Uploaded on

undergraduate course lectures in obstetrics and gynecology prepared by Dr Manal Behery Professor of OB&GYNE ,Faculty of medicine,Zagazig University

undergraduate course lectures in obstetrics and gynecology prepared by Dr Manal Behery Professor of OB&GYNE ,Faculty of medicine,Zagazig University

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
No Downloads

Views

Total Views
380
On Slideshare
0
From Embeds
0
Number of Embeds
0

Actions

Shares
Downloads
30
Comments
0
Likes
2

Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
    No notes for slide

Transcript

  • 1. Hydrops Fetalis Dr Manal Behery 2014
  • 2. Hydrops = Generalized subcutaneous edema in the fetus or neonate
  • 3. Definition 1. Excess serous fluid in at least one space (ascites, pleural effusion, or pericardial effusion) + skin edema (> 5 mm thick) 1. Excess fluid in two spaces without edema
  • 4. Hydrops Fetalis Non Immune Hydrops Fetalis (90%( Immune Hydrops Fetalis (10%(
  • 5. Etiology 1. Hematologic: Due to anemia (10% of cases) : A. Isoimmune hemolytic disease (RH incompatibility). 2.Cardiovascular: Due to heart failure (20% cases) A. Rhythm disturbances B. Major cardiac disease
  • 6. 3. Infection (10% of cases) TORCH-Syphilis- Congenital Hepatitis, Parvovirus…. 4. Chromosomal (5% of cases) : Turner syndrome, trisomy 13,18,21
  • 7. 5. Pulmonary (5% of cases) Chylothorax, diaphragmatic hernia 6. Gastrointestinal (5% of cases) : Meconium peritonitis 7. Renal (5% of cases) Nephrosis, RVT, urinary obstruction …..
  • 8. 7. Maternal conditions (5% of cases) : Toxemia, diabetes, thyrotoxicosis 8. Miscellaneous (10% of cases) : Cystic hygroma, wilms’ tumor – teratoma 9. -Unknown (20% of cases) :
  • 9. Rh (Rhesus) Isoimmunization:
  • 10. Four blood types ( A, B, AB, and O) Each blood type is additionally classified according to the presence or absence of the Rh factor
  • 11. CDE (Rhesus) System • Clinically Important • Includes c, C, D, e, E • Rh negative status indicates the absence of D antigen • 87% of Caucasians carry the D antigen
  • 12. •Rh Disease •Alloimmunization •Isoimmunization •HDFN •Erythroblastosis Fetalis Confusing Terminology
  • 13. When the mother produces Abs directed against fetus RBC surface Ag. Isoimmunization
  • 14. Rh Incompatibility Exposure to fetal antigens causes the mother to produce antibodies
  • 15. The placenta usually acts as a barrier to fetal blood entering the maternal circulation.
  • 16. Fetal cells can enter the maternal circulation through a “break” in the “placental barrier”.
  • 17. Maternal production of Rhesus antibodies following introduction of Rhesus positive blood
  • 18. Maternal production of Rhesus antibodies following introduction of Rhesus positive blood
  • 19. Causes of RBC Transfer: “A break in the barrier” • Abortion/Ectopic Pregnancy • Partial molar pregnancy • Blighted ovum • Antepartum bleeding • Procedures (amniocentesis, cordocentesis, CVS) • External version • Platelet transfusion • Abdominal trauma • Inadvertent transfusion Rh+ blood • Postpartum (Rh+baby)
  • 20. Sensitized pregnancy Non- Sensitized pregnancy Rh Incompatibility Sensitization = Rh neg person exponsed to the Rh (D) antigen and makes antibodies against that protein (antigen).
  • 21. Rh Negative Women Man Rh positive ⇓ Fetus Rh positive Fetus → Rh+ve R.B.C.s enter Maternal circulation⇐ previously sensitized 2nd immune response IgM…IgG antibodies ⇓ Non sensitized Mother Primary immune response 1st Baby usually escapes. Mother gets sensitized? ± Fetus Haemolysis ⇓ Pathogenesis Of Rh Iso - immunisation Rh –VE Fetus no harm
  • 22. Presentation Mild jaundice Erythroblastosis Fetalis Generalized Edema Hepatomegaly Ascites
  • 23. Natural History •50%of affected infants have mild anemia, requiring either phototherapy or no treatment. •25%have hepatosplenomegaly , moderate anemia and progressive jundice ending in kernicterus, neonatal death •25%are hydropic and die in utero or in the neonatal period
  • 24. RhoGAM has decreased HDFN caused by anti-D Give 300 mcg dose within 72 hrs of delivery to unsensitized Rh (-) women (Rh positive infant) • ACOG: 300 mcg at 28 weeks UNLESS father known to be Rh (-)
  • 25. Mechanism of action • Administered antibodies will bind the fetal Rh- positive cells • Spleen captured these cells by Fc-receptors • Suppressor T cell response is stimulated • Spleen remove anti-D coated red cells prior to contact with antigen presenting cells “antigen deviation”
  • 26. Kleihauer-Betke Test • % fetal RBC in maternal circulation • Fetal erythrocytes contain Hbg F which is more resistant to acid elution than HbgA so after exposure to acid, only fetal cells remain & can be identified with stain • 1/1000 deliveries result in fetal hemorrhage > 30ml • Risk factors only identify 50%
  • 27. 1.1-Direct Coomb’s Test (DAT( Detects RBCs that have already been sensitized with IgG Demonstrates that in vivo coating of RBC by Ab has occurred but does NOT identify the antibody Deepa Babin @TMC Kollam 28
  • 28.  Detects antibodies to RBC antigens present in the patient’s serum  Detects in vitro red cell sensitization if red cells contain antigen corresponding to serum antibody  Procedure:  STEP 1: patient’s serum (with unknown Ab) + RBC (with known Ag)  STEP 2: product of step 1 + Coomb’s reagent IAT((2. Indirect Coomb’s Test Deepa Babin @TMC Kollam 29
  • