‚Ļ   Folic supplementation : started at least
    one month prior to conception and continue
    throughout the first trimester.

ï‚Ļ   Dose 4 mg daily
Prevention of neural tube defects

Primary prevention in low risk women
ï‚Ļ   Folic supplementation should be started at
    least one month prior to conception and
    continue throughout the first trimester.
ï‚Ļ   Dose 400g(0.4mg) daily
DOWN SYNDROME AND
ABNORMAL FETAL
KARYOTYPE
Who should be worked up
RISK FACTORS FOR GENETIC DISORDERS


ï‚Ļ   Advanced Maternal Age
ï‚Ļ   Previous Pregnancy Affected by Chromosomal
    Abnormality
ï‚Ļ   History of Early Pregnancy Loss
ï‚Ļ   Advanced Paternal Age
ï‚Ļ   Ethnicity



                      Suchila Sritippayawan   2/1/2011
Women with Increased Risk of Fetal Aneuploidy

Singleton pregnancy and maternal age older than 35 at delivery

Dizygotic twin pregnancy and maternal age older than 31 at delivery

Previous autosomal trisomy birth

Previous 47,XXX or 47,XXY birth

Patient or partner is carrier of chromosome translocation

Patient or partner is carrier of chromosomal inversion

History of triploidy

Some cases of repetitive early pregnancy losses

Patient or partner has aneuploidy

Major fetal structural defect by sonography
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 40 āļ›āļĩ G1P0 GA 8 weeks
āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒ āļ„āļĢāļąāđ‰āļ‡āđāļĢāļ āļāļąāļ‡āļ§āļĨāļ§āđˆāļēāļĨāļđāļāļˆāļ°āđ€āļ›āđ‡āļ™Down
syndrome
āļˆāļ‡āļšāļ­āļāđ‚āļ­āļāļēāļŠāļ—āļĩāđˆāļˆāļ°āļ—āļēāļĢāļāļˆāļ°āđ€āļ›āđ‡āļ™ Down syndromeāđ€āļĄāļ·āđˆāļ­
āļ„āļĨāļ­āļ”
      a.   1:50
      b.   1:100
      c.   1:200
      d.   1:300
      e.   1:400
Singleton Gestation—Maternal Age-Related Risk for Down Syndrome
                                  and
               Any Aneuploidy at Midtrimester and at Term

                      Down Syndrome               Any Aneuploidy

Maternal Age     Midtrimester     Term      Midtrimester     Term
    35             1/250         1/384        1/132         1/204
    36             1/192         1/303        1/105         1/167
    37             1/149         1/227         1/83         1/130
    38             1/115         1/175         1/65         1/103
    39              1/89         1/137         1/53          1/81
    40              1/69         1/106         1/40          1/63
    41              1/53         1/81          1/31          1/50
    42              1/41         1/64          1/25          1/39
    43              1/31         1/50          1/19          1/30
    44              1/25         1/38          1/15          1/24
    45              1/19         1/30          1/12          1/19
āđ‚āļˆāļ—āļĒāđŒ āļ™āļēāļ‡āļŠāļĄāļĻāļĢāļĩāļ­āļēāļĒāļļ 48āļ›āļĩ āļŠāļēāļĄāļĩāļ­āļēāļĒāļļ 50āļ›āļĩ āļ›āļĢāļ°āļ§āļąāļ•āļīāļĄāļĩāļĨāļđāļāļ„āļ™āđāļĢāļ
āđ€āļ›āđ‡āļ™Down syndrome āļ‚āļ“āļ°āļ™āļĩāđ‰āļ­āļēāļĒāļļ2āļ›āļĩ āļ­āļĒāļēāļāļĄāļĩāļĨāļđāļāļ„āļ™āļ—āļĩ2 āļ—āđˆāļēāļ™
                                                 āđˆ
āļˆāļ°āđƒāļŦāđ‰āļ„āļēāđāļ™āļ°āļ™āļēāļ­āļĒāđˆāļēāļ‡āđ„āļĢ

     a.   āļāļēāļāļ„āļĢāļĢāļ āđŒāļ•āļēāļĄāļ›āļāļ•āļī
     b.   āļ•āļĢāļ§āļˆāđ‚āļ„āļĢāđ‚āļĄāđ‚āļ‹āļĄāđ€āļ”āđ‡āļāļ—āļēāļĢāļ
     c.   āđāļ™āļ°āļ™āļēāļœāļŠāļĄāđ€āļ—āļĩāļĒāļĄāđ‚āļ”āļĒāđƒāļŠāđ‰āļ­āļŠāļļāļˆāļīāļœāļđāđ‰āļ­āļ·āđˆāļ™
     d.   āđāļ™āļ°āļ™āļēāļ—āļēIVFāđ‚āļ”āļĒāđƒāļŠāđ‰āđ„āļ‚āđˆāļ‚āļ­āļ‡āļœāļđāđ‰āļšāļĢāļīāļˆāļēāļ„
     e.   āđ„āļĄāđˆāļ•āđ‰āļ­āļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒ
Prenatal Diagnosisāļ—āļĩāđˆāļ„āļ§āļĢāļĢāļđāđ‰
ï‚Ļ   Down syndrome
    ï‚Ī Screening     test : NT,serum markers,US
     ïŪ First   trimester
     ïŪ Second     trimester

    ï‚Ī Diagnostic     test
     ïŪ First   trimester : CVS
     ïŪ Second     trimester : amniocentesis
Strategy                         Analytes                       DR (%)

First-trimester screen   NT, PAPP-A, hCG or free -hCG                 79–87
  NT (First trimester)   NT                                           64–70
       Triple test       MSAFP, hCG or free -hCG, uE3                 60–69
Quadruple (Quad) test    MSAFP, hCG or free -hCG, uE3, inh            67–81
                         First-trimester screen & Quad test—
  Integrated screen                                                   94–96
                         results withheld until Quad test completed
                         First-trimester screen & Quad test
                         — 1% offered diagnostic test after first
 Stepwise sequential
                         trimester screen — 99% proceed to Quad       90–95
       screen
                         test, results withheld until Quad test
                         completed

                         First-trimester screen & Quad test
                         — 1% offered diagnostic test after first-
Contingent sequential    trimester screen — 15% proceed to Quad
                                                                      88–94
       screen            test, results withheld until Quad test
                         completed — 84% have no additional test
                         after first-trimester screen
First-Trimester Screening

ï‚Ļ   GA 11 - 14 weeks.
    ï‚Ī hCG or free ïĒ-hCG

    ï‚Ī and PAPP-A(pregnancy-associated plasma
      protein A )
    ï‚Ī sonographic evaluation : NT

    ï‚Ī or a combination of both.


In the first trimester, for Down syndrome fetus
â€Ē serum hCG levels are >2.0 MoM
â€Ē PAPP-A levels are < 0.4 MoM
First-Trimester Screening

ï‚Ļ   NT measurement ï‚ģ 3.5 mm with a normal
    karyotype  targeted us examination , fetal
    echocardiography or both
                                  measured between
                                  GA11(0/7)and 13(6/7) wks.
ï‚Ļ   ïƒą nuchal translucency is associated :
    ï‚Ī structural   cardiac abnormalities
    ï‚Ī skeletal   dysplasias
2nd trimester screening

Test values for triple markers
screen
        Test             Unconjugated
                MSAFP                    hCG
                            Estriol

Trisomy 18         ï‚Ŋ           ï‚Ŋ          ï‚Ŋ

    NTD                      ↔          ↔
Trisomy 21         ï‚Ŋ           ï‚Ŋ          
Aneuploidy Risk Associated with
                        Selected Major Fetal Anomalies

      Abnormality       Approximate Population   Aneuploidy Risk   Common Aneuploidiesa
                              Incidence            (Percent)

                         1/300 Early US;1/2000
Cystic hygroma                                         50          45X,21,18,13, triploidy
                                 Birth
Nonimmune hydrops           1/1500–4000 B            10–20         21,18,13,45X triploidy

Ventriculomegaly             1/700–3000 B             5–25           13,18,21, triploidy

Holoprosencephaly             1/16,000 B             40–60           13,18,22, triploidy

Dandy Walker complex          1/30,000 B             30–50           18,13,21, triploidy

Cleft lip/palate             1/500–3000 B             5–15                 18,13

Cardiac defects                                      10–30           21,18,13,45X, 22q
                              5–8/1000 B
                                                                       microdeletion

Diaphragmatic hernia       1/2500–10,000 B            5–15                18,13,21

Esophageal atresia          1/2000–4000 B            10–40                 18,21

Duodenal atresia               1/5000 B              30–40                   21

Jejunal/ileal atresia          1/3000 B             Minimal                None

Gastroschisis               1/2000–5000 B           Minimal                None

Omphalocele                    1/4000 B              30–50           18,13,21, triploidy

Clubfoot                       1/1000 B               5–20                 18,13
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒG2P0A1 GA 25 wk. G1 āđāļ—āđ‰āļ‡āļˆāļēāļāļ—āļēāļĢāļ
āļšāļ§āļĄāļ™āđ‰āļē āļˆāļ°āļ•āļĢāļ§āļˆāļ§āđˆāļēāļĨāļđāļāđƒāļ™āļ—āđ‰āļ­āļ‡āļĄāļĩāļ āļēāļ§āļ°āļšāļ§āļĄāļ™āđ‰āļēāđ„āļ”āđ‰āļ­āļĒāđˆāļēāļ‡āđ„āļĢ



A.Amniocentesis
B.Cordocentesis
C.āļ•āļĢāļ§āļˆfetal cells āļˆāļēāļāđ€āļĨāļ·āļ­āļ”āđāļĄāđˆ
D.Ultrasound
Hydrops fetalis
Non immune hydrops             Immune hydrops
ï‚Ļ Cardiovascular disease       ïą Rh isoimmunization

ï‚Ļ Abnormal fetal karyotype

ï‚Ļ Chondrodysplasias

ï‚Ļ Twin pregnancy

ï‚Ļ Hematologic disease
                             Williams Obstetrics, 23e Chapter 29.
ï‚Ļ Thoracic
                             Diseases and Injuries of the Fetus and
ï‚Ļ Malformation sequence
                             Newborn

  and genetic syndrome
ï‚Ļ Metabolic

ï‚Ļ Urinary tract

ï‚Ļ Infection
Diagnosis

ï‚Ļ   targeted sonographic
ï‚Ļ   laboratory evaluations
HYPERTENSION IN
PREGNANCY
APPROACH
HYPERTENSION IN
PREGNANCY
â€Ē   Who have risk factor?

â€Ē   Classification of hypertension in pregnancy and
    criteria for diagnosis

â€Ē   Who should be investigation of preeclampsia?

â€Ē   How to management when preeclampsia occur ?

â€Ē   When and route of delivery ?
â€Ē   What are complication of preeclampsia?
ï‚Ļ   Nulliparity
ï‚Ļ   Advanced maternal age
ï‚Ļ   Obesity
ï‚Ļ   African – American ethnicity
ï‚Ļ   Multifetal gestation
ï‚Ļ   Pregnancy-associated factors : Hydatidiform mole ,
    Hydrops fetalis , Multifetal gestation
ï‚Ļ   Specific medical conditions: GDM, type I diabetes, obesity,
    chronic hypertension, renal disease, thrombophilias and
    APS
āđ‚āļˆāļ—āļĒāđŒ Predisposing factor of pre-eclampsia is
   A. Anemia
   B. Multigravida
   C.Dead fetus in utero
   D.Multiple pregnancy
   E. Chronic renal failure
Classifies HT in pregnancy
ï‚Ī Gestational   hypertension

ï‚Ī Preeclampsia    : mild / severe

ï‚Ī Eclampsia

ï‚Ī Chronic   hypertension

ï‚Ī Chronic   hypertension with superimposed
 preeclampsia
ï‚Ī HELLP   syndrome
āđ‚āļˆāļ—āļĒāđŒ Earliest sign of preeclampsia

A.Hypertension
B.Proteinuria
C.Headache
D.Visual disturbance
E.---
Common pathophysiologic changes seen
    in patients with preeclampsia

ï‚Ļ   Cardiovascular effects:

        Vasoconstriction and  cardiac output.




                       BP

      the earliest clinical finding of preeclampsia
āđ‚āļˆāļ—āļĒāđŒ āļœāļđāđ‰āļ›āđˆāļ§āļĒāļŦāļāļīāļ‡āļ­āļēāļĒāļļ 33 āļ›āļĩ GA 33weeks āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒ
āļ§āļąāļ”āļ„āļ§āļēāļĄāļ”āļąāļ™āđ‚āļĨāļŦāļīāļ•āđ„āļ”āđ‰ 140 / 90 mmHg, āļžāļąāļ 15 āļ™āļēāļ—āļĩāļ§āļąāļ”āļ‹āđ‰āļēāļāđ‡āļĒāļąāļ‡āđ„āļ”āđ‰
āđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ āļ•āļĢāļ§āļˆāđ‚āļ›āļĢāļ•āļĩāļ™āđƒāļ™āļ›āļąāļŠāļŠāļēāļ§āļ°āđ„āļ”āđ‰ 1 +
āļˆāļ‡āđƒāļŦāđ‰āļāļēāļĢāļ§āļīāļ™āļīāļˆāļ‰āļąāļĒ
   a.    Eclampsia
   b.    Mild preeclampsia
   c.    Severe preeclampsia
   d.    Gestational hypertension
Am J Obstet Gynecol 2000;183:S1-22.
                  Suchila Sritippayawan   01/02/54   72
Preeclampsia : Management
                 Gestational age


Term (GA â‰Ĩ 37 wks)                 Term (GA>37 wks)
                     yes
Delivery&MgSO4                Severe disease present ?
                                            no
                               Expectant Rx until term
Mild preeclampsia GA < 37 wk.

ï‚Ļ   Bed rest
ï‚Ļ   BP monitoring
ï‚Ļ   Urine monitoring
ï‚Ļ   Lab evaluation
ï‚Ļ   Fetal surveillance : NST
āļāļēāļĢāļ”āļđāđāļĨāđƒāļ™āļĢāļ°āļĒāļ°Intrapartum
ï‚Ļ āđ€āļāđ‰āļēāļĢāļ°āļ§āļąāļ‡āļ āļēāļ§āļ°severe preeclampsia /eclampsia
  (BP, sign and symptom)
ï‚Ļ Prophylaxis seizure : MgSO4

ï‚Ļ Controlled BP if BP â‰Ĩ160/110 mmHg):

  Hydralazine /Antihypertensive drugs
ï‚Ļ Monitor : vital signs,reflex,sign Magnesium

  toxicity
ï‚Ļ Continuous fetal monitor
Severe Preeclampsia :
Management
ï‚Ļ   Admit
ï‚Ļ   Stabilized MgSO4 for seizure prevention
ï‚Ļ   BP control
ï‚Ļ   Work up lab
ï‚Ļ   Termination of pregnancy
Severe Preeclampsia :
Management(Preterm)
 No severe conditions which should immediately delivery



                                    GA 24 - wks.
                                           steroids


                                           delivery
Severe preeclampsia :
Management
ï‚Ļ   Termination of pregnancy when :
    ï‚Ī Term   pregnancy
    ï‚Ī Severe preclampsia with sign of acute renal failure
      , thrombocytopenia , pulmonary edema,hepatic
      injury,DIC
    ï‚Ī Suspected abruptio placenta
    ï‚Ī Eclampsia
    ï‚Ī HELLP syndrome

    ï‚Ī Non reassuring fetal status
    ï‚Ī Severe IUGR
    ï‚Ī Labor or labor of rupture of membranes
Indications for delivery in preeclampsia

āļ”āđ‰āļēāļ™āđāļĄāđˆ                       āļ”āđ‰āļēāļ™āļĨāļđāļ
ï‚Ļ āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ â‰Ĩ 38 āļŠāļąāļ›āļ”āļēāļŦāđŒ
                              ï‚Ļ   āļĄāļĩāļ āļēāļ§āļ° Severe fetal
ï‚Ļ āļ„āļ§āļšāļ„āļļāļĄāļ„āļ§āļēāļĄāļ”āļąāļ™āđ‚āļĨāļŦāļīāļ•āđ„āļĄāđˆāđ„āļ”āđ‰
                                  growth restriction
ï‚Ļ Severe preeclampsia
                              ï‚Ļ   āļĄāļĩāļ āļēāļ§āļ° Nonreassuring
   (āļ­āļēāļāļēāļĢāđāļĨāļ°āļ­āļēāļāļēāļĢāđāļŠāļ”āļ‡, lab)
                                  results from fetal
ï‚Ļ Eclampsia
                                  testing
ï‚Ļ HELLP syndrome

ï‚Ļ Placental abruption
                              ï‚Ļ   Oligohydramnios
Route of delivery
    ï‚Ļ      Vaginal route delivery is preferred
    ï‚Ļ      Unfavorable cervix  ripening cervix
    ï‚Ļ      Depen on maternal and fetal condition
    ï‚Ļ      āļ‚āđ‰āļ­āļ„āļ§āļĢāļĢāļ°āļ§āļąāļ‡ : āđ„āļĄāđˆāđƒāļŦāđ‰ ERGOMETRINE
           āđƒāļŦāđ‰oxytocin āđāļ—āļ™


            C/S delivery reserved for OB indication

01/02/54                     Suchila Sritippayawan    81
āļāļēāļĢāļ”āļđāđāļĨāđƒāļ™āļĢāļ°āļĒāļ°Postpartum
ï‚Ļ   Most Rapid improved / Some may worsening
ï‚Ļ   Continue MgSO4 for 24 hr
ï‚Ļ   Monitoring of
    ï‚Ī Blood pressure

       Hydralazine or nifedipine PRN BP > 160/110
    ï‚Ī maternal symptoms

    ï‚Ī measurements of fluid intake and urine output.

ï‚Ļ   Follow up 2 wk after discharge
    If hypertension persist , give thiazide or beta-
    blockers or nifedipine
Management : eclampsia

ï‚Ļ   Prevention of maternal hypoxia and
    trauma
ï‚Ļ   Blood pressure control
ï‚Ļ   Prevention of recurrent seizures
ï‚Ļ   Delivery when : stabilized and seizures
    have been controlled
Management : eclampsia

Mode of delivery depend on
ï‚Ļ   Gestational age
ï‚Ļ   Bishop score, whether the patient is in
    labor
ï‚Ļ   Fetal condition and position
Management : eclampsia

 The definitive treatment of eclampsia is
 delivery, irrespective of gestational age

The best way to treat the fetus is to
stabilized the mother

C/S should be reserved for OB condition
Management : eclampsia
Stabilizing the mother by administering anticonvulsant drugs
and oxygen      Treating severe hypertension (if present)



can help the fetus recover in-utero from the effects of
maternal hypoxia, hypercarbia, and uterine hyperstimulation


   if10 – 15 min with no improvement despite maternal
   and fetal resuscitative interventions
                              occult abruption ?

      emergent delivery should be considered
A. Oral antihypertensive drug
B. Diuretics
C. MgSO4
D. Induction of labor
E. Expectation with materno-fetal
   observe
āđ‚āļˆāļ—āļĒāđŒ āļœāļđāđ‰āļ›āđˆāļ§āļĒāļŦāļāļīāļ‡āļ­āļēāļĒāļļ 31 āļ›āļĩ GA 32weeks āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒāļ•āļēāļĄāļ™āļąāļ”
āļ§āļąāļ”āļ„āļ§āļēāļĄāļ”āļąāļ™āđ‚āļĨāļŦāļīāļ•āđ„āļ”āđ‰ 130 / 90 mmHg, āļ•āļĢāļ§āļˆāđ‚āļ›āļĢāļ•āļĩāļ™āđƒāļ™āļ›āļąāļŠāļŠāļēāļ§āļ°āđ„āļ”āđ‰ 1 +
āđ„āļĄāđˆāļĄāļĩāļ­āļēāļāļēāļĢāļ›āļ§āļ”āļĻāļĩāļĢāļĐāļ° āļ•āļēāļĄāļąāļ§ āļˆāļļāļāđāļ™āđˆāļ™āđƒāļ•āđ‰āļĨāļīāđ‰āļ™āļ›āļĩāđˆ āđ„āļĄāđˆāļĄāļĩāļ•āļāļ‚āļēāļ§ āļ„āļąāļ™āļŠāđˆāļ­āļ‡āļ„āļĨāļ­āļ”
āļ›āļąāļŠāļŠāļēāļ§āļ°āđ„āļĄāđˆāđāļŠāļšāļ‚āļąāļ” āđāļžāļ—āļĒāđŒāđāļ™āļ°āļ™āļēāđƒāļŦāđ‰āđ„āļ›āļ§āļąāļ”āļ„āļ§āļēāļĄāļ”āļąāļ™āđ‚āļĨāļŦāļīāļ•āļ—āļĩāđˆ
āļŠāļ–āļēāļ™āļĩāļ­āļ™āļēāļĄāļąāļĒāđƒāļāļĨāđ‰āļšāđ‰āļēāļ™ āđāļĨāļ°āļ™āļąāļ”āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒāļ­āļĩāļ 1 lāļŠāļąāļ›āļ”āļēāļŦāđŒāļ•āđˆāļ­āļĄāļē
āļ§āļąāļ”āļ„āļ§āļēāļĄāļ”āļąāļ™āđ‚āļĨāļŦāļīāļ•āđ„āļ”āđ‰ 170 / 110 mmHg, āļ•āļĢāļ§āļˆāđ‚āļ›āļĢāļ•āļĩāļ™āđƒāļ™āļ›āļąāļŠāļŠāļēāļ§āļ°āđ„āļ”āđ‰ 3+
āļ—āđˆāļēāļ™āļˆāļ°āđƒāļŦāđ‰āļāļēāļĢāļ”āļđāđāļĨāļœāļđāđ‰āļ›āđˆāļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰āļ­āļĒāđˆāļēāļ‡āđ„āļĢ

      a.   āđƒāļŦāđ‰ MgSO4
      b.   āđƒāļŦāđ‰ Pethidine
      c.   āđƒāļŦāđ‰ Oxytocin
      d.   āđƒāļŦāđ‰ Diazepam
āđ‚āļˆāļ—āļĒāđŒ A 32-week primigravida comes to the antenatal clinic
  for her regular appointment. The physical examination
  shows 2 kg weight gain in 2 wks, BP 160/110 mmHg,
  edema over all extremities, 3+ DTR, and 2+ proteinuria.
  The most appropriate initial management is
       A. Diazepam
       B. Furosemide
       C.Hydralazine
       D.Calcium gluconate
       E. Magnesium sulfate
A.   Observed
B.   C/S emergency
C.   MgSO4 then observe
D.   MgSO4then try ND
E.   MgSO4then C/S
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 18āļ›āļĩ G1P0 āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 30
āļŠāļąāļ›āļ”āļēāļŦāđŒ āļĄāļēāļŦāđ‰āļ­āļ‡āļ„āļĨāļ­āļ”āļ”āđ‰āļ§āļĒāļ­āļēāļāļēāļĢāļ›āļ§āļ”āļĻāļĩāļĢāļĐāļ°
āļ§āļąāļ”BPāđ„āļ”āđ‰ 160/110 mm Hg
āđ€āļˆāļēāļ°āđ€āļĨāļ·āļ­āļ”āļ•āļĢāļ§āļˆ āļžāļšāļ§āđˆāļēāļĄāļĩelevated liver function test
āđāļĨāļ°Platelet count 60,000/mm3
āļāļēāļĢāļ”āļđāđāļĨāļ—āļĩāđˆāđ€āļŦāļĄāļēāļ°āļŠāļĄāļŠāļēāļŦāļĢāļąāļšāļœāļđāđ‰āļ›āļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰āļ„āļ·āļ­
                             āđˆ


  a.   āđƒāļŦāđ‰oral antihypertensive therapy
  b.   platelet transfusion
  c.   MgSO4 therapy and induction of labor
  d.   IV Immunoglobulin therapy
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 30āļ›āļĩ G1P0 āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 29
āļŠāļąāļ›āļ”āļēāļŦāđŒ āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒāļ•āļēāļĄāļ™āļąāļ” āļ§āļąāļ”BPāđ„āļ”āđ‰ 140/90 mm Hg
āđ€āļˆāļēāļ°āđ€āļĨāļ·āļ­āļ”āļ•āļĢāļ§āļˆ liver function test āđāļĨāļ°Platelet count
āļ›āļāļ•āļī Urine protein 2+
āļāļēāļĢāļ”āļđāđāļĨāļ—āļĩāđˆāđ€āļŦāļĄāļēāļ°āļŠāļĄāļŠāļēāļŦāļĢāļąāļšāļœāļđāđ‰āļ›āļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰āļ„āļ·āļ­
                            āđˆ

  a. Induction of labor
  b. Cesarean section
  c. Antihypertensive therapy
  d. Expectant management
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 25āļ›āļĩ G1P0 āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 38
āļŠāļąāļ›āļ”āļēāļŦāđŒ āļĄāļĩāļ­āļēāļāļēāļĢāļ›āļ§āļ”āļĻāļĩāļĢāļĐāļ° āļĢāļđāđ‰āļŠāļķāļāļ§āđˆāļēāļĨāļđāļāļ”āļīāļ™āļ™āđ‰āļ­āļĒāļĨāļ‡
                                      āđ‰
āļ§āļąāļ”BPāđ„āļ”āđ‰ 180/110 mm Hg uterine size ~ date ,
DTR +3,Urine protein 2+
āļ„āļ§āļĢāđƒāļŦāđ‰āļĒāļēāđƒāļ”
   a. Diazepam
   b. MgSO4
   c. Antihypertensive drug
   d. ------
   e. -------
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 26āļ›āļĩ G2P1āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 32āļŠāļąāļ›āļ”āļēāļŦāđŒ āļĄāļēāļāļēāļ
āļ„āļĢāļĢāļ āđŒāļ•āļēāļĄāļ™āļąāļ”āđāļžāļ—āļĒāđŒāđƒāļŦāđ‰āļ™āļ­āļ™āđ‚āļĢāļ‡āļžāļĒāļēāļšāļēāļĨāđ€āļžāļĢāļēāļ°āļ§āļąāļ” BPāļžāļšāļ§āđˆāļēBPāđ„āļ”āđ‰
170/110 mm Hg āđ„āļĄāđˆāļĄāļĩāļ­āļēāļāļēāļĢāļœāļīāļ”āļ›āļāļ•āļīāđƒāļ”āđ† āļŦāļĨāļąāļ‡āļžāļąāļ āļ§āļąāļ” BPāļ‹āđ‰āļē =
150/98 mmHg proteinuria = 1 + āđāļžāļ—āļĒāđŒāļŠāļ‡labāđāļĨāļ°āđƒāļŦāđ‰āļ™āļ­āļ™āļžāļąāļ
                                       āđˆ
āđƒāļ™āđ‚āļĢāļ‡āļžāļĒāļēāļšāļēāļĨ āļ‚āđ‰āļ­āđƒāļ”āđ€āļ›āđ‡āļ™āļ‚āļąāđ‰āļ™āļ•āļ­āļ™āļ•āđˆāļ­āđ„āļ›āļ‚āļ­āļ‡āļāļēāļĢāļ”āļđāđāļĨāļœāļđāđ‰āļ›āđˆāļ§āļĒāļĢāļēāļĒāļ™āļĩ


         a.   Induced labor : vaginal delivery
         b.   Cesarean section
         c.   Phenytoin
         d.   Labetalol
         e.   Dexamethasone
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 32 āļ›āļĩ G3P2 GA 35 wk.
underlying CHT āļŠāđˆāļ§āļ‡ANC BPāđ„āļĄāđˆāđ€āļāļīāļ™ 140/90 mmHg,no
proteinuria āļĄāļēANC āļ„āļĢāļąāđ‰āļ‡āļĨāđˆāļēāļŠāļļāļ” BP > 140/83 mmHg urine
protein 24āļŠāļĄ.=0.35 g
āļāļēāļĢāļ”āļđāđāļĨāļ‚āļąāļ™āļ•āļ­āļ™āļ•āđˆāļ­āđ„āļ›āļ„āļ·āļ­
         āđ‰
 (A) Administer oral furosemide
 (B) Prepare for emergent delivery
 (C) Restart the patient‘s prepregnancy
 antihypertensive
 regimen
 (D) Restricted activity and close monitoring as
 an outpatient following initial inpatient
 evaluation
 (E) Start hydralazine
DM IN PREGNANCY
Approach Diabetes in
     pregnancy




97                     2/1/2011
ï‚Ļ   Finding : who has risk of DM in pregnancy
     ï‚Ļ   Screening GDM : 50 gm GCT
     ï‚Ļ   Confirm diagnosis : who has positive 50gm
         GCT(100gm OGTT)
     ï‚Ļ   Classified type of DM : GDM A1,A2 ,PGDM
     ï‚Ļ   Management :
         ï‚Ī   antepartum ,intrapartum ,postpartum
         ï‚Ī   Maternal and fetus


98                                          2/1/2011
āļŠāļīāđˆāļ‡āļ—āļĩāđˆāļ„āļ§āļĢāļĢāļđāđ‰

ï‚Ļ   Classification of DM : overt DM (PGDM),GDM

ï‚Ļ   Screening GDM : who,when ,how

ï‚Ļ   Complication of DM : Maternal , fetus

ï‚Ļ   Interpretation of BS

ï‚Ļ   Management : control DM , monitor
    complication,time of delivery and route of delivery
āđ‚āļˆāļ—āļĒāđŒ āļœāļđāđ‰āļ›āđˆāļ§āļĒāļŦāļāļīāļ‡āļ­āļēāļĒāļļ 39 āļ›āļĩ āļ™āđ‰āļēāļŦāļ™āļąāļ 65 āļāļ.āļŠāļđāļ‡ 152 āļ‹āļĄ.
āļ›āđ‰āļēāđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™ āļĨāļđāļāļ„āļ™āđāļĢāļāļ™āđ‰āļēāļŦāļ™āļąāļāđāļĢāļāļ„āļĨāļ­āļ” 4200 āļ.
āļ‚āđ‰āļ­āđƒāļ”āđ€āļ›āđ‡āļ™āļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āļ•āđˆāļ­āļāļēāļĢāđ€āļ›āđ‡āļ™āđ‚āļĢāļ„āđ€āļšāļēāļŦāļ§āļēāļ™āļ‚āļ­āļ‡āļœāļđāđ‰āļ›āđˆāļ§āļĒ
āļĢāļēāļĒāļ™āļĩāđ‰āļĄāļēāļāļ—āļĩāļŠāļļāļ”
a.   āļ­āđ‰āļ§āļ™
b.   āđ€āļ•āļĩāđ‰āļĒ
c.   āļ›āđ‰āļēāđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™
d.   āļĨāļđāļāļ„āļ™āđāļĢāļāđ€āļ›āđ‡āļ™macrosomia
e.   āļ­āļēāļĒāļļāđāļĄāđˆ> 25āļ›āļĩ
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 30 āļ›āļĩ G3P2 GA 25wk. āļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļī
āļ„āļĢāļĢāļ āđŒāļ—āļĩāđˆāđāļĨāđ‰āļ§āđ€āļ›āđ‡āļ™GDM
āļ„āļĢāļĢāļ āđŒāļ™āļĩāđ‰ āđ€āļĄāļ·āđˆāļ­ GA 10 wk.FBS=110 mg/dL,no glucouria
āļœāļđāđ‰āļ›āđˆāļ§āļĒāļ„āļļāļĄāļ­āļēāļŦāļēāļĢāđ€āļ­āļ‡ 2-3 wk.PTA āļĄāļĩāļ­āļēāļāļēāļĢ
polyuria,fatigue
āļˆāļ°āļ”āļđāđāļĨāļœāļđāđ‰āļ›āļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰āļ­āļĒāđˆāļēāļ‡āđ„āļĢāļ•āđˆāļ­āđ„āļ›
           āđˆ

(A) Administer a 3-hour glucose tolerance test
(B) Administer a 50-g 1-hour glucose tolerance test
(C) Begin insulin therapy
(D) Check a urinalysis and start insulin if urinalysis
reveals glucose in the urine
(E) Prescribe metformin to be taken daily
āļāļĨāļļāđˆāļĄāļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āļ•āđˆāļē (āļžāļšāļ—āļļāļāļ‚āđ‰āļ­āļ•āđˆāļ­āđ„āļ›āļ™āļĩāđ‰) āļ—āļĩāđˆāđāļ™āļ°āļ™āļēāļ§āđˆāļē
       āļ­āļēāļˆāđ„āļĄāđˆāļˆāļēāđ€āļ›āđ‡āļ™āļ•āđ‰āļ­āļ‡āļ•āļĢāļ§āļˆāļ„āļąāļ”āļāļĢāļ­āļ‡
102


 ï‚Ļ    āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ<25āļ›āļĩ
 ï‚Ļ    āļĄāļĩāđ€āļŠāļ·āđ‰āļ­āļŠāļēāļ•āļīāļ—āļĩāđˆāļĄāļĩāļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āļ•āđˆāļē ( āļĒāļāđ€āļ§āđ‰āļ™āđ€āļŠāļ·āđ‰āļ­āļŠāļēāļ•āļī Hispanic, African, Native
      American, South or East Asian origins)
 ï‚Ļ    āđ„āļĄāđˆāļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāļ„āļĢāļ­āļšāļ„āļĢāļąāļ§ āļāļēāļ•āļīāđƒāļāļĨāđ‰āļŠāļīāļ”āđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™
 ï‚Ļ    āļ™āļ™.āļāđˆāļ­āļ™āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāđāļĨāļ°āļ™āļ™.āļ—āļĩāđˆāđ€āļžāļīāđˆāļĄāļĢāļ°āļŦāļ§āđˆāļēāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ›āļāļ•āļī (BMI< 26 kg./m2)
 ï‚Ļ    āđ„āļĄāđˆāļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāļ—āļēāļ‡āļŠāļđāļ•āļīāļĻāļēāļŠāļ•āļĢāđŒāļ—āļĩāđˆāļœāļīāļ”āļ›āļāļ•āļīāļ—āļĩāđˆāđ€āļāļĩāđˆāļĒāļ§āļ‚āđ‰āļ­āļ‡āļāļąāļš
      GDM(macrosomia,stillbirth,malformation)
 ï‚Ļ    āđ„āļĄāđˆāđ€āļ„āļĒāļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāļĢāļ°āļ”āļąāļšāļ™āđ‰āļēāļ•āļēāļĨāđƒāļ™āđ€āļĨāļ·āļ­āļ”āļœāļīāļ”āļ›āļāļ•āļī


                                            ADA ,Diabetic
                                        Suchila Sritippayawan   care 2004;(Suppl 1):S88 – 90
                                                                 2/1/2011
      2/1/2011
                                             Chula
Recommended Screening Strategy Based on Risk
  Assessment for Detecting Gestational Diabetes

  High Risk
  Perform blood glucose testing as soon as feasible. If
  gestational diabetes is not diagnosed, blood glucose
  testing should be repeated at 24-28 weeks or at any
  time a patient has symptoms or signs suggestive of
  hyperglycemia


  High risk — women with marked obesity, strong family
  history of type 2 diabetes, prior gestational diabetes,
  or glucosuria
103                                     2/1/2011
ï‚Ļ    The best time to screen for DM during
      pregnancy :
      ï‚Ī   GA 24 – 28 weeks
 ï‚Ļ    Patient with â‰Ĩ 1 risk factors for developing
      GDM should be screened at
      ï‚Ī   The first prenatal visit and
      ï‚Ī   GA 24 – 28 weeks or
      ï‚Ī   symptoms or signs suggestive of
104       hyperglycemia               2/1/2011
Who have risk factor of GDM



                 50 gm glucose challenge test
                                                     for 80% detection
                   āļ„āđˆāļēāļœāļīāļ”āļ›āļāļ•āļī â‰Ĩ 140 mg/dL


                      100 gm OGTT Diagnostic test
105                          Suchila Sritippayawan   2/1/2011
      2/1/2011
100 gm OGTT
                 Fasting plasma glucose              105 mg/dL
                 1 hour                              190 mg/dL
                 2 hour                              165mg/dL
                 3 hour                              145mg/dL



                    āļœāļīāļ”āļ›āļāļ•āļī āļ•āļąāđ‰āļ‡āđāļ•āđˆ 2 āļ„āđˆāļēāļ‚āļķāđ‰āļ™āđ„āļ›
                                                        GDMA1
                           GDM
106                          Suchila Sritippayawan
                                                         GDMA2
                                                      2/1/2011
      2/1/2011
āđ‚āļˆāļ—āļĒāđŒ āļœāļđāđ‰āļ›āļ§āļĒāļŦāļāļīāļ‡āļ­āļēāļĒāļļ38āļ›āļĩ āđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™ āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒ GA
          āđˆ
30wks. āļĄāļēāļ”āđ‰āļ§āļĒāđ€āļˆāđ‡āļšāļ„āļĢāļĢāļ āđŒāļ„āļĨāļ­āļ”āđāļĨāļ°āļ›āļąāļŠāļŠāļēāļ§āļ°āļšāđˆāļ­āļĒ āļ•āļĢāļ§āļˆ
āļžāļšāļĄāļ”āļĨāļđāļāļ­āļĒāļđāđˆāļĢāļ°āļ”āļąāļšāļĨāļīāļ™āļ›āļĩāđˆ āļ„āļĨāļēāļŠāđˆāļ§āļ™āļ‚āļ­āļ‡āļ—āļēāļĢāļāđ„āļĄāđˆāļŠāļąāļ” FHS
                  āđ‰
152/min Uterine contraction 1āļ„āļĢāļąāđ‰āļ‡āđƒāļ™ 30āļ™āļēāļ—āļĩ
PV: cervix dilated 1cm , effacement 50% āļ­āļĒāļēāļ
āļ—āļĢāļēāļšāļ§āđˆāļēāļŠāļēāđ€āļŦāļ•āļļāļ—āļĩāđˆāļ—āļēāđƒāļŦ āđ‰āđ€āļāļīāļ” āļĨāļąāļāļĐāļ“āļ°āđƒāļ™āļœāļđāđ‰āļ›āļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰āļ„āļ·āļ­
                                       āđˆ

         A.   Macrosomia
         B.   Twin pregnancy
         C.   Myoma uteri
         D.   Polyhydramnios
         E.   Urinary tract infection
Etiology of polyhydramnios
       Etiology       %
      Idiopathic      60
    Maternal DM       19
       Multiple       7.5
   gestation(TTTS)
     Blood group      5
    incompatibility
      Congenital      8.5
     malformation
Fetal malformations associated with
             polyhydramnios
                    anencephaly , encephalocele Iniencephaly
  CNS defects       ,hydranencephaly
                    esophageal atresia, duodenal atresia ,small
                    bowel obstruction ,omphalocele ,
 GI obstruction
                    gastroschisis,cleft palate, diaphragmatic
                    hernia
                    cystic adenomatoid malformation of the
Respiratory tract   lungs,chylothorax
                    Fetal renal harmatoma, Unilateral
    GU tract        ureteriopelvic junction obstruction
Cardiovascular      vulvular incompetence,Ebstein’s anomaly ,
    system          arrythmias,TTTS
                    fetal akinesia , skeletal dysplasia,myotonic
Musculoskeletal
                    dystrophy
   system
Diagnosis polyhydramnios

        Technique              cm.

             AFI            >24 - 25 cm
Vertical single deepest
pocket volume :
   ïą Mild                 8 -11cm (80%)
   ïą Moderate             12 – 15 cm (15%)
   ïą Severe               â‰Ĩ 16 cm (5%)
Evaluation
 ïķScreening        DM
 ïķ Detailed    sonographic examination for
  anomalies
 ïķ Fetal   karyotype (in case severe
  polyhydramnios,fetal anomaly)
 ïķ Coombs’test     : Rh isoimmunization
 ïķ Infection   screening : syphilis
Screening GDM

ï‚Ļ   50 g GCT
ï‚Ļ   Positive screening : ï‚ģ 140 mg/dL
āļāļĨāļļāđˆāļĄāļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āļ•āđˆāļē (āļžāļšāļ—āļļāļāļ‚āđ‰āļ­āļ•āđˆāļ­āđ„āļ›āļ™āļĩāđ‰) āļ—āļĩāđˆāđāļ™āļ°āļ™āļēāļ§āđˆāļē
       āļ­āļēāļˆāđ„āļĄāđˆāļˆāļēāđ€āļ›āđ‡āļ™āļ•āđ‰āļ­āļ‡āļ•āļĢāļ§āļˆāļ„āļąāļ”āļāļĢāļ­āļ‡
113


 ï‚Ļ    āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ<25āļ›āļĩ
 ï‚Ļ    āļĄāļĩāđ€āļŠāļ·āđ‰āļ­āļŠāļēāļ•āļīāļ—āļĩāđˆāļĄāļĩāļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āļ•āđˆāļē ( āļĒāļāđ€āļ§āđ‰āļ™āđ€āļŠāļ·āđ‰āļ­āļŠāļēāļ•āļī Hispanic, African, Native
      American, South or East Asian origins)
 ï‚Ļ    āđ„āļĄāđˆāļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāļ„āļĢāļ­āļšāļ„āļĢāļąāļ§ āļāļēāļ•āļīāđƒāļāļĨāđ‰āļŠāļīāļ”āđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™
 ï‚Ļ    āļ™āļ™.āļāđˆāļ­āļ™āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāđāļĨāļ°āļ™āļ™.āļ—āļĩāđˆāđ€āļžāļīāđˆāļĄāļĢāļ°āļŦāļ§āđˆāļēāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ›āļāļ•āļī (BMI< 26 kg./m2)
 ï‚Ļ    āđ„āļĄāđˆāļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāļ—āļēāļ‡āļŠāļđāļ•āļīāļĻāļēāļŠāļ•āļĢāđŒāļ—āļĩāđˆāļœāļīāļ”āļ›āļāļ•āļīāļ—āļĩāđˆāđ€āļāļĩāđˆāļĒāļ§āļ‚āđ‰āļ­āļ‡āļāļąāļš
      GDM(macrosomia,stillbirth,malformation)
 ï‚Ļ    āđ„āļĄāđˆāđ€āļ„āļĒāļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāļĢāļ°āļ”āļąāļšāļ™āđ‰āļēāļ•āļēāļĨāđƒāļ™āđ€āļĨāļ·āļ­āļ”āļœāļīāļ”āļ›āļāļ•āļī


                                            ADA ,Diabetic
                                        Suchila Sritippayawan   care 2004;(Suppl 1):S88 – 90
                                                                 2/1/2011
      2/1/2011
                                             Chula
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 32 āļ›āļĩ āļĄāļēANC GA 22 wk. āļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāđ€āļ›āđ‡āļ™
DM āļĄāļē 3 āļ›āļĩāđƒāļŠāđ‰ insulināļĄāļēāļ•āļĨāļ­āļ” FBS 105 mg/dL,2hr.PP BS
139 mg/dL


  āļˆāļ°investigation āļ­āļ°āđ„āļĢāđ€āļžāļīāđˆāļĄāđ€āļ•āļīāļĄ

A. BPP
B. Maternal serum triple screening test
C. Maternal serum AFP
D. Fetal Doppler US
E. Fetal echocardiography                         
a.   āļ­āđ‰āļ§āļ™                     BMI 28.1 āļāļ./āļ•āļēāļĢāļēāļ‡āđ€āļĄāļ•āļĢ
b.   āđ€āļ•āļĩāđ‰āļĒ
c.   āļ›āđ‰āļēāđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™
d.   āļĨāļđāļāļ„āļ™āđāļĢāļāđ€āļ›āđ‡āļ™macrosomia
e.   āļ­āļēāļĒāļļāđāļĄāđˆ> 25āļ›āļĩ
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 30 āļ›āļĩ G2P1 12 weeks āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒ
āđ€āļ„āļĒāļ„āļĨāļ­āļ”āļ—āļēāļĢāļāļŦāļ™āļąāļ 3900 āļāļĢāļąāļĄ āļĄāļĩāļ›āđ‰āļēāđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™
āļœāļđāđ‰āļ›āđˆāļ§āļĒāļŦāļ™āļąāļ 72 āļāļ. āļŠāļđāļ‡ 155 āļ‹āļĄ.
āļ‚āđ‰āļ­āđƒāļ”āđ€āļ›āđ‡āļ™āļ›āļąāļˆāļˆāļąāļĒāđ€āļŠāļĩāđˆāļĒāļ‡āļ—āļĩāđˆāļ•āđ‰āļ­āļ‡āļ„āļąāļ”āļāļĢāļ­āļ‡āđ€āļšāļēāļŦāļ§āļēāļ™
     a.   āļ­āđ‰āļ§āļ™                   BMI 29.96 āļāļ./āļ•āļĢ.āđ€āļĄāļ•āļĢ
     b.   āđ€āļ•āļĩāđŠāļĒ
     c.   āļ›āđ‰āļēāđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™
     d.   āđ€āļ„āļĒāļ„āļĨāļ­āļ”āļ—āļēāļĢāļāļ•āļąāļ§āđ‚āļ•
āđ‚āļˆāļ—āļĒāđŒ āļ‚āđ‰āļ­āđƒāļ”āđ„āļĄāđˆāđƒāļŠāđˆ indication āđƒāļ™āļāļēāļĢāļ•āļĢāļ§āļˆ screening GCT in
  pregnancy
   A. History of preterm labour
   B. History of stillbirth
   C.History of LGA
   D.Family history of DM
   E. Persistent glucosuria
DIABETES                                   INSULI
                                            DURATI VASCULAR
        CLASS             ONSET AGE                                     N
                                            ON (Y)  DISEASE
                              (Y)                                      NEED
Gestational diabetes
          A1               Any                 Any                0     0
          A2               Any                 Any                0     +
Pregestational diabetes

           B               >20                 <10                0     +
          C               10-19        or    10-19                0     +
          D                <10         or      >20                +     +
           F               Any                 Any                +     +
          R                Any                 Any                +     +
           T               Any                 Any                +     +
          H                Any Suchila Sritippayawan
                                                Any    2/1/2011   +     +
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡ 32 āļ›āļĩ āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒāļ„āļĢāļąāđ‰āļ‡āđāļĢāļāļ•āļ­āļ™āļ™āļĩāđ‰āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 22 wks
āļœāļđāđ‰āļ›āđˆāļ§āļĒāđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™āļĄāļē 3 āļ›āļĩ āđ„āļ”āđ‰ Insulin āļĄāļēāļ•āļĨāļ­āļ” āļ•āļĢāļ§āļˆ FBS =105
mg/dl 2 hour glucose = 139 mg/dl āļˆāļ° investigation āļ­āļ°āđ„āļĢ
āđ€āļžāļīāđˆāļĄāđ€āļ•āļīāļĄ
    1. BPP
    2. Maternal serum triple test
    3. Maternal serum AFP
    4. Fetal Doppler U/S
    5. Fetal echography
Complication :Pregestational Diabetes Mellitus
                  (PGDM)
 ï‚Ļ Malformation :

      Caudal   regression syndrome (rare)
      Sirenomelia   (rare)
      cardiovascular   malformations (↑occur 2- 5
      fold
       compared to the non-diabetic population)
      genitourinary   tract
      musculoskeletal    anomalies
                           Suchila Sritippayawan   2/1/2011
Complication :Pregestational Diabetes Mellitus
                      (PGDM)


Maternal effect :

ï‚Ļ   Chronic hypertension
ï‚Ļ   Preeclampsia
ï‚Ļ   Microalbuminuria and diabetic nephropathy may
    complicate pregnancy prognosis
ï‚Ļ   Diabetic retinopathy

                           Suchila Sritippayawan   2/1/2011
Complication :Pregestational Diabetes Mellitus
                      (PGDM)

Maternal effect :
ï‚Ļ Ketoacidosis: (insulin resistance ï‚Ū insulin
  deficiency)
    ïŪ Common   risk factors : new onset diabetes;
     infections(influenza and UTI); poor patient
     compliance; insulin pump failure; and
     treatment with Îē-mimetic tocolytic
     medications and antenatal corticosteroids
                        Suchila Sritippayawan   2/1/2011
Complication :Pregestational Diabetes
Mellitus (PGDM)
Maternal effect :

ï‚Ļ   Infection (DM type 1)
    Common infection : candida vulvovaginitis , UTI ,
    URI ,puerperal and pelvic infection
    4% antepartum pyelonephritis develop (with DM
    type 1)
    ï‚Ū screening for asymptomatic bacteriuria

                            Suchila Sritippayawan   2/1/2011
Management

Goal :

ï‚Ļ   to lower the likelihood of Macrosomia

ï‚Ļ   To reduce neonatal hypoglycemia




                       Suchila Sritippayawan   2/1/2011
Management :
Pregestational Diabetes Mellitus

ï‚Ļ   Prepregnancy counseling
ï‚Ļ   Glycemic control during gestation : Diet ,insulin
ï‚Ļ   Fetal assessment
ï‚Ļ   Timing and mode of delivery
ï‚Ļ   Glycemic management during labor
ï‚Ļ   Postpartum care and lactation
ï‚Ļ   Contraception



                        Suchila Sritippayawan   2/1/2011
Prepregnancy counseling
ï‚Ļ   Optimal care and patient education : prevent early
    pregnancy loss and congenital malformation
ï‚Ļ   Preconceptional glucose control
    ï‚Ī Prepandial glucose : 70 – 100 mg/dl
    ï‚Ī Postpandrial glucose : 1 hr. < 140 mg/dl

                              2 hr. < 120 mg/dl
    ï‚Ī Glycated Hb : within 3 SD of normal mean

ï‚Ļ   Folic acid supplement 400 g/day
    (periconception – during early pregnancy) to
    decrease NTD
                           Suchila Sritippayawan   2/1/2011
Glycemic management during pregnancy
PGDM

ï‚Ļ   The management of diabetes in pregnancy
    must focus on excellent glucose control
    achieved using a careful combination of
     diet, exercise, and insulin therapy




                       Suchila Sritippayawan   2/1/2011
Glycemic management during pregnancy
    PGDM


ï‚Ļ   Caloric requirement :
    ï‚Ī   usually require 30–35 kcal/kg/d.

ï‚Ļ   Caloric composition includes
    ï‚Ī   40–50% from complex,high-fiber carbohydrates

    ï‚Ī   20% from protein
    ï‚Ī   30–40% from primarily unsaturated fats.

                               Suchila Sritippayawan   2/1/2011
Fetal assessment

ï‚Ļ   Early US : fetal viability and to accurate date the
    pregnancy
ï‚Ļ   Target US GA 18 – 20 weeks
ï‚Ļ   Periodic US : to confirm fetal growth
ï‚Ļ   Antepartum fetal monitoring :
    ï‚Ī   Initiation of testing at GA 32–34 weeks
    ï‚Ī   Earlier GA in high risk conditions.
    ï‚Ī   Daily fetal movement count


                               Suchila Sritippayawan   2/1/2011
Indication for delivery in diabetes pregnancy


Fetal        Non reactive , positive CST
             Reactive positive CST, mature fetus

             GA 40 – 41 weeks

             U/S evidence of Fetal growth arrest

             Decline in fetal growth rate with decreased AF

Maternal     Severe preeclampsia,

             Mild preeclampsia mature fetus

             Markedly falling renal function( Cr clearance <
            40 ml/min)
Obstetric      Preterm labor with failure of tocolysis
               Mature fetus , inducible cervix
                            Suchila Sritippayawan   2/1/2011
Timing and route of delivery

ï‚Ļ   Early delivery may be indicated :
    ï‚Ī in   patients with vasculopathy, nephropathy
    ï‚Ī poor    glucose control
    ï‚Ī prior   stillbirth
ï‚Ļ   patients with well-controlled may be allowed to
    progress to their expected date of delivery as
    long as antenatal testing remains reassuring


                           Suchila Sritippayawan   2/1/2011
Timing and route of delivery

ï‚Ļ   To prevent traumatic birth injury :
    Cesarean delivery may be considered if the
    EFW > 4,500 g in women with diabetes.
ï‚Ļ   Notify neonatologist
ï‚Ļ   Stop insulin after placental was removal
ï‚Ļ   Beware shoulder dystocia


                         Suchila Sritippayawan   2/1/2011
INFECTION OF PREGNANCY
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ­āļēāļĒāļļ 34 āļ›āļĩ āļĄāļĩāļ­āļēāļāļēāļĢāļ›āļąāļŠāļŠāļēāļ§āļ°āđāļŠāļšāļ‚āļąāļ”āđāļĨāļ°āđ€āļˆāđ‡āļšāļ—āļĩāđˆāļšāļĢāļīāđ€āļ§āļ“
āļŠāđˆāļ­āļ‡āļ„āļĨāļ­āļ” āļ•āļĢāļ§āļˆāļĢāđˆāļēāļ‡āļāļēāļĒāļžāļš vesicular lesion with shallow
ulcer at vulva

āļˆāļ‡āđƒāļŦāđ‰āļāļēāļĢāļ§āļīāļ™āļīāļˆāļ‰āļąāļĒ
A. Herpatic vulva

B. Molluscum contagiosum

C. Candiadiasis at vulva

D. Syphilis
Genital Herpes        Candidiasis vulvovaginitis

                 Syphilis ulcer
Central dimpling bumps   multiple umbilicated flesh-
Diameter 2-5 mm, firm    colored or hypopigmented
Painless                          papules.
Candida vulvovaginitis

ï‚Ļ   Hx : Vulvar pruritus is the dominant feature of
    vulvovaginal candidiasis
ï‚Ļ   PE : erythema of the vulva and vaginal
    mucosa and vulvar edema
ï‚Ļ   Discharge : thick, adherent, and "cottage
    cheese-like
āđ‚āļˆāļ—āļĒāđŒ GA 20 weeks āļĄāļĩāļāļĨāļīāđˆāļ™āđāļĨāļ°āļ„āļąāļ™āļ—āļĩāđˆāļŠāđˆāļ­āļ‡āļ„āļĨāļ­āļ”āļĄāļē 2
āļŠāļąāļ›āļ”āļēāļŦāđŒ āļ•āļĢāļ§āļˆāļĢāđˆāļēāļ‡āļāļēāļĒāļžāļšāļ§āđˆāļē āđāļ”āļ‡āļ—āļĩāđˆāļ›āļēāļāļŠāđˆāļ­āļ‡āļ„āļĨāļ­āļ” āļ•āļ
āļ‚āļēāļ§āļŠāļĩāđ€āļŦāļĨāļ·āļ­āļ‡āđ€āļ‚āļĩāļĒāļ§ āļĄāļĩāļŸāļ­āļ‡ āļŠāđˆāļ­āļ‡āļ„āļĨāļ­āļ”āđāļ”āļ‡ cervix āļŠāļĩ
āđāļ”āļ‡āļ„āļĨāđ‰āļē (āđ„āļĄāđˆāļšāļ­āļāļ§āđˆāļēāļĄāļĩ curd) āļˆāļ°āđƒāļŦāđ‰āļĒāļēāļ­āļ°āđ„āļĢāļĢāļąāļāļĐāļē
     1. oral doxycycline
     2. oral tinidazole
     3. oral ketoconazole
     4. oral fluconazole
     5. clotrimazole Vg
Vulvaginal infections in pregnancy

ï‚Ļ   Bacterial vaginosis :
    ï‚Ī   In pregnancy, it is associated with preterm birth

    ï‚Ī   treatment does not reduce preterm birth, and routine screening is not
        recommended

    ï‚Ī   Rx(symptomatic) : Metronidazole 500 mg twice daily orally for 7 days

ï‚Ļ   Candidiasis :
    ï‚Ī   Asymptomatic colonization : no treatment

    ï‚Ī   Characteristic : profuse, irritating discharge associated with a pruritic,
        tender, edematous vulva

    ï‚Ī   Topical treatment is recommended (Clotrimazole, miconazole, nystatin,
        and terconazole)
Vulvaginal infections in pregnancy

ï‚Ļ   Trichomoniasis :
    ï‚Ī   Characteristic : foamy leukorrhea with pruritus and irritation

    ï‚Ī   (Some studies) In pregnancy, it is associated with preterm birth

        but treatment has not decreased this risk

    ï‚Ī   screening and treatment of asymptomatic women is not
        recommended during pregnancy

    ï‚Ī   Rx : single 2-g dose of Metronidazole
āđ‚āļˆāļ—āļĒāđŒ āļœāļđāđ‰āļ›āđˆāļ§āļĒāļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 19 āļ›āļĩ GA 40 wk. āļĄāļĩ
genital lesion herpes āđ€āļ›āđ‡āļ™āļ„āļĢāļąāđ‰āļ‡āđāļĢāļ āļˆāļ°āļ§āļēāļ‡āđāļœāļ™āļ”āļđāđāļĨ
āļœāļđāđ‰āļ›āđˆāļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰āļ­āļĒāđˆāļēāļ‡āđ„āļĢ
       a.   Cesarean section
       b.   Oxytocin
       c.   Prostaglandin
       d.   Amniotomy
       e.   āļĢāļ­āļˆāļ™āđ€āļˆāđ‡āļšāļ—āđ‰āļ­āļ‡āļ„āļĨāļ­āļ”
Rx         Dx          BV                 CV                  TV

                   Metronidazole  Clotrimazole(100mg)   Metronidazole
Non pregnanct    (500mg) 1X2 oral       1tab vg         2 g orally in a
                     x7 days         suppo.x7days        single dose

                                    The same as non     Treat (symptom)
  pregnant       Treat (symptom)
                                       pregnant


Sexual partner      Not treat          Not treat             Treat

                                                        The same as HIV
                 The same as HIV    The same as HIV           neg
     HIV
                       neg                neg

                                    When persist or
     F/U               no                                     no
                                   recur within 2 mo.
Genital HSV infection and pregnancy

ï‚Ļ   Fetal and neonatal effect :
    ï‚Ī Fetal infection : congenital HSV (hydrops fetalis , fetal
      demise,survivor (skin lesion,CNS manifestration)
    ï‚Ī Neonatal infection : SEM ,manifestration , CNS
      manifestration (meningoencephalitis) , disseminated
      disease
ï‚Ļ   When the risk of neonatal infection occur
ï‚Ļ   Route of delivery
ï‚Ļ   Treatment for prevention or decreased risk of
    neonatal infection
Risk factors for neonatal herpes

ï‚Ļ   The risks are greatest :
     women with primary genital herpes in the 3rd
    trimester particularly within 6 weeks of
    delivery),
Approach pregnant women with Hx HSV infection



           women without symptoms and
             signs of genital herpes or
               prodromal symptoms




          They can be deliver vaginally
Recommendation of CDC and ACOG



                           Cesarean delivery should
                                  be offered




                             Who have history of        Who have ruptured of
                               genital herpes
                                                       membranes > 6 hours,
 Who have active lesions              or
                                                      (although the benefit is not
                            prodromal symptoms at
                              the time of delivery          clearly proven)
Approach pregnant women with Hx HSV infection


                   Cesarean delivery

                  not recommended for




           women with recurrent genital herpes
            and active nongenital HSV lesions
Treatment

ï‚Ļ   In women with first episode genital HSV :

    Acyclovir (400 mg PO three times daily) 7 - 14 days , regardless of
    the timing of infection during pregnancy

    ( to decrease duration of lesion and viral shedding)

ï‚Ļ   In women with a history of recurrent genital HSV, or primary
    infection during pregnancy:

    suppressive Acyclovir (400 mg three times daily) be given at GA 36
    weeks through delivery

ï‚Ļ   Women who do not have a history of genital herpes but HSV-2
    seropositive : not recommend antiviral therapy
Recommended doses of antiviral medication for
          Herpes in pregnancy


   Indication      Acyclovir    Valacyclovir
Primary or 1st   400 mg po tid 1 g bid for 7-14
episode HSV            for           days
                   7-14 days
Symptomatic      400 mg po tid 500 mg po bid
recurrent HSV      for 5 days     for 5 days

Daily            400 mg po tid    500 mg po bid
suppressive       from GA 36       from GA 36
therapy          wk.to delivery   wk.to delivery

                            Obstet Gynecol 2005;106:845-56
A.   āļŠāđˆāļ‡UAāļŦāļē UTI
B.   āđƒāļŠāđ‰āļ–āļļāļ‡āļĒāļēāļ‡āļ­āļ™āļēāļĄāļąāļĒāđ€āļ§āļĨāļēāļĄāļĩāđ€āļžāļĻāļŠāļąāļĄāļžāļąāļ™āļ˜āđŒ
C.   āļ•āļĢāļ§āļˆculture GC āļˆāļēāļcervix,urethra
D.   āđāļ™āļ°āļ™āļēāđƒāļŦāđ‰āļŠāļēāļĄāļĩāļĄāļēāļ•āļĢāļ§āļˆSTD
E.   āļ•āļĢāļ§āļˆāđ€āļĨāļ·āļ­āļ”screen STD (syphilis,HIV)āļ•āļēāļĄāļ›āļāļ•āļī
āđ‚āļˆāļ—āļĒāđŒ āļœāļđāđ‰āļŦāļāļīāļ‡āļ­āļēāļĒāļļ 28 āļ›āļĩ āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 28 āļŠāļąāļ›āļ”āļēāļŦāđŒ āļ•āļĢāļ§āļˆ VDRL reactive
titer = 1:32, FTA-ABS positive āđƒāļŦ āđ‰āļāļēāļĢāļĢāļąāļāļĐāļēāđ€āļ›āđ‡āļ™ Benzathine
penicillin 2.4 āļĨ āđ‰āļēāļ™āļŦāļ™āđˆāļ§āļĒ āļ—āļēāļ‡āļāļĨāđ‰āļēāļĄāđ€āļ™āļ·āđ‰āļ­āđ€āļ›āđ‡āļ™āđ€āļ§āļĨāļē 3 āļŠāļąāļ›āļ”āļēāļŦāđŒ āļ•āđˆāļ­āļĄāļē
āļ•āļĢāļ§āļˆāļ‹ āđ‰āļēāļ•āļ­āļ™ āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 32 āļŠāļąāļ›āļ”āļēāļŦāđŒ VDRL = 1:8 āļ—āđˆāļēāļ™āļˆāļ°āđƒāļŦ āđ‰āļāļēāļĢ
āļĢāļąāļāļĐāļēāļ—āļĩāđˆāđ€āļŦāļĄāļēāļ°āļŠāļĄāļ—āļĩāđˆāļŠāļļāļ”āļ­āļĒāđˆāļēāļ‡āđ„āļĢāļ•āđˆāļ­āđ„āļ›
A. āļ§āļąāļ” VDRL āļ‹āđ‰āļē āļ•āļ­āļ™āļŦāļĨāļąāļ‡āļ„āļĨāļ­āļ” 6 āļŠāļąāļ›āļ”āļēāļŦāđŒ
B. āļ‰āļĩāļ” Benzathine penicillin āļ‹āđ‰āļēāđƒāļ™āļ‚āļ™āļēāļ”āđāļĨāļ°āđ€āļ§āļĨāļēāđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ
C. āļ‰āļĩāļ” Benzathine penicillin 2.4 āļŦāļ™āđˆāļ§āļĒ āļ„āļĢāļąāđ‰āļ‡āđ€āļ”āļĩāļĒāļ§
D. āđƒāļŦ āđ‰penicillin āļŦāļĒāļ”āļ—āļēāļ‡āļŦāļĨāļ­āļ”āđ€āļĨāļ·āļ­āļ”āļ” āļē 1.2 āļĨ āđ‰āļēāļ™āļŦāļ™āđˆāļ§āļĒ
āļĢāļ°āļĒāļ°āđ€āļ§āļĨāļē____
E. āđ€āļ›āļĨāļĩāđˆāļĒāļ™āļĒāļēāđ€āļ›āđ‡āļ™ erythromycin āļ§āļąāļ™āļĨāļ° 2 āļāļĢāļąāļĄ 30 āļ§āļąāļ™
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļĄāļĩ genital wart āļˆāļ‡āđƒāļŦāđ‰āļāļēāļĢāļ”āļđāđāļĨ
āļĢāļąāļāļĐāļē
   A.   Podophyllin
   B.   Trichloroacetic acid
   C.   Interferon
   D.   5-FU
   E.   Imiquimod
ï‚Ļ   Podophyllin : a plant-based resin that blocks cell
    division at metaphase and leads

ï‚Ļ   Trichloroacetic acid : destroy the wart tissue via
    chemical coagulation of tissue proteins

ï‚Ļ   5-FU :a pyrimidine antimetabolite that interferes
    with DNA synthesis

ï‚Ļ   Imiquimod :a positive immune response
    modifier, which acts by local cytokine induction
Genital wart during pregnancy

ï‚Ļ   Three important issues
    ï‚Ī Worsening     of the disease in the pregnant state
    ï‚Ī Choice   of safe and effective treatment
    ï‚Ī Potential   vertical transmission to the fetus
External genital warts during pregnancy


ï‚Ļ   During pregnancy ï‚Ū impaired immune ï‚Ū
    increased proliferation of condylomata.

ï‚Ļ   During the post-partum period ï‚Ū spontaneous
    regression.
Treatment

ï‚Ļ   Aims of treatment : debulking symptomatic
    genital warts.
ï‚Ļ   Eradical of warts during pregnancy is not
    always necessary
Treatment
Effective regimen for genital warts :
  ï‚Ī 80-90%   TCA solution applied typically once a
    week
  ï‚Ī Cryotherapy

  ï‚Ī Laser ablation ?

Podophyllin resin
Podofilox – gel or solution          are not
                                     recommended in
5-FU cream                           pregnancy
Imiquimod cream
Route of delivery
Current OB data :
ï‚Ļ   Data support the rarity of
    perinatal HPV transmission      āđ„āļĄāđˆāđāļ™āļ°āļ™āļēāđƒāļŦāđ‰
ï‚Ļ   Limitation understanding of   ➙ āļœāđˆāļēāļ•āļąāļ”āļ„āļĨāļ­āļ”āđ€āļžāļ·āđˆāļ­
                                    āļĨāļ”āļāļēāļĢāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­
    the development of
    laryngeal papillomatosis



           āļāļēāļĢāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­āļ‚āļ­āļ‡āļ—āļēāļĢāļāđ„āļĄāđˆāđ€āļāļĩāđˆāļĒāļ§āļ‚āđ‰āļ­āļ‡āļāļąāļš
           route of delivery
ïą   āļ–āđ‰āļēāđ€āļŦāđ‡āļ™ genital condyloma āđƒāļ™āđ€āļ”āđ‡āļāļ­āļēāļˆ
    āđ€āļ™āļ·āđˆāļ­āļ‡āļˆāļēāļ
    ïķāļŠāļąāļĄāļœāļąāļŠlesionāđƒāļ™āļĢāļ°āļŦāļ§āđˆāļēāļ‡āļ„āļĨāļ­āļ”āļ—āļēāļ‡āļŠāđˆāļ­āļ‡

     āļ„āļĨāļ­āļ”
    ïķāļ–āđ‰āļēāđƒāļ™āđ€āļ”āđ‡āļāđ‚āļ•āđƒāļŦāđ‰   rule out sexual abuse
     āļ”āđ‰āļ§āļĒ
Rubella in pregnancy

āļŠāļīāđˆāļ‡āļ—āļĩāđˆāļ•āđ‰āļ­āļ‡āļĢāļđāđ‰
ï‚Ļ   āļāļēāļĢāđāļ›āļĨāļœāļĨāđ€āļĨāļ·āļ­āļ” āļ„āļ™āļ—āļĩāđˆāđ„āļ›āļŠāļąāļĄāļœāļąāļŠāđ‚āļĢāļ„āļĄāļē

ï‚Ļ   āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒāļ—āļĩāđˆāđāļĄāđˆāđ€āļ›āđ‡āļ™āļœāļ·āđˆāļ™āđāļĨāļ°āļ—āļēāļĢāļāđƒāļ™āļ„āļĢāļĢāļ āđŒāļĄāļĩāđ‚āļ­āļāļēāļŠāļ•āļīāļ”
    āđ€āļŠāļ·āđ‰āļ­

ï‚Ļ   āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒāļ—āļĩāđˆāļĄāļĩāđ‚āļ­āļāļēāļŠāđ€āļāļīāļ”congenital rubella
    syndrome
Rubella in pregnancy
ï‚Ļ   āļŠāļ•āļĢāļĩāļ­āļēāļĒāļļ 26 āļ›āļĩ āđ€āļ›āđ‡āļ™āļ„āļĢāļđāļĢāļ°āļ”āļąāļšāļ›āļĢāļ°āļ–āļĄāļĻāļķāļāļĐāļē āļĄāļēāļ›āļĢāļķāļāļĐāļēāļāđˆāļ­āļ™āļāļēāļĢāļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒ
    āđ€āļĢāļ·āđˆāļ­āļ‡āļŦāļąāļ”āđ€āļĒāļ­āļĢāļĄāļąāļ™
    āļ—āđˆāļēāļ™āļˆāļ°āđāļ™āļ°āļ™āļēāļ­āļĒāđˆāļēāļ‡āđ„āļĢ
                                       -Hx
    āļ .āđ„āļĄāđˆāļĄāļĩāļ„āļ§āļēāļĄāđ€āļŠāļĩāļĒāļ‡āđ„āļĄāđˆāļ•āđ‰āļ­āļ‡āļ•āļĢāļ§āļˆāđ€āļĨāļ·āļ­āļ”
                   āđˆ
                                       -Serologic testing :
    āļ‚. āļ‰āļĩāļ”āļ§āļąāļ„āļ‹āļĩāļ™ āđ„āļĄāđˆāļ•āđ‰āļ­āļ‡āļ„āļļāļĄāļāļēāđ€āļ™āļīāļ”      IgG
    āļ„. āļ‰āļĩāļ”āļ§āļąāļ„āļ‹āļĩāļ™ āļ„āļļāļĄāļāļēāđ€āļ™āļīāļ” 1 āđ€āļ”āļ·āļ­āļ™     -āļ–āđ‰āļēāđ„āļĄāđˆāļĄāļ āļđāļĄāļīāļ„āļļāđ‰āļĄāļāļąāļ™ āļ‰āļĩāļ”āļ§āļąāļ„āļ‹āļĩāļ™āđāļĨāļ°
                                               āļĩ
    āļ‡. āļŠāđˆāļ‡āļ•āļĢāļ§āļˆrubella Ig M             āļ„āļļāļĄāļāļēāđ€āļ™āļīāļ”āļ›āļĢāļ°āļĄāļēāļ“ 1 āđ€āļ”āļ·āļ­āļ™
    āļˆ. āļŠāđˆāļ‡āļ•āļĢāļ§āļˆrubella IgG
Rubella & pregnancy

ï‚Ļ   āļāļēāļĢāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­āļ‚āļ­āļ‡āļ—āļēāļĢāļ āļœāđˆāļēāļ™āļ—āļēāļ‡āļĢāļāđƒāļ™āļ‚āļ“āļ°āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒ
ï‚Ļ   āđ€āļ›āđ‡āļ™āļŠāļēāđ€āļŦāļ•āļļāļ—āļĩāđˆāļ—āļēāđƒāļŦāđ‰āđ€āļāļīāļ”āļ„āļ§āļēāļĄāļžāļīāļāļēāļĢāļ‚āļ­āļ‡āļ—āļēāļĢāļāđāļ•āđˆāļāļēāđ€āļ™āļīāļ”
    āļ—āļĩāđˆāļĢāļļāļ™āđāļĢāļ‡
ï‚Ļ   āļ–āđ‰āļēāļŠāļ•āļĢāļĩāļ•āļ‡āļ„āļĢāļĢāļ āđŒāđ„āļĄāđˆāļĄāļĩāļ āļđāļĄāļīāļ„āļļāđ‰āļĄāļāļąāļ™ āļĄāļĩāļāļēāļĢāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­
              āļąāđ‰
         ïŪ   āļˆāļ°āļ•āļĢāļ§āļˆāļžāļšāđ„āļ§āļĢāļąāļŠāđƒāļ™āđ€āļĨāļ·āļ­āļ”āļāđˆāļ­āļ™āļĄāļĩāļ­āļēāļāļēāļĢ
          āļ‚āļ­āļ‡āđ‚āļĢāļ„ āļ›āļĢāļ°āļĄāļēāļ“1āļŠāļąāļ›āļ”āļēāļŦāđŒ
         ïŪ āļŦāļĨāļąāļ‡āļœāļ·āđˆāļ™āđ€āļĢāļīāđˆāļĄāļ‚āļķāđ‰āļ™ 1-2 āļŠāļąāļ›āļ”āļēāļŦāđŒāļˆāļ°āđ€āļ›āđ‡āļ™āļŠāđˆāļ§āļ‡āļ—āļĩāđˆ
          āļĄāļĩāļĢāļ°āļ”āļąāļš antibodyāļŠāļđāļ‡āļŠāļļāļ”
ï‚Ļ   Incubation period 12-23 days
ï‚Ļ   20 – 50 % of infections may be asymptomatic
āļœāļĨāļ•āđˆāļ­āļ—āļēāļĢāļ

ï‚Ļ āļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āļ‚āļ­āļ‡āļ—āļēāļĢāļāđƒāļ™āļ„āļĢāļĢāļ āđŒāļ—āļĩāđˆāļˆāļ°āļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­āđāļĨāļ°āļĄāļĩ
  āļ„āļ§āļēāļĄāļžāļīāļāļēāļĢāđāļ•āđˆāļāļēāđ€āļ™āļīāļ”āļ‚āļķāđ‰āļ™āļāļąāļšāļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒāļ‚āļ“āļ°āļ—āļĩāđˆāđāļĄāđˆ
  āđ€āļ›āđ‡āļ™āļœāļ·āđˆāļ™
ï‚Ļ Risk of fetal infection

       GA < 12 wks. Risk = 80%
       GA 13-14 wks. Risk = 54%
       2nd trimester Risk = 25%
ï‚Ļ   Consequence of fetal infection
         spontaneous infection
         seropositive , normal –appearing
          infant(infection may remain subclinical for
          months)
       Congenital    rubella infection
Congenital rubella infection
Findings :
  ï‚Ī Eye : cataract and congenital glaucoma
  ï‚Ī Heart disease : pulmonary artery stenosis

  ï‚Ī Sensorineural deafness : the most common single
    defect
  ï‚Ī CNS defect : microcephaly,paraencephalitis, brain
    calcification, mental retardation
  ï‚Ī Pigment retinopathy

  ï‚Ī purpura

  ï‚Ī Hepatosplenomegaly and jaundice

  ï‚Ī Radiolucent bone disease

  ï‚Ī Symmetrical IUGR
āļœāļĨāļ•āđˆāļ­āļ—āļēāļĢāļ

ï‚Ļ   āļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āļ‚āļ­āļ‡āļ—āļēāļĢāļāđƒāļ™āļ„āļĢāļĢāļ āđŒāļ—āļĩāđˆāļˆāļ°āļĄāļĩāļ„āļ§āļēāļĄāļžāļīāļāļēāļĢāđāļ•āđˆ
    āļāļēāđ€āļ™āļīāļ” (congenital rubella syndrome)
       āļ–āđ‰āļēāļ—āļēāļĢāļāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­āļ—āļĩāđˆGA < 11 wks. āļžāļšāļžāļīāļāļēāļĢāļ—āļļāļāļĢāļēāļĒ
       āļ–āđ‰āļēāļ—āļēāļĢāļāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­āļ—āļĩāđˆ GA 13-16 wks. āļžāļšāļžāļīāļāļēāļĢ =
        35%
       āļ–āđ‰āļēāļ—āļēāļĢāļāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­āļ—āļĩāđˆ GA > 16 wks. āļˆāļ°āđ„āļĄāđˆāļžāļšāļ„āļ§āļēāļĄ
        āļžāļīāļāļēāļĢāđ€āļĨāļĒ
āļāļēāļĢāļ§āļīāļ™āļīāļˆāļ‰āļąāļĒ

ï‚Ļ   āļ„āļ§āļĢāļ•āļĢāļ§āļˆantibodyāļ•āļąāđ‰āļ‡āđāļ•āđˆ āļ āļēāļĒāđƒāļ™2-3āļ§āļąāļ™āļŦāļĨāļąāļ‡āļœāļ·āđˆāļ™āđ€āļĢāļīāđˆāļĄ
    āļ‚āļķāđ‰āļ™

    āđāļĨāļ°āļ•āļĢāļ§āļˆāļ‹āđ‰āļēāļŦāļĨāļąāļ‡āļˆāļēāļāļ™āļąāđ‰āļ™āļ­āļĩāļ 1 āļŠāļąāļ›āļ”āļēāļŦāđŒāđ€āļžāļ·āđˆāļ­āļ”āļđāļāļēāļĢ
    āđ€āļžāļīāđˆāļĄāļ‚āļķāđ‰āļ™āļ‚āļ­āļ‡āļĢāļ°āļ”āļąāļšantibody

ï‚Ļ   IgM āļˆāļ°āļžāļšāđ„āļ”āđ‰āļ•āļąāđ‰āļ‡āđāļ•āđˆāđ€āļĢāļīāđˆāļĄāļĄāļĩāļœāļ·āđˆāļ™āļˆāļ™āļāļĢāļ°āļ—āļąāđˆāļ‡4 āļŠāļąāļ›āļ”āļēāļŦāđŒāļŦāļĨāļąāļ‡
    āđ€āļĢāļīāđˆāļĄāļĄāļĩāļœāļ·āđˆāļ™

ï‚Ļ   IgG āļžāļšāđ„āļ”āđ‰āļ•āļąāđ‰āļ‡āđāļ•āđˆāđ€āļĢāļīāļĄāļĄāļĩāļœāļ·āđˆāļ™āđāļĨāļ°āļĒāļąāļ‡āļ„āļ‡āļ­āļĒāļđāđˆāļ•āļĨāļ­āļ”āļŠāļĩāļ§āļ•
                       āđˆ                         āļī
āđ€āļĄāļ·āđˆāļ­āļœāļđāđ‰āļ›āđˆāļ§āļĒāļĄāļĩāļĨāļąāļāļĐāļ“āļ°āļ—āļēāļ‡āļ„āļĨāļīāļ™āļāļŠāļ‡āļŠāļąāļĒāļ§āđˆāļēāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­āļŦāļąāļ”āđ€āļĒāļ­āļĢāļĄāļąāļ™
                              āļī
 āļĢāļ°āļĒāļ°āđ€āļ§āļĨāļēāļ—āļĩāđˆāļĄāļēāļžāļš
                    1st HAI titer   2nd HAI titer             āđāļ›āļĨāļœāļĨ
 āđāļžāļ—āļĒāđŒāļŦāļĨāļąāļ‡āļœāļ·āđˆāļ™āļ‚āļķāļ™
                āđ‰

                    <1:8(1:10)       āđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ       āđ„āļĄāđˆāđƒāļŠāđˆrubella , no immune
      <3āļ§āļąāļ™
                    <1:8(1:10)        4-fold       āđ€āļ›āđ‡āļ™ rubella
(āļ•āļĢāļ§āļˆāļ‹āđ‰āļēāļ­āļĩāļāđƒāļ™1wk)
                    â‰Ĩ 1:8(1:10)      āđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ       āđ„āļĄāđˆāđƒāļŠāđˆrubella , āļĄāļĩimmune

                    <1:8(1:10)       āđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ       āđ„āļĄāđˆāđƒāļŠāđˆrubella , no immune

     3-7āļ§āļąāļ™           1:8-1:32
(āļ•āļĢāļ§āļˆāļ‹āđ‰āļēāļ­āļĩāļāđƒāļ™1wk)   (1:10-1:140)
                                     āđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ       āđ„āļĄāđˆāđƒāļŠāđˆrubella , āļĄāļĩimmune

                    â‰Ĩ1:64(1:80)     āļŠāļđāļ‡āļāļ§āđˆāļēāđ€āļ”āļīāļĄ     āđ„āļĄāđˆāđāļ™āđˆ ,āļ•āļĢāļ§āļˆIgM
                    <1:8(1:10)           -          āđ„āļĄāđˆāđƒāļŠāđˆrubella , no immune

      >7āļ§āļąāļ™           1:8-1:32
                    (1:10-1:140)
                                         -          āđ„āļĄāđˆāđƒāļŠāđˆrubella , āļĄāļĩimmune
āļĄāļēāļŸāļąāļ‡āļœāļĨāđƒāļ™1-2wk.

                    â‰Ĩ1:64(1:80)          -          āļ­āļēāļˆāđ€āļ›āđ‡āļ™rubella,āļ•āļĢāļ§āļˆIgM
āļĢāļēāļĒāļ—āļĩāđˆāļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāđ„āļ›āļŠāļąāļĄāļœāļąāļŠāđ‚āļĢāļ„āļĄāļē

         1st HAI            2nd HAI               āđāļ›āļĨāļœāļĨ

        <1:8(1:10)          āđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ      āđ„āļĄāđˆāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­,āļĒāļąāļ‡āđ„āļĄāđˆāļĄāļĩāļ āļđāļĄāļī
        <1:8(1:10)        āļŠāļđāļ‡āļāļ§āđˆāļēāđ€āļ”āļīāļĄ            āļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­
        â‰Ĩ 1:8(1:10)         āđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ      āđ„āļĄāđˆāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­,āļĄāļĩāļ āļđāļĄāļīāđāļĨāđ‰āļ§
        â‰Ĩ 1:8(1:10)        1:64(1:80)         āļ•āļĢāļ§āļˆāļŦāļēIgM

1st HAI <1:8 āđ€āļˆāļēāļ°āđ€āļĨāļ·āļ­āļ”āļ„āļĢāļąāđ‰āļ‡āļ—āļĩāđˆāļŠāļ­āļ‡āđ€āļĄāļ·āđˆāļ­āļ„āļĢāļš 1āļ” āļŦāļĨāļąāļ‡āđ„āļ›āļŠāļąāļĄāļœāļąāļŠāđ‚āļĢāļ„āļĄāļē
1st HAI â‰Ĩ 1:8 āđ€āļˆāļēāļ°āđ€āļĨāļ·āļ­āļ”āļ„āļĢāļąāđ‰āļ‡āļ—āļĩāđˆāļŠāļ­āļ‡āđƒāļ™āļ§āļąāļ™āļ—āļĩāđˆāļĄāļēāļŸāļąāļ‡āļœāļĨ
IgM āļœāļĨ + = āđ€āļžāļīāđˆāļ‡āđ€āļ›āđ‡āļ™rubellaāļĄāļē 4-6wks.
IgM āļœāļĨ - = āđ€āļ›āđ‡āļ™rubellaāļĄāļēāđ€āļāļīāļ™ 4-6wks
Prevention
ï‚Ļ   Rubella vaccination should be avoided 1
    month before or during pregnancy (attenuated
    live virus) (CDC 2000)
TWIN PREGNANCY
āđ‚āļˆāļ—āļĒāđŒ Most common cause of perinatal
     death in twin pregnancy

a.   Antepartum hemorrhage
b.   Birth asphyxia
c.   IUGR
d.   Prematurity
e.   Twin – twin transfusion
āđ‚āļˆāļ—āļĒāđŒ “Locked twins”āļ—āļēāļĢāļāđāļāļ”āļ„āļ™āļ—āļĩāđˆāļŦāļ™āļķāđˆāļ‡
     āđāļĨāļ°āļŠāļ­āļ‡āļˆāļ°āļ­āļĒāļđāđˆāđƒāļ™āļ—āđˆāļēāđƒāļ”
a.   Cephalic – Breech
b.   Breech – Breech
c.   Cephalic – Cephalic
d.   Breech – Cephalic
e.   Cephalic - Transverse
―Locked twins‖

         Breech – Cephalic

            ✔
āđ‚āļˆāļ—āļĒāđŒ the most common presentation at
     delivery of near term twins are
                                vertex - vertex       40%

a.   Both cephalic     ✔        vertex - breech
                                breech - vertex
                                                      26%
                                                      10%
                                breech - breech       10%
b.   Both breech                vertex - transverse    8%
                                others                 6%
c.   One cephalic , one breech
d.   One cephalic , one transverse
e.   One breech , one transverse
OTHERS
āļŦāļāļīāļ‡āđ„āļ—āļĒ G2 āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒ GA 18 wk āļ•āļĢāļ§āļˆāđ€āļĨāļ·āļ­āļ”
āđāļĄāđˆ A- āļžāđˆāļ­ B+ (āļ­āļēāļˆāļŠāļĨāļąāļšāļāļąāļ™ āļ›āļĢāļ°āļĄāļēāļ“āļ™āļĩ) āļ–āļēāļĄ
                                  āđ‰
āļ—āļēāđ„āļĢāļ•āđˆāļ­
    1. Anti D
    2. Cordocentesis
    3. direct comb
    4. Amniocentesis
    5. indirect coomb
ï‚Ļ   The direct Coombs' test : detection of antibody on the
    surface of the RBC

ï‚Ļ   The indirect Coombs’test : detection antibodies
    against RBCs that are present unbound in the patient's
    serum.

ï‚Ļ   The indirect Coombs’test is used to screen pregnant
    women for antibodies that may cause hemolytic
    diseasee of the newborn
Isoimmunization

ï‚Ļ   Etiology : maternal Ab production in response
    to exposure to RBC Ag

ï‚Ļ   Rh isoimmunization : Ab against to Rh group

ï‚Ļ   Rh Ag are present on fetal cells by the 38th
    day postconception
Rh isoimmunization

             Fetus : Rh
              positive




             Mother : Rh
          negative and RBC
            sensitization




          Hemolytic disease
Hemolytic disease of the newborn
(Erythroblastosis fetalis
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 20 āļ›āļĩ G1P0 GA 38 wk. car
accident āļĄāļēāļ—āļĩāđˆāļŦāđ‰āļ­āļ‡āļ‰āļļāļāđ€āļ‰āļīāļ™ āļĄāļĩāđ€āļĨāļ·āļ­āļ”āļ­āļ­āļāļ—āļēāļ‡āļŠāđˆāļ­āļ‡āļ„āļĨāļ­āļ” āļ•āđˆāļ­āļĄāļē
āļ„āļĨāļ­āļ”āļšāļļāļ•āļĢ āđ€āļŠāļĩāļĒāđ€āļĨāļ·āļ­āļ” 900ml āļ‚āļ“āļ°āļ™āļĩāđ‰āļœāļđāđ‰āļ›āđˆāļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰āļ›āļĨāļ­āļ”āļ āļąāļĒāđāļĨāđ‰āļ§
āļ—āļĢāļēāļšāļ‚āđ‰āļ­āļĄāļđāļĨāļˆāļēāļāļāļēāļĢāļāļēāļāļ„āļĢāļĢāļ āđŒ āļžāļšāļ§āđˆāļēRh negative Anti D
negative
āļ‚āļąāđ‰āļ™āļ•āļ­āļ™āļ•āđˆāļ­āđ„āļ›āđƒāļ™āļāļēāļĢāļ”āļđāđāļĨāļœāļđāđ‰āļ›āđˆāļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰
      a. Perform CBC
      b. Transfuse PRC
      c. Performed Kleihauer-Betke test
      d. Give additional Rh immune globulin
      e. Assess neonatal Rh Ag status
Kleihauer-Betke test : the number of fetal red cells
in the maternal circulation to measure the amount of
fetal Hb transferred from a fetus to a mother's
bloodstream
â€Ē the differential resistance of fetal hemoglobin to
acid
â€ĒPositive test : the rosette test
â€ĒMaternal red blood cells
 appear as pale "‖
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 27 āļ›āļĩ G1P0 GA 27 wk. āļĄāļēāļ—āļĩāđˆERāđ€āļ™āļ·āđˆāļ­āļ‡āļˆāļēāļ
āļ­āļļāļšāļąāļ•āļīāđ€āļŦāļ•āļļāļˆāļēāļāļĢāļ–MC āđ„āļĄāđˆāļĄāļĩāļ­āļēāļāļēāļĢāļ›āļ§āļ”āļ—āđ‰āļ­āļ‡ āļ—āđ‰āļ­āļ‡āđāļ‚āđ‡āļ‡ āđ„āļĄāđˆāļĄāļĩāđ€āļĨāļ·āļ­āļ”āļ­āļ­āļ
FHSāļ­āļĒāļđāđˆāđƒāļ™āđ€āļāļ“āļ‘āđŒāļ›āļāļ•āļī āļ•āļĢāļ§āļˆāļĢāđˆāļēāļ‡āļāļēāļĒ Abd :not tender
PV cervix:os close no effacement ,no bleeding per vagina
Lab : Rh +(āđ„āļĄāđˆāļĢāļđāđ‰āļœāļĨāļ‚āļ­āļ‡āļžāđˆāļ­) āđ„āļĄāđˆāļĄāļĩHx blood transfusion ,
Kleihauer-Betke test shows a combination
of pale and stained RBCs.
(A) Administer   an appropriate dose of IM Rh0(D) immune globulin
(B) Amniocentesis to measure the amniotic fluid bilirubin level
(C) Emergent cesarean section
(D) Induction of vaginal labor with prostaglandins and oxytocin
(E) Treatment with betamethasone
Indication for Anti-D immunoglobulin in
unsensitized pregnant women


ï‚Ļ   Abortion

ï‚Ļ   Ectopic pregnancy

ï‚Ļ   Antepartum bleeding(1st ,2nd trimester)

ï‚Ļ   Abdominal trauma

ï‚Ļ   After amniocentesis,CVS
ï‚Ļ   After external cephalic version
Management : maternal Rh neg
with unsensitized
ï‚Ļ   Treat with Rh immunoglobulin at GA 28 wk.
    and after delivery(within /72 hr.) if the Fetal is
    Rh positive

ï‚Ļ   Dose 300g of Rh immunoglobulin can protect
    from an exposure of up to 30 ml of fetal blood
Management : maternal Rh neg
with sensitized
                    Assess GA
                      by US



                      Check
                     paternal
                    blood type


                         Paternal Rh :
        Paternal
                      homozygous for D or
        Rh neg
                       heterozygous for D


       No further           Assess
       manageme             prior OB
           nt                  Hx


                                Serial
                            maternal Ab
                           titer ,US ,MCA
                               Doppler
                             velocimetry
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 31āļ›āļĩ GA 4 wk. ,kANC
underlying disease SLEāļĄāļē 5 āļ›āļĩ āļāļīāļ™ low dose
Prednisone āļĄāļĩ renal insufficiency(Cr = 1.3 mg/dL)
clinical SLE stableāļĄāļēāļ›āļĢāļ°āļĄāļēāļ“ 6 āđ€āļ”āļ·āļ­āļ™
āļ—āļēāļĢāļāļĄāļĩāļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āđƒāļ™āļ‚āđ‰āļ­āđƒāļ”āļ•āđˆāļ­āđ„āļ›āļ™āļĩāđ‰āđ€āļžāļīāđˆāļĄāļ‚āļķāđ‰āļ™

(A) Acute renal failure
(B) Chorioretinitis
(C) Complete heart block
(D) Ebstein’s anomaly
(E) Rash
ï‚Ļ   Chorioretinitis : Toxoplasmosis infection,CMV
    infection
ï‚Ļ   Ebstein’s anomaly (malformation
     of the tricuspid valve and right ventricle) :
    Lithium
ï‚Ļ   Rash : neonatal lupus āļĄāļĩ erythematous annular
    lesions on the scalp and periorbital area. the
    rash is typically mild and resolves by 6–8
    months of age.
ULTRASOUND IN OB
āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ­āļēāļĒāļļ 26 āļ›āļĩ āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 8 āļŠāļąāļ›āļ”āļēāļŦāđŒ āļāļēāļĢāļ•āļĢāļ§āļˆ
ultrasoundāđ€āļžāļ·āđˆāļ­āļ›āļĢāļ°āđ€āļĄāļīāļ™āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ āļ‚āđ‰āļ­āđƒāļ”āđāļĄāđˆāļ™āļĒāļēāļ—āļĩāđˆāļŠāļļāļ”

    a.   Femur length
    b.   Biparietal diameter
    c.   Crown rump length
    d.   Abdominal circumference
    e.   Head circumference
āļāļēāļĢāļ›āļĢāļ°āđ€āļĄāļīāļ™āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒāđāļĨāļ°āļĨāļąāļāļĐāļ“āļ°āļ—āļĩāđˆāļžāļšāđƒāļ™āļĢāļ°āļĒāļ°
āđ„āļ•āļĢāļĄāļēāļŠāđāļĢāļ(TVS)
ï‚Ļ   4 - 5 wk by LMP : āđ€āļŦāđ‡āļ™ gestational sac
ï‚Ļ   5 – 6 wk by LMP: āđ€āļŦāđ‡āļ™ yolk sac (hCG ~7,200 mU/ml)
ï‚Ļ   6 – 7 wk by LMP : āđ€āļŦāđ‡āļ™ fetal echo ,fetal heart beat
    ï‚Ī   MSD > 20 mm.
    ï‚Ī   hCG ~10,800 mU/ml
    ï‚Ī   CRL āļ•āļąāđ‰āļ‡āđāļ•āđˆ 5 mm.āļ„āļ§āļĢāļˆāļ°āđ€āļŦāđ‡āļ™fetal heart beat āļ—āļļāļāļĢāļēāļĒ
ï‚Ļ   7 – 8 wk. by LMP : āđ€āļŦāđ‡āļ™ fetal movement āđ„āļ”āđ‰
    ï‚Ī   MSD > 30 mm. Rhombencephalon āļˆāļ°āđ€āļ”āđˆāļ™
ï‚Ļ   8 – 9 wk. by LMP : āđ€āļŦāđ‡āļ™ physiologic omphalocele ,āđāļ‚āļ™āļ‚āļē
    choroid plexus,āđāļ™āļ§āđ„āļ‚āļŠāļąāļ™āļŦāļĨāļąāļ‡
āļāļēāļĢāļ›āļĢāļ°āđ€āļĄāļīāļ™āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒāđƒāļ™āļĢāļ°āļĒāļ°āđ„āļ•āļĢāļĄāļēāļŠāđāļĢāļ
Crown – rump – length(CRL)
  ï‚Īāđ€āļŦāļĄāļēāļ°āļŠāļĄāļŠāļēāļŦāļĢāļąāļšāļāļēāļĢāļ›āļĢāļ°āđ€āļĄāļīāļ™
   āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 7 – 14 āļŠāļąāļ›āļ”āļēāļŦāđŒ āļĄāļĩ
   āļ„āļ§āļēāļĄāđāļĄāđˆāļ™āļĒāļēāđƒāļ™āļāļēāļĢāļ—āļēāļ™āļēāļĒ
   āļĄāļēāļ

                         ✔
  ï‚ĪāļĄāļĩāļ„āļ§āļēāļĄāđāļĄāđˆāļ™āļĒāļēāļ—āļĩāđˆāļŠāļļāļ”āļ—āļĩāđˆāļ­āļēāļĒāļļ
   āļ„āļĢāļĢāļ āđŒ 6.5 – 10 āļŠāļąāļ›āļ”āļēāļŦāđŒ
  ï‚Ī Menstrual age (weeks) =

      CRL (cm) + 6.5
āļāļēāļĢāļ›āļĢāļ°āđ€āļĄāļīāļ™āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒāđƒāļ™āļĢāļ°āļĒāļ°āđ„āļ•āļĢāļĄāļēāļŠāļ—āļĩāđˆāļŠāļ­āļ‡āđāļĨāļ°āļŠāļēāļĄ




                                              BPD , HC


      A                                         FL
      C
āđ‚āļˆāļ—āļĒāđŒ Transvaginal USG at GA 8 wk āļžāļš sac 30 mm.
 āđ„āļĄāđˆāļĄāļĩ embryonic echo āļ—āļēāļ­āļ°āđ„āļĢ


A.Transquillizer and rest
B.Progestin and rest
C.Laparoscopy
D.Medical or surgical termination of pregnancy
E.Serial B-HCG
Abnormal pregnancy during 1st trimester

ï‚Ļ   Viable pregnancy : āđ€āļŦāđ‡āļ™   yolk sac , fetal echo.fetal
    heart
ï‚Ļ   Nonviable pregnancy : early embryonic death , blighted
    ovum, ectopic pregnancy,molar pregnancy


         Diagnosis early embryonic death :
         TAS CRL 9 mm āđ„āļĄāđˆāđ€āļŦāđ‡āļ™ fetal heart
         TVS CRL 5 mm āđ„āļĄāđˆāđ€āļŦāđ‡āļ™ fetal heart
Mean gestational sac diameter



     MSD(mm)                 GA(wk)

        2                       4

        5                       5

        10   āļ•āđ‰āļ­āļ‡āđ€āļŦāđ‡āļ™ yolk      6
                sacāđāļĨāđ‰āļ§
        20                      7

        25                      8

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National licensce ii 2554 print meng

  • 1. NATIONAL LICENSE II 2554 Sritippayawan S.
  • 3. Prenatal diagnosis āļ—āļĩāđˆāļ„āļ§āļĢāļĢāļđāđ‰ ï‚Ļ Thalassemia ï‚Ļ Abnormal fetal karyotype ï‚Ļ Other fetal anomalies : NTDs,heart diseases,cleft lip/cleft palate
  • 4. How to approach ï‚Ļ History taking : patient history,family history,ethnic background ï‚Ļ Risk factors: advanced maternal , prior affected pregnancy,drugs and toxin exposure
  • 5. Diagnostic tests ï‚Ļ Screening test : maternal serum markers, US(NT) ï‚Ļ Diagnostic test : US , Amniocentesis , CVS,cordocentesis
  • 6. DDx ï‚Ļ Chromosome anomalies : ï‚Ī Autosomal: Trisomy 13,18,21 ï‚Ī Sex chromosome : 45,X,47,XXY ï‚Ļ Genetic disorders : ï‚Ī AD ï‚Ī AR : thalassemia ï‚Ī X-linked dominant ï‚Ī X-linked recessive ï‚Ī Multifactorial : NTD ,cleft lip/cleft palate,heart disease
  • 7. Procedures ï‚Ļ Invasive procedure : ï‚Ī CVS ï‚Ī Amniocentesis ï‚Ī Cordocentesis
  • 8. Complication Complication : ï‚Ļ Mother : Placental abruption , Isoimmunization ï‚Ļ Fetus : prematurity,stillbirth Prognosis : ï‚Ļ depend on diagnosis
  • 9. Management ï‚Ļ Option of terminate pregnancy,further investigation,delivery at tertiary center ï‚Ļ Genetic counseling ï‚Ļ Pediatric surgery consultation ï‚Ļ Rho(D) Immune Globulin for prevent isoimmunization ï‚Ļ Subsequent management : recurrent rate
  • 10. Prenatal Diagnosis of thalassemia ï‚Ļ Thalassemia ï‚Ī Screening test – interpretation ï‚Ī Diagnostic test – interpretation ï‚Ī Who are couple at risk for severe thalassemia
  • 11. Prenatal diagnosis of NTD Who have risk of fetal NTDs? How to know ?
  • 12. Prenatal Diagnosis of Down syndrome ï‚Ļ Down syndrome ï‚Ī Who have risk of Abnormal fetal karyotype? ï‚Ī Screening test : NT,serum markers.US ïŪ First trimester ïŪ Second trimester ï‚Ī Diagnostic test ïŪ First trimester : CVS ïŪ Second trimester : amniocentesis
  • 13. THALASSEMIA IN PREGNANCY SRITIPPAYAWAN S.
  • 14. Severe thalassemia in Thailand ï‚Ļ Hb Bart ‗s hydrops fetalis ï‚Ļ Homozygous beta thalassemia ï‚Ļ Beta thalassemia Hb E
  • 15. Alpha thalassemia diseases THALASSEMIA GENOTYPE Hb Bart ‗s hydrops fetalis ïĄ-thal 1 / ïĄ-thal 1) Hb H disease ïĄ-thal 1 / ïĄ-thal 2 Hb H disease with ïĄ-thal 1 / Hb CS Hb Constant Spring Homozygous Hb Constant Hb CS / Hb CS Spring
  • 16. Screening thalassemia ï‚Ļ OF test , MCV ï‚Ļ DCIP , Hb E screening
  • 17. āļāļēāļĢāđ€āļ‚āļĩāļĒāļ™genotype Beta thalassemia ï‚Ļ Normal ï‚Ļ Heterozygous Beta thalassemia (beta trait) ï‚Ļ Homozygous Beta thalassemia ï‚Ļ Beta thalassemia hemoglobin E (Beta thal Hb E)
  • 18. āļāļēāļĢāđ€āļ‚āļĩāļĒāļ™genotype Beta thalassemia āļŠāļąāļāļĨāļąāļāļĐāļ“āđŒ āļŦāļĄāļēāļĒāļ–āļķāļ‡ ïĒ orïĒA or ïĒN Gene ïĒ globin āļ›āļāļ•āļī ïĒT orïĒthal Gene ïĒ thalassemia  ïĒ0 – thalassemia OR ïĒ0 orïĒ+ ïĒ+- thalassemia ïĒE Gene Hb E
  • 19. āļāļēāļĢāđ€āļ‚āļĩāļĒāļ™genotype Beta thalassemia āļŠāļąāļāļĨāļąāļāļĐāļ“āđŒ āļŦāļĄāļēāļĒāļ–āļķāļ‡ ïĒE/ïĒE HbE homozygoys ïĒA/ïĒE HbE heterozygous ïĒA/ïĒ+/0 or ïĒA/ ïĒthal ïĒ thal heterozygous ïĒ+/0/ïĒE or ïĒthal/ïĒE ïĒ thal /Hb E disease ïĒA/ïĒA normal homozygous ïĒ thal ïĒthal /ïĒthal or ïĒ+/0/ïĒ+/0 disease
  • 20. āļāļēāļĢāđ€āļ‚āļĩāļĒāļ™genotype Alpha thalassemia āļŠāļąāļāļĨāļąāļāļĐāļ“āđŒ āļŦāļĄāļēāļĒāļ–āļķāļ‡ ï€ ïĄ Gene ï€ ïĄ globin āļ›āļāļ•āļī Gene ï€ ïĄ globin āļ—āļĩāđˆ 2 āļ•āļēāđāļŦāļ™āđˆāļ‡ ï€ ïĄï€ ïĄ (ïĄï€ globin haplotype) - -, or ï€ ïĄ -thal 1 ï€ ïĄ -thal 1 haplotype -ïĄ ,or ï€ ïĄ -thal 2 ï€ ïĄ -thal 2 haplotype ïĄ cs Gene Hb constant Spring ïĄ csï€ ïĄ Hb constant Spring haplotype
  • 21. āđ‚āļˆāļ—āļĒāđŒ āļžāđˆāļ­āđ€āļ›āđ‡āļ™ïĄï€ thal-1 trait (- - / ïĄïĄ) āđāļĄāđˆāđ€āļ›āđ‡āļ™ ïĄï€ thal-2 trait (- ïĄ / ïĄïĄ) āļĨāļđāļāļ„āļ™āđāļĢāļāđ€āļ›āđ‡āļ™ Hb H disease (- - / - ïĄ) āļ–āđ‰āļēāļˆāļ°āļĄāļĩāļĨāļđāļāļ„āļ™āļ•āđˆāļ­āđ„āļ›āļˆāļ°āļĄāļĩāđ‚āļ­āļāļēāļŠāđ€āļ›āđ‡āļ™ Hb H disease āļāļĩāđˆ % A. 0% B. 25%  C. 50% D. 75% E. 100%
  • 22. āļāļēāļĢāļ„āļēāļ™āļ§āļ“āļ­āļąāļ•āļĢāļēāđ€āļŠāļĩāđˆāļĒāļ‡āļ‚āļ­āļ‡āļĨāļđāļāļ•āđˆāļ­āļŠāļēāļĄāļĩāļ•āđˆāļ­āļāļēāļĢāļĄāļĩgenotype āļŠāļ™āļīāļ”āļ•āđˆāļēāļ‡āđ† āļ‚āļ­āļ‡āļ­āļąāļĨāļŸāļē āļ˜āļēāļĨāļąāļŠāļ‹āļĩāđ€āļĄāļĩāļĒāđāļĨāļ°āļŪāļĩāđ‚āļĄāđ‚āļāļĨāļšāļīāļ™āļœāļīāļ”āļ›āļāļ•āļī genotype genotypeāđāļĄāđˆ āļ­āļąāļ•āļĢāļēāđ€āļŠāļĩāđˆāļĒāļ‡āļ‚āļ­āļ‡āļĨāļđāļāļ•āđˆāļ­āļāļēāļĢāļĄāļĩgenotypeāļŠāļ™āļīāļ”āļ•āđˆāļēāļ‡āđ† āļžāđˆāļ­ --/-ïĄ - ïĄ / ïĄïĄ --/-ïĄ - - / ïĄïĄ -ïĄ/-ïĄ - ïĄ / ïĄïĄ Hb H ïĄ- thal2 trait Hb H ïĄ- thal 1 trait homozygous ïĄ ïĄ - thal2 trait disease (OF -) disease(1/4) (1/4) - thal2 (1/4) (1/4) (OF +) ïĄcsïĄ/ïĄïĄ - -/ïĄCSïĄ - - / ïĄïĄ - ïĄ/ïĄcsïĄ - ïĄ / ïĄïĄ Hb CS trait Hb H disease ïĄ- thal 1 trait ïĄ - thal2 / Hb ïĄ - thal2 trait (OF - ) with Hb CS (1/4) CS(1/4) (1/4) (1/4) - - / ïĄïĄ - ïĄ / ïĄïĄ --/-ïĄ - - / ïĄïĄ - ïĄ / ïĄïĄ ïĄïĄ/ ïĄïĄ ïĄ- thal 1 ïĄ - thal2 trait Hb H ïĄ- thal 1 trait ïĄ - thal2 trait normal (1/4) trait (OF -) disease(1/4) (1/4 ) (1/4) (OF +)
  • 23. āđ‚āļˆāļ—āļĒāđŒ āļœāļĨāļāļēāļĢāļ•āļĢāļ§āļˆāļ„āļąāļ”āļāļĢāļ­āļ‡āļ˜āļēāļĨāļąāļŠāļ‹āļĩāđ€āļĄāļĩāļĒāđƒāļ™āļ„āļđāđˆāļŠāļĄāļĢāļŠ āļžāļšāļ§āđˆāļē āđāļĄāđˆ : OFT +,DCIP -,%HbA2 = 2.8 Not exclude ïĄ-thal1trait) āļžāđˆāļ­ : OFT -,DCIP +,%HbA2 = 22 Hb E trait 1. āļˆāļ‡āđāļ›āļĨāļœāļĨ 2. āđ€āļ›āđ‡āļ™āļ„āļđāđˆāđ€āļŠāļĩāđˆāļĒāļ‡āļ˜āļēāļĨāļąāļŠāļ‹āļĩāđ€āļĄāļĩāļĒāļŠāļ™āļīāļ”āļĢāļļāļ™āđāļĢāļ‡āļŦāļĢāļ·āļ­āđ„āļĄāđˆ
  • 24. āļ–āđ‰āļēāđ€āļĨāļ·āļ­āļ”āđ€āļāđˆāļēāđ€āļāļīāļ™ 3 āļ§āļąāļ™ āļ­āļēāļˆāđƒāļŦāđ‰āļœāļĨāļĨāļšāļĨāļ§āļ‡āđ„āļ”āđ‰ OF āļ—āļąāđ‰āļ‡āļ—āļĩāđˆāļˆāļĢāļīāļ‡ āđ† āđāļĨāđ‰āļ§āđ€āļ›āđ‡āļ™āļžāļēāļŦāļ° ï‚Ļ OF positive ï‚Ļ OF negative ï‚Ī ïĄ - thal trait (~100%) ï‚Ī Hb E trait (30- ï‚ĪïĒ - thal trait (~100%) 40%) ï‚Ī Hb E trait (60-70%) ï‚Ī āđ„āļĄāđˆāđ„āļ”āđ‰āđ€āļ›āđ‡āļ™āļžāļēāļŦāļ°āļ˜āļēāļĨāļąāļŠāļ‹āļĩāđ€āļĄāļĩāļĒ DCIP āļœāļĨāļšāļ§āļ : Hb E, Hb H
  • 25. āļœāļĨāļ•āļĢāļ§āļˆāļ„āļąāļ”āļāļĢāļ­āļ‡āļ—āļĩāđˆāđ€āļ›āđ‡āļ™āļšāļ§āļ(āļœāļīāļ”āļ›āļāļ•āļī) MCV < 80 fL or OF positive And / or DCIP positive Work up : confirm test āļ•āļēāļĄāļŠāļēāļĄāļĩāļĄāļēāļ•āļĢāļ§āļˆ
  • 26. Hb A 2 Result HbA2 Normal <4% ïĄ thal - 1 trait < 4% ïĒ thal trait 4-8% Hb E trait 10 – 30 % ïĒ thal/HbE disease 30-60 % Homozygous Hb E > 60 %
  • 27. āđ‚āļˆāļ—āļĒāđŒ āļ„āļđāđˆāđ€āļŠāļĩāđˆāļĒāļ‡āļ˜āļēāļĨāļąāļŠāļ‹āļĩāđ€āļĄāļĩāļĒāļŠāļ™āļīāļ”āđ„āļŦāļ™ OFT HbE PCR HbE No MCV DCIP % A2 ïĄ-1 ïĄ-1 ïĒ ? ? ? āļ. + ve X X āļŠ. - ve ? āļŠāļēāļĒ % A2 ïĒthal/HbE? Further investigation āļŦāļāļīāļ‡ Hb E /DCIP
  • 29. Neural tube defect(NTD) ï‚Ļ NTDs result from failure of the neural tube to close normally between the 3rd and 4th weeks after conception (the 5th and 6th weeks of gestation). ï‚Ļ Type of NTD : ï‚Ī Spine (Spina bifida, meningomyelocele or myelomeningocele ) , cranium(Anencephaly ,exencephaly, Encephalocele ) ïŪ Open NTDs : often involve spine and cranium ïŪ Closed NTDs are usually localized and confined to the spine
  • 30. NTDs & AFP ï‚Ļ AFP : glycoprotein is synthesized by ï‚Ī Fetal yolk sac ï‚Ī Fetal GI tract and liver ï‚Ļ AFP in fetal serum and AF ïƒą until GA 13 wk. then ïƒē and ï‚Ļ AFPïƒą in maternal serum after 12 wk., peaks between GA 28 -32 weeks and then ïƒē
  • 31. NTDs & AFP NTDs , ventral wall defects permit AFP to leak into the AF, maternal serum ïƒąAFP in maternal serum and AF Women who carry fetuses with NTDs have :MSAFP at GA 16 – 18 wk. > 2.5 MoM
  • 32. Risk factors of NTDs ï‚Ļ 95 % of NTDs occur in the absence of risk factor or family history ï‚Ļ NTDs : genetic causes and multifactorial disorders ï‚Ļ Recurrence rate ï‚Ī 4 % : couple has previous child with NTD ï‚Ī 5 % : either parent was born with NTD ï‚Ī 10% : couple has 2 affected children ï‚Ļ Etiology in some population : mutation MTHFR ï‚Ū impaired homocysteine and folate metabolism
  • 33. Risk Factors for Neural-Tube Defects Family history of neural-tube defects Exposure to certain environmental agents Diabetes (hyperglycemia) Hyperthermia Drugs and medications Genetic syndrome with known recurrence risk Some racial or ethnic groups and/or living in high-risk geographical regions Production of anti- folate receptor antibodies
  • 34. Some Risk Factors for NTDs Genetic cause â€ĒFamily history—multifactorial inheritance â€ĒMTHFR mutation—677CT â€ĒSyndromes with autosomal recessive inheritance : Meckel-Gruber Roberts Joubert Jarcho-Levin HARDE—hydrocephalus–agyria–retinal dysplasia–encephalocele â€ĒAneuploidy Trisomy 13 Trisomy 18 Triploidy Exposure to certain environmental agents â€ĒDiabetes—hyperglycemia â€ĒHyperthermia Hot tub or sauna Fever (controversial) â€ĒMedications Valproic acid Carbamazepine Coumadin Aminopterin Thalidomide Efavirenz Geographical region—ethnicity, diet, other factor â€ĒUnited Kingdom ,India,China,Egypt,Mexico,Southern Appalachian United States
  • 35. Prenatal diagnosis of NTD ï‚Ļ Screening test : maternal serum AFP at 2nd trimester ï‚Ī GA 15 – 20 wk. ï‚Ī Upper normal limit of maternal serum AFP = 2.0- 2.5 MoM( Abnormal if > 2.0 – 2.5 MoM) ï‚Ļ Diagnosis test : ultrasound
  • 36. Screening test : MSAFP at 2nd trimester ï‚Ļ ïƒą MSAFP  risk for NTD and other disorders ï‚Ļ ïƒē MSAFP  risk for Down syndrome
  • 37. Factors influence of the maternal serum AFP level ï‚Ļ Maternal weight : reflect the volume of distribution ï‚Ļ GA : maternal serum AFP 15 % /wk. during the 2nd trimester ï‚Ļ Race or ethnicity : African American women have 10 %  serum AFP (but low risk NTDs) ï‚Ļ DM : serum AFP may be ï‚Ŋ than non DM women ï‚Ļ Twins : ï‚Ū use higher screening threshold (â‰Ĩ 3.5 MoM)
  • 38. Unexplained  Abnormal MSAFP often forcast a poor pregnancy outcome ïŪLow birth weight ïŪOligohydramnios ïŪPlacental abruption ïŪFetal death
  • 39. Maternal serum AFP (MoM) adjusted markers screening for maternal age , (triple screening AFP â‰Ĩ2.0MoM BW,ethinicity,GA, test at GA 15 -20 twins,DM weeks US evaluate to AFPâ‰Ĩ2.5 MoM exclude twins , fetal US (Abnormal result) death and recalculate AFP
  • 40. āđ‚āļˆāļ—āļĒāđŒ āļŠāļ•āļĢāļĩāļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ•āļĢāļ§āļˆ AFP āļžāļšāļ§āđˆāļēāđ€āļ—āđˆāļēāļāļąāļš 3.0 MoM āļˆāļ°āļžāļšāđ„āļ”āđ‰āđƒāļ™āđ‚āļĢāļ„āđƒāļ” a. Cystic fibrosis b. Down syndrome c. Polycystic kidney disease d. Neural tube defect e. Nephroblastoma
  • 41. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 18 āļ›āļĩ G2P1 GA 5 weeks āļ›āļĢāļ°āļ§āļąāļ•āļīāļšāļļāļ•āļĢāļ„āļ™āđāļĢāļ āđ€āļ›āđ‡āļ™ spina bifida āļˆāļ°āđƒāļŦāđ‰āļ„āļēāđāļ™āļ°āļ™āļēāļ­āļ°āđ„āļĢāđ€āļžāļ·āđˆāļ­āļ›āđ‰āļ­āļ‡āļāļąāļ™āļāļēāļĢāđ€āļāļīāļ”āļ āļēāļ§āļ°āļ”āļąāļ‡āļāļĨāđˆāļēāļ§āļ‹āđ‰āļē a. Iron b. Zinc c. Folic acid d. B6 e. Thiamine
  • 42. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 31āļ›āļĩ āļ›āļĢāļ°āļ§āļąāļ•āļīāļšāļļāļ•āļĢāļ„āļ™āđāļĢāļ āđ„āļĄāđˆāļĄāļĩ āļāļĢāļ°āđ‚āļŦāļĨāļāļĻāļĩāļĢāļĐāļ° āļĄāļēāļ•āļĢāļ§āļˆāļāļēāļĢāļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒ āļ„āļ§āļĢāđƒāļŦāđ‰āļāļēāļĢāļ”āļđāđāļĨāļĢāļąāļāļĐāļēāļ­āļĒāđˆāļēāļ‡āđ„āļĢ a. āđƒāļŦāđ‰āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ•āđˆāļ­āđ„āļ›āđ„āļ”āđ‰ b. āļ™āļēāļŠāļēāļĄāļĩ āļ āļĢāļĢāļĒāļēāļĄāļēāļ•āļĢāļ§āļˆāļ„āļ§āļēāļĄāļœāļīāļ”āļ›āļāļ•āļīāļ‚āļ­āļ‡āđ‚āļ„āļĢāđ‚āļĄāđ‚āļ‹āļĄ c. āđƒāļŦāđ‰āļāļīāļ™Folic acidāđ€āļŠāļĢāļīāļĄ d. āđƒāļŦāđ‰āļāļīāļ™āļ˜āļēāļ•āļļāđ€āļŦāļĨāđ‡āļāđ€āļŠāļĢāļīāļĄ e. āđƒāļŦāđ‰āļāļīāļ™āđāļ„āļĨāđ€āļ‹āļĩāļĒāļĄāđ€āļŠāļĢāļīāļĄ
  • 43. Prevention of neural tube defects ï‚Ļ Periconceptional folic acid supplementation reduces the incidence of neural tube defects by 50 - 70 % ï‚Ļ Women who have risk for NTDs : ï‚Ī women with a previously affected child ï‚Ī Women who take anticonvulsant drugs ï‚Ī family history of NTD ï‚Ī insulin-requiring diabetes
  • 44. Prevention of neural tube defects ï‚Ļ Folic supplementation : started at least one month prior to conception and continue throughout the first trimester. ï‚Ļ Dose 4 mg daily
  • 45. Prevention of neural tube defects Primary prevention in low risk women ï‚Ļ Folic supplementation should be started at least one month prior to conception and continue throughout the first trimester. ï‚Ļ Dose 400g(0.4mg) daily
  • 46. DOWN SYNDROME AND ABNORMAL FETAL KARYOTYPE
  • 47. Who should be worked up
  • 48. RISK FACTORS FOR GENETIC DISORDERS ï‚Ļ Advanced Maternal Age ï‚Ļ Previous Pregnancy Affected by Chromosomal Abnormality ï‚Ļ History of Early Pregnancy Loss ï‚Ļ Advanced Paternal Age ï‚Ļ Ethnicity Suchila Sritippayawan 2/1/2011
  • 49. Women with Increased Risk of Fetal Aneuploidy Singleton pregnancy and maternal age older than 35 at delivery Dizygotic twin pregnancy and maternal age older than 31 at delivery Previous autosomal trisomy birth Previous 47,XXX or 47,XXY birth Patient or partner is carrier of chromosome translocation Patient or partner is carrier of chromosomal inversion History of triploidy Some cases of repetitive early pregnancy losses Patient or partner has aneuploidy Major fetal structural defect by sonography
  • 50. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 40 āļ›āļĩ G1P0 GA 8 weeks āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒ āļ„āļĢāļąāđ‰āļ‡āđāļĢāļ āļāļąāļ‡āļ§āļĨāļ§āđˆāļēāļĨāļđāļāļˆāļ°āđ€āļ›āđ‡āļ™Down syndrome āļˆāļ‡āļšāļ­āļāđ‚āļ­āļāļēāļŠāļ—āļĩāđˆāļˆāļ°āļ—āļēāļĢāļāļˆāļ°āđ€āļ›āđ‡āļ™ Down syndromeāđ€āļĄāļ·āđˆāļ­ āļ„āļĨāļ­āļ” a. 1:50 b. 1:100 c. 1:200 d. 1:300 e. 1:400
  • 51. Singleton Gestation—Maternal Age-Related Risk for Down Syndrome and Any Aneuploidy at Midtrimester and at Term Down Syndrome Any Aneuploidy Maternal Age Midtrimester Term Midtrimester Term 35 1/250 1/384 1/132 1/204 36 1/192 1/303 1/105 1/167 37 1/149 1/227 1/83 1/130 38 1/115 1/175 1/65 1/103 39 1/89 1/137 1/53 1/81 40 1/69 1/106 1/40 1/63 41 1/53 1/81 1/31 1/50 42 1/41 1/64 1/25 1/39 43 1/31 1/50 1/19 1/30 44 1/25 1/38 1/15 1/24 45 1/19 1/30 1/12 1/19
  • 52. āđ‚āļˆāļ—āļĒāđŒ āļ™āļēāļ‡āļŠāļĄāļĻāļĢāļĩāļ­āļēāļĒāļļ 48āļ›āļĩ āļŠāļēāļĄāļĩāļ­āļēāļĒāļļ 50āļ›āļĩ āļ›āļĢāļ°āļ§āļąāļ•āļīāļĄāļĩāļĨāļđāļāļ„āļ™āđāļĢāļ āđ€āļ›āđ‡āļ™Down syndrome āļ‚āļ“āļ°āļ™āļĩāđ‰āļ­āļēāļĒāļļ2āļ›āļĩ āļ­āļĒāļēāļāļĄāļĩāļĨāļđāļāļ„āļ™āļ—āļĩ2 āļ—āđˆāļēāļ™ āđˆ āļˆāļ°āđƒāļŦāđ‰āļ„āļēāđāļ™āļ°āļ™āļēāļ­āļĒāđˆāļēāļ‡āđ„āļĢ a. āļāļēāļāļ„āļĢāļĢāļ āđŒāļ•āļēāļĄāļ›āļāļ•āļī b. āļ•āļĢāļ§āļˆāđ‚āļ„āļĢāđ‚āļĄāđ‚āļ‹āļĄāđ€āļ”āđ‡āļāļ—āļēāļĢāļ c. āđāļ™āļ°āļ™āļēāļœāļŠāļĄāđ€āļ—āļĩāļĒāļĄāđ‚āļ”āļĒāđƒāļŠāđ‰āļ­āļŠāļļāļˆāļīāļœāļđāđ‰āļ­āļ·āđˆāļ™ d. āđāļ™āļ°āļ™āļēāļ—āļēIVFāđ‚āļ”āļĒāđƒāļŠāđ‰āđ„āļ‚āđˆāļ‚āļ­āļ‡āļœāļđāđ‰āļšāļĢāļīāļˆāļēāļ„ e. āđ„āļĄāđˆāļ•āđ‰āļ­āļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒ
  • 53. Prenatal Diagnosisāļ—āļĩāđˆāļ„āļ§āļĢāļĢāļđāđ‰ ï‚Ļ Down syndrome ï‚Ī Screening test : NT,serum markers,US ïŪ First trimester ïŪ Second trimester ï‚Ī Diagnostic test ïŪ First trimester : CVS ïŪ Second trimester : amniocentesis
  • 54. Strategy Analytes DR (%) First-trimester screen NT, PAPP-A, hCG or free -hCG 79–87 NT (First trimester) NT 64–70 Triple test MSAFP, hCG or free -hCG, uE3 60–69 Quadruple (Quad) test MSAFP, hCG or free -hCG, uE3, inh 67–81 First-trimester screen & Quad test— Integrated screen 94–96 results withheld until Quad test completed First-trimester screen & Quad test — 1% offered diagnostic test after first Stepwise sequential trimester screen — 99% proceed to Quad 90–95 screen test, results withheld until Quad test completed First-trimester screen & Quad test — 1% offered diagnostic test after first- Contingent sequential trimester screen — 15% proceed to Quad 88–94 screen test, results withheld until Quad test completed — 84% have no additional test after first-trimester screen
  • 55. First-Trimester Screening ï‚Ļ GA 11 - 14 weeks. ï‚Ī hCG or free ïĒ-hCG ï‚Ī and PAPP-A(pregnancy-associated plasma protein A ) ï‚Ī sonographic evaluation : NT ï‚Ī or a combination of both. In the first trimester, for Down syndrome fetus â€Ē serum hCG levels are >2.0 MoM â€Ē PAPP-A levels are < 0.4 MoM
  • 56. First-Trimester Screening ï‚Ļ NT measurement ï‚ģ 3.5 mm with a normal karyotype  targeted us examination , fetal echocardiography or both measured between GA11(0/7)and 13(6/7) wks.
  • 57. ï‚Ļ ïƒą nuchal translucency is associated : ï‚Ī structural cardiac abnormalities ï‚Ī skeletal dysplasias
  • 58. 2nd trimester screening Test values for triple markers screen Test Unconjugated MSAFP hCG Estriol Trisomy 18 ï‚Ŋ ï‚Ŋ ï‚Ŋ NTD  ↔ ↔ Trisomy 21 ï‚Ŋ ï‚Ŋ 
  • 59. Aneuploidy Risk Associated with Selected Major Fetal Anomalies Abnormality Approximate Population Aneuploidy Risk Common Aneuploidiesa Incidence (Percent) 1/300 Early US;1/2000 Cystic hygroma 50 45X,21,18,13, triploidy Birth Nonimmune hydrops 1/1500–4000 B 10–20 21,18,13,45X triploidy Ventriculomegaly 1/700–3000 B 5–25 13,18,21, triploidy Holoprosencephaly 1/16,000 B 40–60 13,18,22, triploidy Dandy Walker complex 1/30,000 B 30–50 18,13,21, triploidy Cleft lip/palate 1/500–3000 B 5–15 18,13 Cardiac defects 10–30 21,18,13,45X, 22q 5–8/1000 B microdeletion Diaphragmatic hernia 1/2500–10,000 B 5–15 18,13,21 Esophageal atresia 1/2000–4000 B 10–40 18,21 Duodenal atresia 1/5000 B 30–40 21 Jejunal/ileal atresia 1/3000 B Minimal None Gastroschisis 1/2000–5000 B Minimal None Omphalocele 1/4000 B 30–50 18,13,21, triploidy Clubfoot 1/1000 B 5–20 18,13
  • 60. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒG2P0A1 GA 25 wk. G1 āđāļ—āđ‰āļ‡āļˆāļēāļāļ—āļēāļĢāļ āļšāļ§āļĄāļ™āđ‰āļē āļˆāļ°āļ•āļĢāļ§āļˆāļ§āđˆāļēāļĨāļđāļāđƒāļ™āļ—āđ‰āļ­āļ‡āļĄāļĩāļ āļēāļ§āļ°āļšāļ§āļĄāļ™āđ‰āļēāđ„āļ”āđ‰āļ­āļĒāđˆāļēāļ‡āđ„āļĢ A.Amniocentesis B.Cordocentesis C.āļ•āļĢāļ§āļˆfetal cells āļˆāļēāļāđ€āļĨāļ·āļ­āļ”āđāļĄāđˆ D.Ultrasound
  • 61. Hydrops fetalis Non immune hydrops Immune hydrops ï‚Ļ Cardiovascular disease ïą Rh isoimmunization ï‚Ļ Abnormal fetal karyotype ï‚Ļ Chondrodysplasias ï‚Ļ Twin pregnancy ï‚Ļ Hematologic disease Williams Obstetrics, 23e Chapter 29. ï‚Ļ Thoracic Diseases and Injuries of the Fetus and ï‚Ļ Malformation sequence Newborn and genetic syndrome ï‚Ļ Metabolic ï‚Ļ Urinary tract ï‚Ļ Infection
  • 62. Diagnosis ï‚Ļ targeted sonographic ï‚Ļ laboratory evaluations
  • 65. â€Ē Who have risk factor? â€Ē Classification of hypertension in pregnancy and criteria for diagnosis â€Ē Who should be investigation of preeclampsia? â€Ē How to management when preeclampsia occur ? â€Ē When and route of delivery ? â€Ē What are complication of preeclampsia?
  • 66. ï‚Ļ Nulliparity ï‚Ļ Advanced maternal age ï‚Ļ Obesity ï‚Ļ African – American ethnicity ï‚Ļ Multifetal gestation ï‚Ļ Pregnancy-associated factors : Hydatidiform mole , Hydrops fetalis , Multifetal gestation ï‚Ļ Specific medical conditions: GDM, type I diabetes, obesity, chronic hypertension, renal disease, thrombophilias and APS
  • 67. āđ‚āļˆāļ—āļĒāđŒ Predisposing factor of pre-eclampsia is A. Anemia B. Multigravida C.Dead fetus in utero D.Multiple pregnancy E. Chronic renal failure
  • 68. Classifies HT in pregnancy ï‚Ī Gestational hypertension ï‚Ī Preeclampsia : mild / severe ï‚Ī Eclampsia ï‚Ī Chronic hypertension ï‚Ī Chronic hypertension with superimposed preeclampsia ï‚Ī HELLP syndrome
  • 69. āđ‚āļˆāļ—āļĒāđŒ Earliest sign of preeclampsia A.Hypertension B.Proteinuria C.Headache D.Visual disturbance E.---
  • 70. Common pathophysiologic changes seen in patients with preeclampsia ï‚Ļ Cardiovascular effects: Vasoconstriction and  cardiac output.  BP the earliest clinical finding of preeclampsia
  • 71. āđ‚āļˆāļ—āļĒāđŒ āļœāļđāđ‰āļ›āđˆāļ§āļĒāļŦāļāļīāļ‡āļ­āļēāļĒāļļ 33 āļ›āļĩ GA 33weeks āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒ āļ§āļąāļ”āļ„āļ§āļēāļĄāļ”āļąāļ™āđ‚āļĨāļŦāļīāļ•āđ„āļ”āđ‰ 140 / 90 mmHg, āļžāļąāļ 15 āļ™āļēāļ—āļĩāļ§āļąāļ”āļ‹āđ‰āļēāļāđ‡āļĒāļąāļ‡āđ„āļ”āđ‰ āđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ āļ•āļĢāļ§āļˆāđ‚āļ›āļĢāļ•āļĩāļ™āđƒāļ™āļ›āļąāļŠāļŠāļēāļ§āļ°āđ„āļ”āđ‰ 1 + āļˆāļ‡āđƒāļŦāđ‰āļāļēāļĢāļ§āļīāļ™āļīāļˆāļ‰āļąāļĒ a. Eclampsia b. Mild preeclampsia c. Severe preeclampsia d. Gestational hypertension
  • 72. Am J Obstet Gynecol 2000;183:S1-22. Suchila Sritippayawan 01/02/54 72
  • 73. Preeclampsia : Management Gestational age Term (GA â‰Ĩ 37 wks) Term (GA>37 wks) yes Delivery&MgSO4 Severe disease present ? no Expectant Rx until term
  • 74. Mild preeclampsia GA < 37 wk. ï‚Ļ Bed rest ï‚Ļ BP monitoring ï‚Ļ Urine monitoring ï‚Ļ Lab evaluation ï‚Ļ Fetal surveillance : NST
  • 75.
  • 76. āļāļēāļĢāļ”āļđāđāļĨāđƒāļ™āļĢāļ°āļĒāļ°Intrapartum ï‚Ļ āđ€āļāđ‰āļēāļĢāļ°āļ§āļąāļ‡āļ āļēāļ§āļ°severe preeclampsia /eclampsia (BP, sign and symptom) ï‚Ļ Prophylaxis seizure : MgSO4 ï‚Ļ Controlled BP if BP â‰Ĩ160/110 mmHg): Hydralazine /Antihypertensive drugs ï‚Ļ Monitor : vital signs,reflex,sign Magnesium toxicity ï‚Ļ Continuous fetal monitor
  • 77. Severe Preeclampsia : Management ï‚Ļ Admit ï‚Ļ Stabilized MgSO4 for seizure prevention ï‚Ļ BP control ï‚Ļ Work up lab ï‚Ļ Termination of pregnancy
  • 78. Severe Preeclampsia : Management(Preterm) No severe conditions which should immediately delivery GA 24 - wks. steroids delivery
  • 79. Severe preeclampsia : Management ï‚Ļ Termination of pregnancy when : ï‚Ī Term pregnancy ï‚Ī Severe preclampsia with sign of acute renal failure , thrombocytopenia , pulmonary edema,hepatic injury,DIC ï‚Ī Suspected abruptio placenta ï‚Ī Eclampsia ï‚Ī HELLP syndrome ï‚Ī Non reassuring fetal status ï‚Ī Severe IUGR ï‚Ī Labor or labor of rupture of membranes
  • 80. Indications for delivery in preeclampsia āļ”āđ‰āļēāļ™āđāļĄāđˆ āļ”āđ‰āļēāļ™āļĨāļđāļ ï‚Ļ āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ â‰Ĩ 38 āļŠāļąāļ›āļ”āļēāļŦāđŒ ï‚Ļ āļĄāļĩāļ āļēāļ§āļ° Severe fetal ï‚Ļ āļ„āļ§āļšāļ„āļļāļĄāļ„āļ§āļēāļĄāļ”āļąāļ™āđ‚āļĨāļŦāļīāļ•āđ„āļĄāđˆāđ„āļ”āđ‰ growth restriction ï‚Ļ Severe preeclampsia ï‚Ļ āļĄāļĩāļ āļēāļ§āļ° Nonreassuring (āļ­āļēāļāļēāļĢāđāļĨāļ°āļ­āļēāļāļēāļĢāđāļŠāļ”āļ‡, lab) results from fetal ï‚Ļ Eclampsia testing ï‚Ļ HELLP syndrome ï‚Ļ Placental abruption ï‚Ļ Oligohydramnios
  • 81. Route of delivery ï‚Ļ Vaginal route delivery is preferred ï‚Ļ Unfavorable cervix  ripening cervix ï‚Ļ Depen on maternal and fetal condition ï‚Ļ āļ‚āđ‰āļ­āļ„āļ§āļĢāļĢāļ°āļ§āļąāļ‡ : āđ„āļĄāđˆāđƒāļŦāđ‰ ERGOMETRINE āđƒāļŦāđ‰oxytocin āđāļ—āļ™ C/S delivery reserved for OB indication 01/02/54 Suchila Sritippayawan 81
  • 82. āļāļēāļĢāļ”āļđāđāļĨāđƒāļ™āļĢāļ°āļĒāļ°Postpartum ï‚Ļ Most Rapid improved / Some may worsening ï‚Ļ Continue MgSO4 for 24 hr ï‚Ļ Monitoring of ï‚Ī Blood pressure Hydralazine or nifedipine PRN BP > 160/110 ï‚Ī maternal symptoms ï‚Ī measurements of fluid intake and urine output. ï‚Ļ Follow up 2 wk after discharge If hypertension persist , give thiazide or beta- blockers or nifedipine
  • 83. Management : eclampsia ï‚Ļ Prevention of maternal hypoxia and trauma ï‚Ļ Blood pressure control ï‚Ļ Prevention of recurrent seizures ï‚Ļ Delivery when : stabilized and seizures have been controlled
  • 84. Management : eclampsia Mode of delivery depend on ï‚Ļ Gestational age ï‚Ļ Bishop score, whether the patient is in labor ï‚Ļ Fetal condition and position
  • 85. Management : eclampsia The definitive treatment of eclampsia is delivery, irrespective of gestational age The best way to treat the fetus is to stabilized the mother C/S should be reserved for OB condition
  • 86. Management : eclampsia Stabilizing the mother by administering anticonvulsant drugs and oxygen Treating severe hypertension (if present) can help the fetus recover in-utero from the effects of maternal hypoxia, hypercarbia, and uterine hyperstimulation if10 – 15 min with no improvement despite maternal and fetal resuscitative interventions occult abruption ? emergent delivery should be considered
  • 87. A. Oral antihypertensive drug B. Diuretics C. MgSO4 D. Induction of labor E. Expectation with materno-fetal observe
  • 88. āđ‚āļˆāļ—āļĒāđŒ āļœāļđāđ‰āļ›āđˆāļ§āļĒāļŦāļāļīāļ‡āļ­āļēāļĒāļļ 31 āļ›āļĩ GA 32weeks āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒāļ•āļēāļĄāļ™āļąāļ” āļ§āļąāļ”āļ„āļ§āļēāļĄāļ”āļąāļ™āđ‚āļĨāļŦāļīāļ•āđ„āļ”āđ‰ 130 / 90 mmHg, āļ•āļĢāļ§āļˆāđ‚āļ›āļĢāļ•āļĩāļ™āđƒāļ™āļ›āļąāļŠāļŠāļēāļ§āļ°āđ„āļ”āđ‰ 1 + āđ„āļĄāđˆāļĄāļĩāļ­āļēāļāļēāļĢāļ›āļ§āļ”āļĻāļĩāļĢāļĐāļ° āļ•āļēāļĄāļąāļ§ āļˆāļļāļāđāļ™āđˆāļ™āđƒāļ•āđ‰āļĨāļīāđ‰āļ™āļ›āļĩāđˆ āđ„āļĄāđˆāļĄāļĩāļ•āļāļ‚āļēāļ§ āļ„āļąāļ™āļŠāđˆāļ­āļ‡āļ„āļĨāļ­āļ” āļ›āļąāļŠāļŠāļēāļ§āļ°āđ„āļĄāđˆāđāļŠāļšāļ‚āļąāļ” āđāļžāļ—āļĒāđŒāđāļ™āļ°āļ™āļēāđƒāļŦāđ‰āđ„āļ›āļ§āļąāļ”āļ„āļ§āļēāļĄāļ”āļąāļ™āđ‚āļĨāļŦāļīāļ•āļ—āļĩāđˆ āļŠāļ–āļēāļ™āļĩāļ­āļ™āļēāļĄāļąāļĒāđƒāļāļĨāđ‰āļšāđ‰āļēāļ™ āđāļĨāļ°āļ™āļąāļ”āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒāļ­āļĩāļ 1 lāļŠāļąāļ›āļ”āļēāļŦāđŒāļ•āđˆāļ­āļĄāļē āļ§āļąāļ”āļ„āļ§āļēāļĄāļ”āļąāļ™āđ‚āļĨāļŦāļīāļ•āđ„āļ”āđ‰ 170 / 110 mmHg, āļ•āļĢāļ§āļˆāđ‚āļ›āļĢāļ•āļĩāļ™āđƒāļ™āļ›āļąāļŠāļŠāļēāļ§āļ°āđ„āļ”āđ‰ 3+ āļ—āđˆāļēāļ™āļˆāļ°āđƒāļŦāđ‰āļāļēāļĢāļ”āļđāđāļĨāļœāļđāđ‰āļ›āđˆāļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰āļ­āļĒāđˆāļēāļ‡āđ„āļĢ a. āđƒāļŦāđ‰ MgSO4 b. āđƒāļŦāđ‰ Pethidine c. āđƒāļŦāđ‰ Oxytocin d. āđƒāļŦāđ‰ Diazepam
  • 89. āđ‚āļˆāļ—āļĒāđŒ A 32-week primigravida comes to the antenatal clinic for her regular appointment. The physical examination shows 2 kg weight gain in 2 wks, BP 160/110 mmHg, edema over all extremities, 3+ DTR, and 2+ proteinuria. The most appropriate initial management is A. Diazepam B. Furosemide C.Hydralazine D.Calcium gluconate E. Magnesium sulfate
  • 90. A. Observed B. C/S emergency C. MgSO4 then observe D. MgSO4then try ND E. MgSO4then C/S
  • 91. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 18āļ›āļĩ G1P0 āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 30 āļŠāļąāļ›āļ”āļēāļŦāđŒ āļĄāļēāļŦāđ‰āļ­āļ‡āļ„āļĨāļ­āļ”āļ”āđ‰āļ§āļĒāļ­āļēāļāļēāļĢāļ›āļ§āļ”āļĻāļĩāļĢāļĐāļ° āļ§āļąāļ”BPāđ„āļ”āđ‰ 160/110 mm Hg āđ€āļˆāļēāļ°āđ€āļĨāļ·āļ­āļ”āļ•āļĢāļ§āļˆ āļžāļšāļ§āđˆāļēāļĄāļĩelevated liver function test āđāļĨāļ°Platelet count 60,000/mm3 āļāļēāļĢāļ”āļđāđāļĨāļ—āļĩāđˆāđ€āļŦāļĄāļēāļ°āļŠāļĄāļŠāļēāļŦāļĢāļąāļšāļœāļđāđ‰āļ›āļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰āļ„āļ·āļ­ āđˆ a. āđƒāļŦāđ‰oral antihypertensive therapy b. platelet transfusion c. MgSO4 therapy and induction of labor d. IV Immunoglobulin therapy
  • 92. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 30āļ›āļĩ G1P0 āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 29 āļŠāļąāļ›āļ”āļēāļŦāđŒ āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒāļ•āļēāļĄāļ™āļąāļ” āļ§āļąāļ”BPāđ„āļ”āđ‰ 140/90 mm Hg āđ€āļˆāļēāļ°āđ€āļĨāļ·āļ­āļ”āļ•āļĢāļ§āļˆ liver function test āđāļĨāļ°Platelet count āļ›āļāļ•āļī Urine protein 2+ āļāļēāļĢāļ”āļđāđāļĨāļ—āļĩāđˆāđ€āļŦāļĄāļēāļ°āļŠāļĄāļŠāļēāļŦāļĢāļąāļšāļœāļđāđ‰āļ›āļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰āļ„āļ·āļ­ āđˆ a. Induction of labor b. Cesarean section c. Antihypertensive therapy d. Expectant management
  • 93. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 25āļ›āļĩ G1P0 āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 38 āļŠāļąāļ›āļ”āļēāļŦāđŒ āļĄāļĩāļ­āļēāļāļēāļĢāļ›āļ§āļ”āļĻāļĩāļĢāļĐāļ° āļĢāļđāđ‰āļŠāļķāļāļ§āđˆāļēāļĨāļđāļāļ”āļīāļ™āļ™āđ‰āļ­āļĒāļĨāļ‡ āđ‰ āļ§āļąāļ”BPāđ„āļ”āđ‰ 180/110 mm Hg uterine size ~ date , DTR +3,Urine protein 2+ āļ„āļ§āļĢāđƒāļŦāđ‰āļĒāļēāđƒāļ” a. Diazepam b. MgSO4 c. Antihypertensive drug d. ------ e. -------
  • 94. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 26āļ›āļĩ G2P1āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 32āļŠāļąāļ›āļ”āļēāļŦāđŒ āļĄāļēāļāļēāļ āļ„āļĢāļĢāļ āđŒāļ•āļēāļĄāļ™āļąāļ”āđāļžāļ—āļĒāđŒāđƒāļŦāđ‰āļ™āļ­āļ™āđ‚āļĢāļ‡āļžāļĒāļēāļšāļēāļĨāđ€āļžāļĢāļēāļ°āļ§āļąāļ” BPāļžāļšāļ§āđˆāļēBPāđ„āļ”āđ‰ 170/110 mm Hg āđ„āļĄāđˆāļĄāļĩāļ­āļēāļāļēāļĢāļœāļīāļ”āļ›āļāļ•āļīāđƒāļ”āđ† āļŦāļĨāļąāļ‡āļžāļąāļ āļ§āļąāļ” BPāļ‹āđ‰āļē = 150/98 mmHg proteinuria = 1 + āđāļžāļ—āļĒāđŒāļŠāļ‡labāđāļĨāļ°āđƒāļŦāđ‰āļ™āļ­āļ™āļžāļąāļ āđˆ āđƒāļ™āđ‚āļĢāļ‡āļžāļĒāļēāļšāļēāļĨ āļ‚āđ‰āļ­āđƒāļ”āđ€āļ›āđ‡āļ™āļ‚āļąāđ‰āļ™āļ•āļ­āļ™āļ•āđˆāļ­āđ„āļ›āļ‚āļ­āļ‡āļāļēāļĢāļ”āļđāđāļĨāļœāļđāđ‰āļ›āđˆāļ§āļĒāļĢāļēāļĒāļ™āļĩ a. Induced labor : vaginal delivery b. Cesarean section c. Phenytoin d. Labetalol e. Dexamethasone
  • 95. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 32 āļ›āļĩ G3P2 GA 35 wk. underlying CHT āļŠāđˆāļ§āļ‡ANC BPāđ„āļĄāđˆāđ€āļāļīāļ™ 140/90 mmHg,no proteinuria āļĄāļēANC āļ„āļĢāļąāđ‰āļ‡āļĨāđˆāļēāļŠāļļāļ” BP > 140/83 mmHg urine protein 24āļŠāļĄ.=0.35 g āļāļēāļĢāļ”āļđāđāļĨāļ‚āļąāļ™āļ•āļ­āļ™āļ•āđˆāļ­āđ„āļ›āļ„āļ·āļ­ āđ‰ (A) Administer oral furosemide (B) Prepare for emergent delivery (C) Restart the patient‘s prepregnancy antihypertensive regimen (D) Restricted activity and close monitoring as an outpatient following initial inpatient evaluation (E) Start hydralazine
  • 97. Approach Diabetes in pregnancy 97 2/1/2011
  • 98. ï‚Ļ Finding : who has risk of DM in pregnancy ï‚Ļ Screening GDM : 50 gm GCT ï‚Ļ Confirm diagnosis : who has positive 50gm GCT(100gm OGTT) ï‚Ļ Classified type of DM : GDM A1,A2 ,PGDM ï‚Ļ Management : ï‚Ī antepartum ,intrapartum ,postpartum ï‚Ī Maternal and fetus 98 2/1/2011
  • 99. āļŠāļīāđˆāļ‡āļ—āļĩāđˆāļ„āļ§āļĢāļĢāļđāđ‰ ï‚Ļ Classification of DM : overt DM (PGDM),GDM ï‚Ļ Screening GDM : who,when ,how ï‚Ļ Complication of DM : Maternal , fetus ï‚Ļ Interpretation of BS ï‚Ļ Management : control DM , monitor complication,time of delivery and route of delivery
  • 100. āđ‚āļˆāļ—āļĒāđŒ āļœāļđāđ‰āļ›āđˆāļ§āļĒāļŦāļāļīāļ‡āļ­āļēāļĒāļļ 39 āļ›āļĩ āļ™āđ‰āļēāļŦāļ™āļąāļ 65 āļāļ.āļŠāļđāļ‡ 152 āļ‹āļĄ. āļ›āđ‰āļēāđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™ āļĨāļđāļāļ„āļ™āđāļĢāļāļ™āđ‰āļēāļŦāļ™āļąāļāđāļĢāļāļ„āļĨāļ­āļ” 4200 āļ. āļ‚āđ‰āļ­āđƒāļ”āđ€āļ›āđ‡āļ™āļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āļ•āđˆāļ­āļāļēāļĢāđ€āļ›āđ‡āļ™āđ‚āļĢāļ„āđ€āļšāļēāļŦāļ§āļēāļ™āļ‚āļ­āļ‡āļœāļđāđ‰āļ›āđˆāļ§āļĒ āļĢāļēāļĒāļ™āļĩāđ‰āļĄāļēāļāļ—āļĩāļŠāļļāļ” a. āļ­āđ‰āļ§āļ™ b. āđ€āļ•āļĩāđ‰āļĒ c. āļ›āđ‰āļēāđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™ d. āļĨāļđāļāļ„āļ™āđāļĢāļāđ€āļ›āđ‡āļ™macrosomia e. āļ­āļēāļĒāļļāđāļĄāđˆ> 25āļ›āļĩ
  • 101. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 30 āļ›āļĩ G3P2 GA 25wk. āļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļī āļ„āļĢāļĢāļ āđŒāļ—āļĩāđˆāđāļĨāđ‰āļ§āđ€āļ›āđ‡āļ™GDM āļ„āļĢāļĢāļ āđŒāļ™āļĩāđ‰ āđ€āļĄāļ·āđˆāļ­ GA 10 wk.FBS=110 mg/dL,no glucouria āļœāļđāđ‰āļ›āđˆāļ§āļĒāļ„āļļāļĄāļ­āļēāļŦāļēāļĢāđ€āļ­āļ‡ 2-3 wk.PTA āļĄāļĩāļ­āļēāļāļēāļĢ polyuria,fatigue āļˆāļ°āļ”āļđāđāļĨāļœāļđāđ‰āļ›āļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰āļ­āļĒāđˆāļēāļ‡āđ„āļĢāļ•āđˆāļ­āđ„āļ› āđˆ (A) Administer a 3-hour glucose tolerance test (B) Administer a 50-g 1-hour glucose tolerance test (C) Begin insulin therapy (D) Check a urinalysis and start insulin if urinalysis reveals glucose in the urine (E) Prescribe metformin to be taken daily
  • 102. āļāļĨāļļāđˆāļĄāļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āļ•āđˆāļē (āļžāļšāļ—āļļāļāļ‚āđ‰āļ­āļ•āđˆāļ­āđ„āļ›āļ™āļĩāđ‰) āļ—āļĩāđˆāđāļ™āļ°āļ™āļēāļ§āđˆāļē āļ­āļēāļˆāđ„āļĄāđˆāļˆāļēāđ€āļ›āđ‡āļ™āļ•āđ‰āļ­āļ‡āļ•āļĢāļ§āļˆāļ„āļąāļ”āļāļĢāļ­āļ‡ 102 ï‚Ļ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ<25āļ›āļĩ ï‚Ļ āļĄāļĩāđ€āļŠāļ·āđ‰āļ­āļŠāļēāļ•āļīāļ—āļĩāđˆāļĄāļĩāļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āļ•āđˆāļē ( āļĒāļāđ€āļ§āđ‰āļ™āđ€āļŠāļ·āđ‰āļ­āļŠāļēāļ•āļī Hispanic, African, Native American, South or East Asian origins) ï‚Ļ āđ„āļĄāđˆāļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāļ„āļĢāļ­āļšāļ„āļĢāļąāļ§ āļāļēāļ•āļīāđƒāļāļĨāđ‰āļŠāļīāļ”āđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™ ï‚Ļ āļ™āļ™.āļāđˆāļ­āļ™āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāđāļĨāļ°āļ™āļ™.āļ—āļĩāđˆāđ€āļžāļīāđˆāļĄāļĢāļ°āļŦāļ§āđˆāļēāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ›āļāļ•āļī (BMI< 26 kg./m2) ï‚Ļ āđ„āļĄāđˆāļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāļ—āļēāļ‡āļŠāļđāļ•āļīāļĻāļēāļŠāļ•āļĢāđŒāļ—āļĩāđˆāļœāļīāļ”āļ›āļāļ•āļīāļ—āļĩāđˆāđ€āļāļĩāđˆāļĒāļ§āļ‚āđ‰āļ­āļ‡āļāļąāļš GDM(macrosomia,stillbirth,malformation) ï‚Ļ āđ„āļĄāđˆāđ€āļ„āļĒāļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāļĢāļ°āļ”āļąāļšāļ™āđ‰āļēāļ•āļēāļĨāđƒāļ™āđ€āļĨāļ·āļ­āļ”āļœāļīāļ”āļ›āļāļ•āļī ADA ,Diabetic Suchila Sritippayawan care 2004;(Suppl 1):S88 – 90 2/1/2011 2/1/2011 Chula
  • 103. Recommended Screening Strategy Based on Risk Assessment for Detecting Gestational Diabetes High Risk Perform blood glucose testing as soon as feasible. If gestational diabetes is not diagnosed, blood glucose testing should be repeated at 24-28 weeks or at any time a patient has symptoms or signs suggestive of hyperglycemia High risk — women with marked obesity, strong family history of type 2 diabetes, prior gestational diabetes, or glucosuria 103 2/1/2011
  • 104. ï‚Ļ The best time to screen for DM during pregnancy : ï‚Ī GA 24 – 28 weeks ï‚Ļ Patient with â‰Ĩ 1 risk factors for developing GDM should be screened at ï‚Ī The first prenatal visit and ï‚Ī GA 24 – 28 weeks or ï‚Ī symptoms or signs suggestive of 104 hyperglycemia 2/1/2011
  • 105. Who have risk factor of GDM 50 gm glucose challenge test for 80% detection āļ„āđˆāļēāļœāļīāļ”āļ›āļāļ•āļī â‰Ĩ 140 mg/dL 100 gm OGTT Diagnostic test 105 Suchila Sritippayawan 2/1/2011 2/1/2011
  • 106. 100 gm OGTT Fasting plasma glucose 105 mg/dL 1 hour 190 mg/dL 2 hour 165mg/dL 3 hour 145mg/dL āļœāļīāļ”āļ›āļāļ•āļī āļ•āļąāđ‰āļ‡āđāļ•āđˆ 2 āļ„āđˆāļēāļ‚āļķāđ‰āļ™āđ„āļ› GDMA1 GDM 106 Suchila Sritippayawan GDMA2 2/1/2011 2/1/2011
  • 107. āđ‚āļˆāļ—āļĒāđŒ āļœāļđāđ‰āļ›āļ§āļĒāļŦāļāļīāļ‡āļ­āļēāļĒāļļ38āļ›āļĩ āđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™ āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒ GA āđˆ 30wks. āļĄāļēāļ”āđ‰āļ§āļĒāđ€āļˆāđ‡āļšāļ„āļĢāļĢāļ āđŒāļ„āļĨāļ­āļ”āđāļĨāļ°āļ›āļąāļŠāļŠāļēāļ§āļ°āļšāđˆāļ­āļĒ āļ•āļĢāļ§āļˆ āļžāļšāļĄāļ”āļĨāļđāļāļ­āļĒāļđāđˆāļĢāļ°āļ”āļąāļšāļĨāļīāļ™āļ›āļĩāđˆ āļ„āļĨāļēāļŠāđˆāļ§āļ™āļ‚āļ­āļ‡āļ—āļēāļĢāļāđ„āļĄāđˆāļŠāļąāļ” FHS āđ‰ 152/min Uterine contraction 1āļ„āļĢāļąāđ‰āļ‡āđƒāļ™ 30āļ™āļēāļ—āļĩ PV: cervix dilated 1cm , effacement 50% āļ­āļĒāļēāļ āļ—āļĢāļēāļšāļ§āđˆāļēāļŠāļēāđ€āļŦāļ•āļļāļ—āļĩāđˆāļ—āļēāđƒāļŦ āđ‰āđ€āļāļīāļ” āļĨāļąāļāļĐāļ“āļ°āđƒāļ™āļœāļđāđ‰āļ›āļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰āļ„āļ·āļ­ āđˆ A. Macrosomia B. Twin pregnancy C. Myoma uteri D. Polyhydramnios E. Urinary tract infection
  • 108. Etiology of polyhydramnios Etiology % Idiopathic 60 Maternal DM 19 Multiple 7.5 gestation(TTTS) Blood group 5 incompatibility Congenital 8.5 malformation
  • 109. Fetal malformations associated with polyhydramnios anencephaly , encephalocele Iniencephaly CNS defects ,hydranencephaly esophageal atresia, duodenal atresia ,small bowel obstruction ,omphalocele , GI obstruction gastroschisis,cleft palate, diaphragmatic hernia cystic adenomatoid malformation of the Respiratory tract lungs,chylothorax Fetal renal harmatoma, Unilateral GU tract ureteriopelvic junction obstruction Cardiovascular vulvular incompetence,Ebstein’s anomaly , system arrythmias,TTTS fetal akinesia , skeletal dysplasia,myotonic Musculoskeletal dystrophy system
  • 110. Diagnosis polyhydramnios Technique cm. AFI >24 - 25 cm Vertical single deepest pocket volume : ïą Mild 8 -11cm (80%) ïą Moderate 12 – 15 cm (15%) ïą Severe â‰Ĩ 16 cm (5%)
  • 111. Evaluation ïķScreening DM ïķ Detailed sonographic examination for anomalies ïķ Fetal karyotype (in case severe polyhydramnios,fetal anomaly) ïķ Coombs’test : Rh isoimmunization ïķ Infection screening : syphilis
  • 112. Screening GDM ï‚Ļ 50 g GCT ï‚Ļ Positive screening : ï‚ģ 140 mg/dL
  • 113. āļāļĨāļļāđˆāļĄāļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āļ•āđˆāļē (āļžāļšāļ—āļļāļāļ‚āđ‰āļ­āļ•āđˆāļ­āđ„āļ›āļ™āļĩāđ‰) āļ—āļĩāđˆāđāļ™āļ°āļ™āļēāļ§āđˆāļē āļ­āļēāļˆāđ„āļĄāđˆāļˆāļēāđ€āļ›āđ‡āļ™āļ•āđ‰āļ­āļ‡āļ•āļĢāļ§āļˆāļ„āļąāļ”āļāļĢāļ­āļ‡ 113 ï‚Ļ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ<25āļ›āļĩ ï‚Ļ āļĄāļĩāđ€āļŠāļ·āđ‰āļ­āļŠāļēāļ•āļīāļ—āļĩāđˆāļĄāļĩāļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āļ•āđˆāļē ( āļĒāļāđ€āļ§āđ‰āļ™āđ€āļŠāļ·āđ‰āļ­āļŠāļēāļ•āļī Hispanic, African, Native American, South or East Asian origins) ï‚Ļ āđ„āļĄāđˆāļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāļ„āļĢāļ­āļšāļ„āļĢāļąāļ§ āļāļēāļ•āļīāđƒāļāļĨāđ‰āļŠāļīāļ”āđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™ ï‚Ļ āļ™āļ™.āļāđˆāļ­āļ™āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāđāļĨāļ°āļ™āļ™.āļ—āļĩāđˆāđ€āļžāļīāđˆāļĄāļĢāļ°āļŦāļ§āđˆāļēāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ›āļāļ•āļī (BMI< 26 kg./m2) ï‚Ļ āđ„āļĄāđˆāļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāļ—āļēāļ‡āļŠāļđāļ•āļīāļĻāļēāļŠāļ•āļĢāđŒāļ—āļĩāđˆāļœāļīāļ”āļ›āļāļ•āļīāļ—āļĩāđˆāđ€āļāļĩāđˆāļĒāļ§āļ‚āđ‰āļ­āļ‡āļāļąāļš GDM(macrosomia,stillbirth,malformation) ï‚Ļ āđ„āļĄāđˆāđ€āļ„āļĒāļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāļĢāļ°āļ”āļąāļšāļ™āđ‰āļēāļ•āļēāļĨāđƒāļ™āđ€āļĨāļ·āļ­āļ”āļœāļīāļ”āļ›āļāļ•āļī ADA ,Diabetic Suchila Sritippayawan care 2004;(Suppl 1):S88 – 90 2/1/2011 2/1/2011 Chula
  • 114. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 32 āļ›āļĩ āļĄāļēANC GA 22 wk. āļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāđ€āļ›āđ‡āļ™ DM āļĄāļē 3 āļ›āļĩāđƒāļŠāđ‰ insulināļĄāļēāļ•āļĨāļ­āļ” FBS 105 mg/dL,2hr.PP BS 139 mg/dL āļˆāļ°investigation āļ­āļ°āđ„āļĢāđ€āļžāļīāđˆāļĄāđ€āļ•āļīāļĄ A. BPP B. Maternal serum triple screening test C. Maternal serum AFP D. Fetal Doppler US E. Fetal echocardiography 
  • 115. a. āļ­āđ‰āļ§āļ™ BMI 28.1 āļāļ./āļ•āļēāļĢāļēāļ‡āđ€āļĄāļ•āļĢ b. āđ€āļ•āļĩāđ‰āļĒ c. āļ›āđ‰āļēāđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™ d. āļĨāļđāļāļ„āļ™āđāļĢāļāđ€āļ›āđ‡āļ™macrosomia e. āļ­āļēāļĒāļļāđāļĄāđˆ> 25āļ›āļĩ
  • 116. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 30 āļ›āļĩ G2P1 12 weeks āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒ āđ€āļ„āļĒāļ„āļĨāļ­āļ”āļ—āļēāļĢāļāļŦāļ™āļąāļ 3900 āļāļĢāļąāļĄ āļĄāļĩāļ›āđ‰āļēāđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™ āļœāļđāđ‰āļ›āđˆāļ§āļĒāļŦāļ™āļąāļ 72 āļāļ. āļŠāļđāļ‡ 155 āļ‹āļĄ. āļ‚āđ‰āļ­āđƒāļ”āđ€āļ›āđ‡āļ™āļ›āļąāļˆāļˆāļąāļĒāđ€āļŠāļĩāđˆāļĒāļ‡āļ—āļĩāđˆāļ•āđ‰āļ­āļ‡āļ„āļąāļ”āļāļĢāļ­āļ‡āđ€āļšāļēāļŦāļ§āļēāļ™ a. āļ­āđ‰āļ§āļ™ BMI 29.96 āļāļ./āļ•āļĢ.āđ€āļĄāļ•āļĢ b. āđ€āļ•āļĩāđŠāļĒ c. āļ›āđ‰āļēāđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™ d. āđ€āļ„āļĒāļ„āļĨāļ­āļ”āļ—āļēāļĢāļāļ•āļąāļ§āđ‚āļ•
  • 117. āđ‚āļˆāļ—āļĒāđŒ āļ‚āđ‰āļ­āđƒāļ”āđ„āļĄāđˆāđƒāļŠāđˆ indication āđƒāļ™āļāļēāļĢāļ•āļĢāļ§āļˆ screening GCT in pregnancy A. History of preterm labour B. History of stillbirth C.History of LGA D.Family history of DM E. Persistent glucosuria
  • 118. DIABETES INSULI DURATI VASCULAR CLASS ONSET AGE N ON (Y) DISEASE (Y) NEED Gestational diabetes A1 Any Any 0 0 A2 Any Any 0 + Pregestational diabetes B >20 <10 0 + C 10-19 or 10-19 0 + D <10 or >20 + + F Any Any + + R Any Any + + T Any Any + + H Any Suchila Sritippayawan Any 2/1/2011 + +
  • 119. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡ 32 āļ›āļĩ āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒāļ„āļĢāļąāđ‰āļ‡āđāļĢāļāļ•āļ­āļ™āļ™āļĩāđ‰āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 22 wks āļœāļđāđ‰āļ›āđˆāļ§āļĒāđ€āļ›āđ‡āļ™āđ€āļšāļēāļŦāļ§āļēāļ™āļĄāļē 3 āļ›āļĩ āđ„āļ”āđ‰ Insulin āļĄāļēāļ•āļĨāļ­āļ” āļ•āļĢāļ§āļˆ FBS =105 mg/dl 2 hour glucose = 139 mg/dl āļˆāļ° investigation āļ­āļ°āđ„āļĢ āđ€āļžāļīāđˆāļĄāđ€āļ•āļīāļĄ 1. BPP 2. Maternal serum triple test 3. Maternal serum AFP 4. Fetal Doppler U/S 5. Fetal echography
  • 120. Complication :Pregestational Diabetes Mellitus (PGDM) ï‚Ļ Malformation :  Caudal regression syndrome (rare)  Sirenomelia (rare)  cardiovascular malformations (↑occur 2- 5 fold compared to the non-diabetic population)  genitourinary tract  musculoskeletal anomalies Suchila Sritippayawan 2/1/2011
  • 121. Complication :Pregestational Diabetes Mellitus (PGDM) Maternal effect : ï‚Ļ Chronic hypertension ï‚Ļ Preeclampsia ï‚Ļ Microalbuminuria and diabetic nephropathy may complicate pregnancy prognosis ï‚Ļ Diabetic retinopathy Suchila Sritippayawan 2/1/2011
  • 122. Complication :Pregestational Diabetes Mellitus (PGDM) Maternal effect : ï‚Ļ Ketoacidosis: (insulin resistance ï‚Ū insulin deficiency) ïŪ Common risk factors : new onset diabetes; infections(influenza and UTI); poor patient compliance; insulin pump failure; and treatment with Îē-mimetic tocolytic medications and antenatal corticosteroids Suchila Sritippayawan 2/1/2011
  • 123. Complication :Pregestational Diabetes Mellitus (PGDM) Maternal effect : ï‚Ļ Infection (DM type 1) Common infection : candida vulvovaginitis , UTI , URI ,puerperal and pelvic infection 4% antepartum pyelonephritis develop (with DM type 1) ï‚Ū screening for asymptomatic bacteriuria Suchila Sritippayawan 2/1/2011
  • 124. Management Goal : ï‚Ļ to lower the likelihood of Macrosomia ï‚Ļ To reduce neonatal hypoglycemia Suchila Sritippayawan 2/1/2011
  • 125. Management : Pregestational Diabetes Mellitus ï‚Ļ Prepregnancy counseling ï‚Ļ Glycemic control during gestation : Diet ,insulin ï‚Ļ Fetal assessment ï‚Ļ Timing and mode of delivery ï‚Ļ Glycemic management during labor ï‚Ļ Postpartum care and lactation ï‚Ļ Contraception Suchila Sritippayawan 2/1/2011
  • 126. Prepregnancy counseling ï‚Ļ Optimal care and patient education : prevent early pregnancy loss and congenital malformation ï‚Ļ Preconceptional glucose control ï‚Ī Prepandial glucose : 70 – 100 mg/dl ï‚Ī Postpandrial glucose : 1 hr. < 140 mg/dl 2 hr. < 120 mg/dl ï‚Ī Glycated Hb : within 3 SD of normal mean ï‚Ļ Folic acid supplement 400 g/day (periconception – during early pregnancy) to decrease NTD Suchila Sritippayawan 2/1/2011
  • 127. Glycemic management during pregnancy PGDM ï‚Ļ The management of diabetes in pregnancy must focus on excellent glucose control achieved using a careful combination of diet, exercise, and insulin therapy Suchila Sritippayawan 2/1/2011
  • 128. Glycemic management during pregnancy PGDM ï‚Ļ Caloric requirement : ï‚Ī usually require 30–35 kcal/kg/d. ï‚Ļ Caloric composition includes ï‚Ī 40–50% from complex,high-fiber carbohydrates ï‚Ī 20% from protein ï‚Ī 30–40% from primarily unsaturated fats. Suchila Sritippayawan 2/1/2011
  • 129. Fetal assessment ï‚Ļ Early US : fetal viability and to accurate date the pregnancy ï‚Ļ Target US GA 18 – 20 weeks ï‚Ļ Periodic US : to confirm fetal growth ï‚Ļ Antepartum fetal monitoring : ï‚Ī Initiation of testing at GA 32–34 weeks ï‚Ī Earlier GA in high risk conditions. ï‚Ī Daily fetal movement count Suchila Sritippayawan 2/1/2011
  • 130. Indication for delivery in diabetes pregnancy Fetal  Non reactive , positive CST  Reactive positive CST, mature fetus  GA 40 – 41 weeks  U/S evidence of Fetal growth arrest  Decline in fetal growth rate with decreased AF Maternal  Severe preeclampsia,  Mild preeclampsia mature fetus  Markedly falling renal function( Cr clearance < 40 ml/min) Obstetric  Preterm labor with failure of tocolysis  Mature fetus , inducible cervix Suchila Sritippayawan 2/1/2011
  • 131. Timing and route of delivery ï‚Ļ Early delivery may be indicated : ï‚Ī in patients with vasculopathy, nephropathy ï‚Ī poor glucose control ï‚Ī prior stillbirth ï‚Ļ patients with well-controlled may be allowed to progress to their expected date of delivery as long as antenatal testing remains reassuring Suchila Sritippayawan 2/1/2011
  • 132. Timing and route of delivery ï‚Ļ To prevent traumatic birth injury : Cesarean delivery may be considered if the EFW > 4,500 g in women with diabetes. ï‚Ļ Notify neonatologist ï‚Ļ Stop insulin after placental was removal ï‚Ļ Beware shoulder dystocia Suchila Sritippayawan 2/1/2011
  • 134. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ­āļēāļĒāļļ 34 āļ›āļĩ āļĄāļĩāļ­āļēāļāļēāļĢāļ›āļąāļŠāļŠāļēāļ§āļ°āđāļŠāļšāļ‚āļąāļ”āđāļĨāļ°āđ€āļˆāđ‡āļšāļ—āļĩāđˆāļšāļĢāļīāđ€āļ§āļ“ āļŠāđˆāļ­āļ‡āļ„āļĨāļ­āļ” āļ•āļĢāļ§āļˆāļĢāđˆāļēāļ‡āļāļēāļĒāļžāļš vesicular lesion with shallow ulcer at vulva āļˆāļ‡āđƒāļŦāđ‰āļāļēāļĢāļ§āļīāļ™āļīāļˆāļ‰āļąāļĒ A. Herpatic vulva B. Molluscum contagiosum C. Candiadiasis at vulva D. Syphilis
  • 135. Genital Herpes Candidiasis vulvovaginitis Syphilis ulcer
  • 136. Central dimpling bumps multiple umbilicated flesh- Diameter 2-5 mm, firm colored or hypopigmented Painless papules.
  • 137. Candida vulvovaginitis ï‚Ļ Hx : Vulvar pruritus is the dominant feature of vulvovaginal candidiasis ï‚Ļ PE : erythema of the vulva and vaginal mucosa and vulvar edema ï‚Ļ Discharge : thick, adherent, and "cottage cheese-like
  • 138. āđ‚āļˆāļ—āļĒāđŒ GA 20 weeks āļĄāļĩāļāļĨāļīāđˆāļ™āđāļĨāļ°āļ„āļąāļ™āļ—āļĩāđˆāļŠāđˆāļ­āļ‡āļ„āļĨāļ­āļ”āļĄāļē 2 āļŠāļąāļ›āļ”āļēāļŦāđŒ āļ•āļĢāļ§āļˆāļĢāđˆāļēāļ‡āļāļēāļĒāļžāļšāļ§āđˆāļē āđāļ”āļ‡āļ—āļĩāđˆāļ›āļēāļāļŠāđˆāļ­āļ‡āļ„āļĨāļ­āļ” āļ•āļ āļ‚āļēāļ§āļŠāļĩāđ€āļŦāļĨāļ·āļ­āļ‡āđ€āļ‚āļĩāļĒāļ§ āļĄāļĩāļŸāļ­āļ‡ āļŠāđˆāļ­āļ‡āļ„āļĨāļ­āļ”āđāļ”āļ‡ cervix āļŠāļĩ āđāļ”āļ‡āļ„āļĨāđ‰āļē (āđ„āļĄāđˆāļšāļ­āļāļ§āđˆāļēāļĄāļĩ curd) āļˆāļ°āđƒāļŦāđ‰āļĒāļēāļ­āļ°āđ„āļĢāļĢāļąāļāļĐāļē 1. oral doxycycline 2. oral tinidazole 3. oral ketoconazole 4. oral fluconazole 5. clotrimazole Vg
  • 139. Vulvaginal infections in pregnancy ï‚Ļ Bacterial vaginosis : ï‚Ī In pregnancy, it is associated with preterm birth ï‚Ī treatment does not reduce preterm birth, and routine screening is not recommended ï‚Ī Rx(symptomatic) : Metronidazole 500 mg twice daily orally for 7 days ï‚Ļ Candidiasis : ï‚Ī Asymptomatic colonization : no treatment ï‚Ī Characteristic : profuse, irritating discharge associated with a pruritic, tender, edematous vulva ï‚Ī Topical treatment is recommended (Clotrimazole, miconazole, nystatin, and terconazole)
  • 140. Vulvaginal infections in pregnancy ï‚Ļ Trichomoniasis : ï‚Ī Characteristic : foamy leukorrhea with pruritus and irritation ï‚Ī (Some studies) In pregnancy, it is associated with preterm birth but treatment has not decreased this risk ï‚Ī screening and treatment of asymptomatic women is not recommended during pregnancy ï‚Ī Rx : single 2-g dose of Metronidazole
  • 141. āđ‚āļˆāļ—āļĒāđŒ āļœāļđāđ‰āļ›āđˆāļ§āļĒāļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 19 āļ›āļĩ GA 40 wk. āļĄāļĩ genital lesion herpes āđ€āļ›āđ‡āļ™āļ„āļĢāļąāđ‰āļ‡āđāļĢāļ āļˆāļ°āļ§āļēāļ‡āđāļœāļ™āļ”āļđāđāļĨ āļœāļđāđ‰āļ›āđˆāļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰āļ­āļĒāđˆāļēāļ‡āđ„āļĢ a. Cesarean section b. Oxytocin c. Prostaglandin d. Amniotomy e. āļĢāļ­āļˆāļ™āđ€āļˆāđ‡āļšāļ—āđ‰āļ­āļ‡āļ„āļĨāļ­āļ”
  • 142. Rx Dx BV CV TV Metronidazole Clotrimazole(100mg) Metronidazole Non pregnanct (500mg) 1X2 oral 1tab vg 2 g orally in a x7 days suppo.x7days single dose The same as non Treat (symptom) pregnant Treat (symptom) pregnant Sexual partner Not treat Not treat Treat The same as HIV The same as HIV The same as HIV neg HIV neg neg When persist or F/U no no recur within 2 mo.
  • 143. Genital HSV infection and pregnancy ï‚Ļ Fetal and neonatal effect : ï‚Ī Fetal infection : congenital HSV (hydrops fetalis , fetal demise,survivor (skin lesion,CNS manifestration) ï‚Ī Neonatal infection : SEM ,manifestration , CNS manifestration (meningoencephalitis) , disseminated disease ï‚Ļ When the risk of neonatal infection occur ï‚Ļ Route of delivery ï‚Ļ Treatment for prevention or decreased risk of neonatal infection
  • 144. Risk factors for neonatal herpes ï‚Ļ The risks are greatest : women with primary genital herpes in the 3rd trimester particularly within 6 weeks of delivery),
  • 145. Approach pregnant women with Hx HSV infection women without symptoms and signs of genital herpes or prodromal symptoms They can be deliver vaginally
  • 146. Recommendation of CDC and ACOG Cesarean delivery should be offered Who have history of Who have ruptured of genital herpes membranes > 6 hours, Who have active lesions or (although the benefit is not prodromal symptoms at the time of delivery clearly proven)
  • 147. Approach pregnant women with Hx HSV infection Cesarean delivery not recommended for women with recurrent genital herpes and active nongenital HSV lesions
  • 148. Treatment ï‚Ļ In women with first episode genital HSV : Acyclovir (400 mg PO three times daily) 7 - 14 days , regardless of the timing of infection during pregnancy ( to decrease duration of lesion and viral shedding) ï‚Ļ In women with a history of recurrent genital HSV, or primary infection during pregnancy: suppressive Acyclovir (400 mg three times daily) be given at GA 36 weeks through delivery ï‚Ļ Women who do not have a history of genital herpes but HSV-2 seropositive : not recommend antiviral therapy
  • 149. Recommended doses of antiviral medication for Herpes in pregnancy Indication Acyclovir Valacyclovir Primary or 1st 400 mg po tid 1 g bid for 7-14 episode HSV for days 7-14 days Symptomatic 400 mg po tid 500 mg po bid recurrent HSV for 5 days for 5 days Daily 400 mg po tid 500 mg po bid suppressive from GA 36 from GA 36 therapy wk.to delivery wk.to delivery Obstet Gynecol 2005;106:845-56
  • 150. A. āļŠāđˆāļ‡UAāļŦāļē UTI B. āđƒāļŠāđ‰āļ–āļļāļ‡āļĒāļēāļ‡āļ­āļ™āļēāļĄāļąāļĒāđ€āļ§āļĨāļēāļĄāļĩāđ€āļžāļĻāļŠāļąāļĄāļžāļąāļ™āļ˜āđŒ C. āļ•āļĢāļ§āļˆculture GC āļˆāļēāļcervix,urethra D. āđāļ™āļ°āļ™āļēāđƒāļŦāđ‰āļŠāļēāļĄāļĩāļĄāļēāļ•āļĢāļ§āļˆSTD E. āļ•āļĢāļ§āļˆāđ€āļĨāļ·āļ­āļ”screen STD (syphilis,HIV)āļ•āļēāļĄāļ›āļāļ•āļī
  • 151. āđ‚āļˆāļ—āļĒāđŒ āļœāļđāđ‰āļŦāļāļīāļ‡āļ­āļēāļĒāļļ 28 āļ›āļĩ āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 28 āļŠāļąāļ›āļ”āļēāļŦāđŒ āļ•āļĢāļ§āļˆ VDRL reactive titer = 1:32, FTA-ABS positive āđƒāļŦ āđ‰āļāļēāļĢāļĢāļąāļāļĐāļēāđ€āļ›āđ‡āļ™ Benzathine penicillin 2.4 āļĨ āđ‰āļēāļ™āļŦāļ™āđˆāļ§āļĒ āļ—āļēāļ‡āļāļĨāđ‰āļēāļĄāđ€āļ™āļ·āđ‰āļ­āđ€āļ›āđ‡āļ™āđ€āļ§āļĨāļē 3 āļŠāļąāļ›āļ”āļēāļŦāđŒ āļ•āđˆāļ­āļĄāļē āļ•āļĢāļ§āļˆāļ‹ āđ‰āļēāļ•āļ­āļ™ āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 32 āļŠāļąāļ›āļ”āļēāļŦāđŒ VDRL = 1:8 āļ—āđˆāļēāļ™āļˆāļ°āđƒāļŦ āđ‰āļāļēāļĢ āļĢāļąāļāļĐāļēāļ—āļĩāđˆāđ€āļŦāļĄāļēāļ°āļŠāļĄāļ—āļĩāđˆāļŠāļļāļ”āļ­āļĒāđˆāļēāļ‡āđ„āļĢāļ•āđˆāļ­āđ„āļ› A. āļ§āļąāļ” VDRL āļ‹āđ‰āļē āļ•āļ­āļ™āļŦāļĨāļąāļ‡āļ„āļĨāļ­āļ” 6 āļŠāļąāļ›āļ”āļēāļŦāđŒ B. āļ‰āļĩāļ” Benzathine penicillin āļ‹āđ‰āļēāđƒāļ™āļ‚āļ™āļēāļ”āđāļĨāļ°āđ€āļ§āļĨāļēāđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ C. āļ‰āļĩāļ” Benzathine penicillin 2.4 āļŦāļ™āđˆāļ§āļĒ āļ„āļĢāļąāđ‰āļ‡āđ€āļ”āļĩāļĒāļ§ D. āđƒāļŦ āđ‰penicillin āļŦāļĒāļ”āļ—āļēāļ‡āļŦāļĨāļ­āļ”āđ€āļĨāļ·āļ­āļ”āļ” āļē 1.2 āļĨ āđ‰āļēāļ™āļŦāļ™āđˆāļ§āļĒ āļĢāļ°āļĒāļ°āđ€āļ§āļĨāļē____ E. āđ€āļ›āļĨāļĩāđˆāļĒāļ™āļĒāļēāđ€āļ›āđ‡āļ™ erythromycin āļ§āļąāļ™āļĨāļ° 2 āļāļĢāļąāļĄ 30 āļ§āļąāļ™
  • 152. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļĄāļĩ genital wart āļˆāļ‡āđƒāļŦāđ‰āļāļēāļĢāļ”āļđāđāļĨ āļĢāļąāļāļĐāļē A. Podophyllin B. Trichloroacetic acid C. Interferon D. 5-FU E. Imiquimod
  • 153. ï‚Ļ Podophyllin : a plant-based resin that blocks cell division at metaphase and leads ï‚Ļ Trichloroacetic acid : destroy the wart tissue via chemical coagulation of tissue proteins ï‚Ļ 5-FU :a pyrimidine antimetabolite that interferes with DNA synthesis ï‚Ļ Imiquimod :a positive immune response modifier, which acts by local cytokine induction
  • 154. Genital wart during pregnancy ï‚Ļ Three important issues ï‚Ī Worsening of the disease in the pregnant state ï‚Ī Choice of safe and effective treatment ï‚Ī Potential vertical transmission to the fetus
  • 155. External genital warts during pregnancy ï‚Ļ During pregnancy ï‚Ū impaired immune ï‚Ū increased proliferation of condylomata. ï‚Ļ During the post-partum period ï‚Ū spontaneous regression.
  • 156. Treatment ï‚Ļ Aims of treatment : debulking symptomatic genital warts. ï‚Ļ Eradical of warts during pregnancy is not always necessary
  • 157. Treatment Effective regimen for genital warts : ï‚Ī 80-90% TCA solution applied typically once a week ï‚Ī Cryotherapy ï‚Ī Laser ablation ? Podophyllin resin Podofilox – gel or solution are not recommended in 5-FU cream pregnancy Imiquimod cream
  • 158. Route of delivery Current OB data : ï‚Ļ Data support the rarity of perinatal HPV transmission āđ„āļĄāđˆāđāļ™āļ°āļ™āļēāđƒāļŦāđ‰ ï‚Ļ Limitation understanding of ➙ āļœāđˆāļēāļ•āļąāļ”āļ„āļĨāļ­āļ”āđ€āļžāļ·āđˆāļ­ āļĨāļ”āļāļēāļĢāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­ the development of laryngeal papillomatosis āļāļēāļĢāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­āļ‚āļ­āļ‡āļ—āļēāļĢāļāđ„āļĄāđˆāđ€āļāļĩāđˆāļĒāļ§āļ‚āđ‰āļ­āļ‡āļāļąāļš route of delivery
  • 159. ïą āļ–āđ‰āļēāđ€āļŦāđ‡āļ™ genital condyloma āđƒāļ™āđ€āļ”āđ‡āļāļ­āļēāļˆ āđ€āļ™āļ·āđˆāļ­āļ‡āļˆāļēāļ ïķāļŠāļąāļĄāļœāļąāļŠlesionāđƒāļ™āļĢāļ°āļŦāļ§āđˆāļēāļ‡āļ„āļĨāļ­āļ”āļ—āļēāļ‡āļŠāđˆāļ­āļ‡ āļ„āļĨāļ­āļ” ïķāļ–āđ‰āļēāđƒāļ™āđ€āļ”āđ‡āļāđ‚āļ•āđƒāļŦāđ‰ rule out sexual abuse āļ”āđ‰āļ§āļĒ
  • 160. Rubella in pregnancy āļŠāļīāđˆāļ‡āļ—āļĩāđˆāļ•āđ‰āļ­āļ‡āļĢāļđāđ‰ ï‚Ļ āļāļēāļĢāđāļ›āļĨāļœāļĨāđ€āļĨāļ·āļ­āļ” āļ„āļ™āļ—āļĩāđˆāđ„āļ›āļŠāļąāļĄāļœāļąāļŠāđ‚āļĢāļ„āļĄāļē ï‚Ļ āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒāļ—āļĩāđˆāđāļĄāđˆāđ€āļ›āđ‡āļ™āļœāļ·āđˆāļ™āđāļĨāļ°āļ—āļēāļĢāļāđƒāļ™āļ„āļĢāļĢāļ āđŒāļĄāļĩāđ‚āļ­āļāļēāļŠāļ•āļīāļ” āđ€āļŠāļ·āđ‰āļ­ ï‚Ļ āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒāļ—āļĩāđˆāļĄāļĩāđ‚āļ­āļāļēāļŠāđ€āļāļīāļ”congenital rubella syndrome
  • 161. Rubella in pregnancy ï‚Ļ āļŠāļ•āļĢāļĩāļ­āļēāļĒāļļ 26 āļ›āļĩ āđ€āļ›āđ‡āļ™āļ„āļĢāļđāļĢāļ°āļ”āļąāļšāļ›āļĢāļ°āļ–āļĄāļĻāļķāļāļĐāļē āļĄāļēāļ›āļĢāļķāļāļĐāļēāļāđˆāļ­āļ™āļāļēāļĢāļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒ āđ€āļĢāļ·āđˆāļ­āļ‡āļŦāļąāļ”āđ€āļĒāļ­āļĢāļĄāļąāļ™ āļ—āđˆāļēāļ™āļˆāļ°āđāļ™āļ°āļ™āļēāļ­āļĒāđˆāļēāļ‡āđ„āļĢ -Hx āļ .āđ„āļĄāđˆāļĄāļĩāļ„āļ§āļēāļĄāđ€āļŠāļĩāļĒāļ‡āđ„āļĄāđˆāļ•āđ‰āļ­āļ‡āļ•āļĢāļ§āļˆāđ€āļĨāļ·āļ­āļ” āđˆ -Serologic testing : āļ‚. āļ‰āļĩāļ”āļ§āļąāļ„āļ‹āļĩāļ™ āđ„āļĄāđˆāļ•āđ‰āļ­āļ‡āļ„āļļāļĄāļāļēāđ€āļ™āļīāļ” IgG āļ„. āļ‰āļĩāļ”āļ§āļąāļ„āļ‹āļĩāļ™ āļ„āļļāļĄāļāļēāđ€āļ™āļīāļ” 1 āđ€āļ”āļ·āļ­āļ™ -āļ–āđ‰āļēāđ„āļĄāđˆāļĄāļ āļđāļĄāļīāļ„āļļāđ‰āļĄāļāļąāļ™ āļ‰āļĩāļ”āļ§āļąāļ„āļ‹āļĩāļ™āđāļĨāļ° āļĩ āļ‡. āļŠāđˆāļ‡āļ•āļĢāļ§āļˆrubella Ig M āļ„āļļāļĄāļāļēāđ€āļ™āļīāļ”āļ›āļĢāļ°āļĄāļēāļ“ 1 āđ€āļ”āļ·āļ­āļ™ āļˆ. āļŠāđˆāļ‡āļ•āļĢāļ§āļˆrubella IgG
  • 162. Rubella & pregnancy ï‚Ļ āļāļēāļĢāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­āļ‚āļ­āļ‡āļ—āļēāļĢāļ āļœāđˆāļēāļ™āļ—āļēāļ‡āļĢāļāđƒāļ™āļ‚āļ“āļ°āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒ ï‚Ļ āđ€āļ›āđ‡āļ™āļŠāļēāđ€āļŦāļ•āļļāļ—āļĩāđˆāļ—āļēāđƒāļŦāđ‰āđ€āļāļīāļ”āļ„āļ§āļēāļĄāļžāļīāļāļēāļĢāļ‚āļ­āļ‡āļ—āļēāļĢāļāđāļ•āđˆāļāļēāđ€āļ™āļīāļ” āļ—āļĩāđˆāļĢāļļāļ™āđāļĢāļ‡ ï‚Ļ āļ–āđ‰āļēāļŠāļ•āļĢāļĩāļ•āļ‡āļ„āļĢāļĢāļ āđŒāđ„āļĄāđˆāļĄāļĩāļ āļđāļĄāļīāļ„āļļāđ‰āļĄāļāļąāļ™ āļĄāļĩāļāļēāļĢāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­ āļąāđ‰ ïŪ āļˆāļ°āļ•āļĢāļ§āļˆāļžāļšāđ„āļ§āļĢāļąāļŠāđƒāļ™āđ€āļĨāļ·āļ­āļ”āļāđˆāļ­āļ™āļĄāļĩāļ­āļēāļāļēāļĢ āļ‚āļ­āļ‡āđ‚āļĢāļ„ āļ›āļĢāļ°āļĄāļēāļ“1āļŠāļąāļ›āļ”āļēāļŦāđŒ ïŪ āļŦāļĨāļąāļ‡āļœāļ·āđˆāļ™āđ€āļĢāļīāđˆāļĄāļ‚āļķāđ‰āļ™ 1-2 āļŠāļąāļ›āļ”āļēāļŦāđŒāļˆāļ°āđ€āļ›āđ‡āļ™āļŠāđˆāļ§āļ‡āļ—āļĩāđˆ āļĄāļĩāļĢāļ°āļ”āļąāļš antibodyāļŠāļđāļ‡āļŠāļļāļ”
  • 163. ï‚Ļ Incubation period 12-23 days ï‚Ļ 20 – 50 % of infections may be asymptomatic
  • 164. āļœāļĨāļ•āđˆāļ­āļ—āļēāļĢāļ ï‚Ļ āļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āļ‚āļ­āļ‡āļ—āļēāļĢāļāđƒāļ™āļ„āļĢāļĢāļ āđŒāļ—āļĩāđˆāļˆāļ°āļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­āđāļĨāļ°āļĄāļĩ āļ„āļ§āļēāļĄāļžāļīāļāļēāļĢāđāļ•āđˆāļāļēāđ€āļ™āļīāļ”āļ‚āļķāđ‰āļ™āļāļąāļšāļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒāļ‚āļ“āļ°āļ—āļĩāđˆāđāļĄāđˆ āđ€āļ›āđ‡āļ™āļœāļ·āđˆāļ™ ï‚Ļ Risk of fetal infection  GA < 12 wks. Risk = 80%  GA 13-14 wks. Risk = 54%  2nd trimester Risk = 25%
  • 165. ï‚Ļ Consequence of fetal infection  spontaneous infection  seropositive , normal –appearing infant(infection may remain subclinical for months)  Congenital rubella infection
  • 166. Congenital rubella infection Findings : ï‚Ī Eye : cataract and congenital glaucoma ï‚Ī Heart disease : pulmonary artery stenosis ï‚Ī Sensorineural deafness : the most common single defect ï‚Ī CNS defect : microcephaly,paraencephalitis, brain calcification, mental retardation ï‚Ī Pigment retinopathy ï‚Ī purpura ï‚Ī Hepatosplenomegaly and jaundice ï‚Ī Radiolucent bone disease ï‚Ī Symmetrical IUGR
  • 167. āļœāļĨāļ•āđˆāļ­āļ—āļēāļĢāļ ï‚Ļ āļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āļ‚āļ­āļ‡āļ—āļēāļĢāļāđƒāļ™āļ„āļĢāļĢāļ āđŒāļ—āļĩāđˆāļˆāļ°āļĄāļĩāļ„āļ§āļēāļĄāļžāļīāļāļēāļĢāđāļ•āđˆ āļāļēāđ€āļ™āļīāļ” (congenital rubella syndrome)  āļ–āđ‰āļēāļ—āļēāļĢāļāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­āļ—āļĩāđˆGA < 11 wks. āļžāļšāļžāļīāļāļēāļĢāļ—āļļāļāļĢāļēāļĒ  āļ–āđ‰āļēāļ—āļēāļĢāļāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­āļ—āļĩāđˆ GA 13-16 wks. āļžāļšāļžāļīāļāļēāļĢ = 35%  āļ–āđ‰āļēāļ—āļēāļĢāļāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­āļ—āļĩāđˆ GA > 16 wks. āļˆāļ°āđ„āļĄāđˆāļžāļšāļ„āļ§āļēāļĄ āļžāļīāļāļēāļĢāđ€āļĨāļĒ
  • 168. āļāļēāļĢāļ§āļīāļ™āļīāļˆāļ‰āļąāļĒ ï‚Ļ āļ„āļ§āļĢāļ•āļĢāļ§āļˆantibodyāļ•āļąāđ‰āļ‡āđāļ•āđˆ āļ āļēāļĒāđƒāļ™2-3āļ§āļąāļ™āļŦāļĨāļąāļ‡āļœāļ·āđˆāļ™āđ€āļĢāļīāđˆāļĄ āļ‚āļķāđ‰āļ™ āđāļĨāļ°āļ•āļĢāļ§āļˆāļ‹āđ‰āļēāļŦāļĨāļąāļ‡āļˆāļēāļāļ™āļąāđ‰āļ™āļ­āļĩāļ 1 āļŠāļąāļ›āļ”āļēāļŦāđŒāđ€āļžāļ·āđˆāļ­āļ”āļđāļāļēāļĢ āđ€āļžāļīāđˆāļĄāļ‚āļķāđ‰āļ™āļ‚āļ­āļ‡āļĢāļ°āļ”āļąāļšantibody ï‚Ļ IgM āļˆāļ°āļžāļšāđ„āļ”āđ‰āļ•āļąāđ‰āļ‡āđāļ•āđˆāđ€āļĢāļīāđˆāļĄāļĄāļĩāļœāļ·āđˆāļ™āļˆāļ™āļāļĢāļ°āļ—āļąāđˆāļ‡4 āļŠāļąāļ›āļ”āļēāļŦāđŒāļŦāļĨāļąāļ‡ āđ€āļĢāļīāđˆāļĄāļĄāļĩāļœāļ·āđˆāļ™ ï‚Ļ IgG āļžāļšāđ„āļ”āđ‰āļ•āļąāđ‰āļ‡āđāļ•āđˆāđ€āļĢāļīāļĄāļĄāļĩāļœāļ·āđˆāļ™āđāļĨāļ°āļĒāļąāļ‡āļ„āļ‡āļ­āļĒāļđāđˆāļ•āļĨāļ­āļ”āļŠāļĩāļ§āļ• āđˆ āļī
  • 169. āđ€āļĄāļ·āđˆāļ­āļœāļđāđ‰āļ›āđˆāļ§āļĒāļĄāļĩāļĨāļąāļāļĐāļ“āļ°āļ—āļēāļ‡āļ„āļĨāļīāļ™āļāļŠāļ‡āļŠāļąāļĒāļ§āđˆāļēāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­āļŦāļąāļ”āđ€āļĒāļ­āļĢāļĄāļąāļ™ āļī āļĢāļ°āļĒāļ°āđ€āļ§āļĨāļēāļ—āļĩāđˆāļĄāļēāļžāļš 1st HAI titer 2nd HAI titer āđāļ›āļĨāļœāļĨ āđāļžāļ—āļĒāđŒāļŦāļĨāļąāļ‡āļœāļ·āđˆāļ™āļ‚āļķāļ™ āđ‰ <1:8(1:10) āđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ āđ„āļĄāđˆāđƒāļŠāđˆrubella , no immune <3āļ§āļąāļ™ <1:8(1:10) 4-fold āđ€āļ›āđ‡āļ™ rubella (āļ•āļĢāļ§āļˆāļ‹āđ‰āļēāļ­āļĩāļāđƒāļ™1wk) â‰Ĩ 1:8(1:10) āđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ āđ„āļĄāđˆāđƒāļŠāđˆrubella , āļĄāļĩimmune <1:8(1:10) āđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ āđ„āļĄāđˆāđƒāļŠāđˆrubella , no immune 3-7āļ§āļąāļ™ 1:8-1:32 (āļ•āļĢāļ§āļˆāļ‹āđ‰āļēāļ­āļĩāļāđƒāļ™1wk) (1:10-1:140) āđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ āđ„āļĄāđˆāđƒāļŠāđˆrubella , āļĄāļĩimmune â‰Ĩ1:64(1:80) āļŠāļđāļ‡āļāļ§āđˆāļēāđ€āļ”āļīāļĄ āđ„āļĄāđˆāđāļ™āđˆ ,āļ•āļĢāļ§āļˆIgM <1:8(1:10) - āđ„āļĄāđˆāđƒāļŠāđˆrubella , no immune >7āļ§āļąāļ™ 1:8-1:32 (1:10-1:140) - āđ„āļĄāđˆāđƒāļŠāđˆrubella , āļĄāļĩimmune āļĄāļēāļŸāļąāļ‡āļœāļĨāđƒāļ™1-2wk. â‰Ĩ1:64(1:80) - āļ­āļēāļˆāđ€āļ›āđ‡āļ™rubella,āļ•āļĢāļ§āļˆIgM
  • 170. āļĢāļēāļĒāļ—āļĩāđˆāļĄāļĩāļ›āļĢāļ°āļ§āļąāļ•āļīāđ„āļ›āļŠāļąāļĄāļœāļąāļŠāđ‚āļĢāļ„āļĄāļē 1st HAI 2nd HAI āđāļ›āļĨāļœāļĨ <1:8(1:10) āđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ āđ„āļĄāđˆāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­,āļĒāļąāļ‡āđ„āļĄāđˆāļĄāļĩāļ āļđāļĄāļī <1:8(1:10) āļŠāļđāļ‡āļāļ§āđˆāļēāđ€āļ”āļīāļĄ āļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­ â‰Ĩ 1:8(1:10) āđ€āļ—āđˆāļēāđ€āļ”āļīāļĄ āđ„āļĄāđˆāļ•āļīāļ”āđ€āļŠāļ·āđ‰āļ­,āļĄāļĩāļ āļđāļĄāļīāđāļĨāđ‰āļ§ â‰Ĩ 1:8(1:10) 1:64(1:80) āļ•āļĢāļ§āļˆāļŦāļēIgM 1st HAI <1:8 āđ€āļˆāļēāļ°āđ€āļĨāļ·āļ­āļ”āļ„āļĢāļąāđ‰āļ‡āļ—āļĩāđˆāļŠāļ­āļ‡āđ€āļĄāļ·āđˆāļ­āļ„āļĢāļš 1āļ” āļŦāļĨāļąāļ‡āđ„āļ›āļŠāļąāļĄāļœāļąāļŠāđ‚āļĢāļ„āļĄāļē 1st HAI â‰Ĩ 1:8 āđ€āļˆāļēāļ°āđ€āļĨāļ·āļ­āļ”āļ„āļĢāļąāđ‰āļ‡āļ—āļĩāđˆāļŠāļ­āļ‡āđƒāļ™āļ§āļąāļ™āļ—āļĩāđˆāļĄāļēāļŸāļąāļ‡āļœāļĨ IgM āļœāļĨ + = āđ€āļžāļīāđˆāļ‡āđ€āļ›āđ‡āļ™rubellaāļĄāļē 4-6wks. IgM āļœāļĨ - = āđ€āļ›āđ‡āļ™rubellaāļĄāļēāđ€āļāļīāļ™ 4-6wks
  • 171. Prevention ï‚Ļ Rubella vaccination should be avoided 1 month before or during pregnancy (attenuated live virus) (CDC 2000)
  • 173. āđ‚āļˆāļ—āļĒāđŒ Most common cause of perinatal death in twin pregnancy a. Antepartum hemorrhage b. Birth asphyxia c. IUGR d. Prematurity e. Twin – twin transfusion
  • 174. āđ‚āļˆāļ—āļĒāđŒ “Locked twins”āļ—āļēāļĢāļāđāļāļ”āļ„āļ™āļ—āļĩāđˆāļŦāļ™āļķāđˆāļ‡ āđāļĨāļ°āļŠāļ­āļ‡āļˆāļ°āļ­āļĒāļđāđˆāđƒāļ™āļ—āđˆāļēāđƒāļ” a. Cephalic – Breech b. Breech – Breech c. Cephalic – Cephalic d. Breech – Cephalic e. Cephalic - Transverse
  • 175. ―Locked twins‖ Breech – Cephalic ✔
  • 176. āđ‚āļˆāļ—āļĒāđŒ the most common presentation at delivery of near term twins are vertex - vertex 40% a. Both cephalic ✔ vertex - breech breech - vertex 26% 10% breech - breech 10% b. Both breech vertex - transverse 8% others 6% c. One cephalic , one breech d. One cephalic , one transverse e. One breech , one transverse
  • 177. OTHERS
  • 178. āļŦāļāļīāļ‡āđ„āļ—āļĒ G2 āļĄāļēāļāļēāļāļ„āļĢāļĢāļ āđŒ GA 18 wk āļ•āļĢāļ§āļˆāđ€āļĨāļ·āļ­āļ” āđāļĄāđˆ A- āļžāđˆāļ­ B+ (āļ­āļēāļˆāļŠāļĨāļąāļšāļāļąāļ™ āļ›āļĢāļ°āļĄāļēāļ“āļ™āļĩ) āļ–āļēāļĄ āđ‰ āļ—āļēāđ„āļĢāļ•āđˆāļ­ 1. Anti D 2. Cordocentesis 3. direct comb 4. Amniocentesis 5. indirect coomb
  • 179. ï‚Ļ The direct Coombs' test : detection of antibody on the surface of the RBC ï‚Ļ The indirect Coombs’test : detection antibodies against RBCs that are present unbound in the patient's serum. ï‚Ļ The indirect Coombs’test is used to screen pregnant women for antibodies that may cause hemolytic diseasee of the newborn
  • 180. Isoimmunization ï‚Ļ Etiology : maternal Ab production in response to exposure to RBC Ag ï‚Ļ Rh isoimmunization : Ab against to Rh group ï‚Ļ Rh Ag are present on fetal cells by the 38th day postconception
  • 181. Rh isoimmunization Fetus : Rh positive Mother : Rh negative and RBC sensitization Hemolytic disease
  • 182. Hemolytic disease of the newborn (Erythroblastosis fetalis
  • 183. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 20 āļ›āļĩ G1P0 GA 38 wk. car accident āļĄāļēāļ—āļĩāđˆāļŦāđ‰āļ­āļ‡āļ‰āļļāļāđ€āļ‰āļīāļ™ āļĄāļĩāđ€āļĨāļ·āļ­āļ”āļ­āļ­āļāļ—āļēāļ‡āļŠāđˆāļ­āļ‡āļ„āļĨāļ­āļ” āļ•āđˆāļ­āļĄāļē āļ„āļĨāļ­āļ”āļšāļļāļ•āļĢ āđ€āļŠāļĩāļĒāđ€āļĨāļ·āļ­āļ” 900ml āļ‚āļ“āļ°āļ™āļĩāđ‰āļœāļđāđ‰āļ›āđˆāļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰āļ›āļĨāļ­āļ”āļ āļąāļĒāđāļĨāđ‰āļ§ āļ—āļĢāļēāļšāļ‚āđ‰āļ­āļĄāļđāļĨāļˆāļēāļāļāļēāļĢāļāļēāļāļ„āļĢāļĢāļ āđŒ āļžāļšāļ§āđˆāļēRh negative Anti D negative āļ‚āļąāđ‰āļ™āļ•āļ­āļ™āļ•āđˆāļ­āđ„āļ›āđƒāļ™āļāļēāļĢāļ”āļđāđāļĨāļœāļđāđ‰āļ›āđˆāļ§āļĒāļĢāļēāļĒāļ™āļĩāđ‰ a. Perform CBC b. Transfuse PRC c. Performed Kleihauer-Betke test d. Give additional Rh immune globulin e. Assess neonatal Rh Ag status
  • 184. Kleihauer-Betke test : the number of fetal red cells in the maternal circulation to measure the amount of fetal Hb transferred from a fetus to a mother's bloodstream â€Ē the differential resistance of fetal hemoglobin to acid â€ĒPositive test : the rosette test â€ĒMaternal red blood cells appear as pale "‖
  • 185. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 27 āļ›āļĩ G1P0 GA 27 wk. āļĄāļēāļ—āļĩāđˆERāđ€āļ™āļ·āđˆāļ­āļ‡āļˆāļēāļ āļ­āļļāļšāļąāļ•āļīāđ€āļŦāļ•āļļāļˆāļēāļāļĢāļ–MC āđ„āļĄāđˆāļĄāļĩāļ­āļēāļāļēāļĢāļ›āļ§āļ”āļ—āđ‰āļ­āļ‡ āļ—āđ‰āļ­āļ‡āđāļ‚āđ‡āļ‡ āđ„āļĄāđˆāļĄāļĩāđ€āļĨāļ·āļ­āļ”āļ­āļ­āļ FHSāļ­āļĒāļđāđˆāđƒāļ™āđ€āļāļ“āļ‘āđŒāļ›āļāļ•āļī āļ•āļĢāļ§āļˆāļĢāđˆāļēāļ‡āļāļēāļĒ Abd :not tender PV cervix:os close no effacement ,no bleeding per vagina Lab : Rh +(āđ„āļĄāđˆāļĢāļđāđ‰āļœāļĨāļ‚āļ­āļ‡āļžāđˆāļ­) āđ„āļĄāđˆāļĄāļĩHx blood transfusion , Kleihauer-Betke test shows a combination of pale and stained RBCs. (A) Administer an appropriate dose of IM Rh0(D) immune globulin (B) Amniocentesis to measure the amniotic fluid bilirubin level (C) Emergent cesarean section (D) Induction of vaginal labor with prostaglandins and oxytocin (E) Treatment with betamethasone
  • 186. Indication for Anti-D immunoglobulin in unsensitized pregnant women ï‚Ļ Abortion ï‚Ļ Ectopic pregnancy ï‚Ļ Antepartum bleeding(1st ,2nd trimester) ï‚Ļ Abdominal trauma ï‚Ļ After amniocentesis,CVS ï‚Ļ After external cephalic version
  • 187. Management : maternal Rh neg with unsensitized ï‚Ļ Treat with Rh immunoglobulin at GA 28 wk. and after delivery(within /72 hr.) if the Fetal is Rh positive ï‚Ļ Dose 300g of Rh immunoglobulin can protect from an exposure of up to 30 ml of fetal blood
  • 188. Management : maternal Rh neg with sensitized Assess GA by US Check paternal blood type Paternal Rh : Paternal homozygous for D or Rh neg heterozygous for D No further Assess manageme prior OB nt Hx Serial maternal Ab titer ,US ,MCA Doppler velocimetry
  • 189. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ•āļąāđ‰āļ‡āļ„āļĢāļĢāļ āđŒāļ­āļēāļĒāļļ 31āļ›āļĩ GA 4 wk. ,kANC underlying disease SLEāļĄāļē 5 āļ›āļĩ āļāļīāļ™ low dose Prednisone āļĄāļĩ renal insufficiency(Cr = 1.3 mg/dL) clinical SLE stableāļĄāļēāļ›āļĢāļ°āļĄāļēāļ“ 6 āđ€āļ”āļ·āļ­āļ™ āļ—āļēāļĢāļāļĄāļĩāļ„āļ§āļēāļĄāđ€āļŠāļĩāđˆāļĒāļ‡āđƒāļ™āļ‚āđ‰āļ­āđƒāļ”āļ•āđˆāļ­āđ„āļ›āļ™āļĩāđ‰āđ€āļžāļīāđˆāļĄāļ‚āļķāđ‰āļ™ (A) Acute renal failure (B) Chorioretinitis (C) Complete heart block (D) Ebstein’s anomaly (E) Rash
  • 190. ï‚Ļ Chorioretinitis : Toxoplasmosis infection,CMV infection ï‚Ļ Ebstein’s anomaly (malformation of the tricuspid valve and right ventricle) : Lithium ï‚Ļ Rash : neonatal lupus āļĄāļĩ erythematous annular lesions on the scalp and periorbital area. the rash is typically mild and resolves by 6–8 months of age.
  • 192. āđ‚āļˆāļ—āļĒāđŒ āļŦāļāļīāļ‡āļ­āļēāļĒāļļ 26 āļ›āļĩ āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 8 āļŠāļąāļ›āļ”āļēāļŦāđŒ āļāļēāļĢāļ•āļĢāļ§āļˆ ultrasoundāđ€āļžāļ·āđˆāļ­āļ›āļĢāļ°āđ€āļĄāļīāļ™āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ āļ‚āđ‰āļ­āđƒāļ”āđāļĄāđˆāļ™āļĒāļēāļ—āļĩāđˆāļŠāļļāļ” a. Femur length b. Biparietal diameter c. Crown rump length d. Abdominal circumference e. Head circumference
  • 193. āļāļēāļĢāļ›āļĢāļ°āđ€āļĄāļīāļ™āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒāđāļĨāļ°āļĨāļąāļāļĐāļ“āļ°āļ—āļĩāđˆāļžāļšāđƒāļ™āļĢāļ°āļĒāļ° āđ„āļ•āļĢāļĄāļēāļŠāđāļĢāļ(TVS) ï‚Ļ 4 - 5 wk by LMP : āđ€āļŦāđ‡āļ™ gestational sac ï‚Ļ 5 – 6 wk by LMP: āđ€āļŦāđ‡āļ™ yolk sac (hCG ~7,200 mU/ml) ï‚Ļ 6 – 7 wk by LMP : āđ€āļŦāđ‡āļ™ fetal echo ,fetal heart beat ï‚Ī MSD > 20 mm. ï‚Ī hCG ~10,800 mU/ml ï‚Ī CRL āļ•āļąāđ‰āļ‡āđāļ•āđˆ 5 mm.āļ„āļ§āļĢāļˆāļ°āđ€āļŦāđ‡āļ™fetal heart beat āļ—āļļāļāļĢāļēāļĒ ï‚Ļ 7 – 8 wk. by LMP : āđ€āļŦāđ‡āļ™ fetal movement āđ„āļ”āđ‰ ï‚Ī MSD > 30 mm. Rhombencephalon āļˆāļ°āđ€āļ”āđˆāļ™ ï‚Ļ 8 – 9 wk. by LMP : āđ€āļŦāđ‡āļ™ physiologic omphalocele ,āđāļ‚āļ™āļ‚āļē choroid plexus,āđāļ™āļ§āđ„āļ‚āļŠāļąāļ™āļŦāļĨāļąāļ‡
  • 194. āļāļēāļĢāļ›āļĢāļ°āđ€āļĄāļīāļ™āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒāđƒāļ™āļĢāļ°āļĒāļ°āđ„āļ•āļĢāļĄāļēāļŠāđāļĢāļ Crown – rump – length(CRL) ï‚Īāđ€āļŦāļĄāļēāļ°āļŠāļĄāļŠāļēāļŦāļĢāļąāļšāļāļēāļĢāļ›āļĢāļ°āđ€āļĄāļīāļ™ āļ­āļēāļĒāļļāļ„āļĢāļĢāļ āđŒ 7 – 14 āļŠāļąāļ›āļ”āļēāļŦāđŒ āļĄāļĩ āļ„āļ§āļēāļĄāđāļĄāđˆāļ™āļĒāļēāđƒāļ™āļāļēāļĢāļ—āļēāļ™āļēāļĒ āļĄāļēāļ ✔ ï‚ĪāļĄāļĩāļ„āļ§āļēāļĄāđāļĄāđˆāļ™āļĒāļēāļ—āļĩāđˆāļŠāļļāļ”āļ—āļĩāđˆāļ­āļēāļĒāļļ āļ„āļĢāļĢāļ āđŒ 6.5 – 10 āļŠāļąāļ›āļ”āļēāļŦāđŒ ï‚Ī Menstrual age (weeks) = CRL (cm) + 6.5
  • 196. āđ‚āļˆāļ—āļĒāđŒ Transvaginal USG at GA 8 wk āļžāļš sac 30 mm. āđ„āļĄāđˆāļĄāļĩ embryonic echo āļ—āļēāļ­āļ°āđ„āļĢ A.Transquillizer and rest B.Progestin and rest C.Laparoscopy D.Medical or surgical termination of pregnancy E.Serial B-HCG
  • 197. Abnormal pregnancy during 1st trimester ï‚Ļ Viable pregnancy : āđ€āļŦāđ‡āļ™ yolk sac , fetal echo.fetal heart ï‚Ļ Nonviable pregnancy : early embryonic death , blighted ovum, ectopic pregnancy,molar pregnancy Diagnosis early embryonic death : TAS CRL 9 mm āđ„āļĄāđˆāđ€āļŦāđ‡āļ™ fetal heart TVS CRL 5 mm āđ„āļĄāđˆāđ€āļŦāđ‡āļ™ fetal heart
  • 198. Mean gestational sac diameter MSD(mm) GA(wk) 2 4 5 5 10 āļ•āđ‰āļ­āļ‡āđ€āļŦāđ‡āļ™ yolk 6 sacāđāļĨāđ‰āļ§ 20 7 25 8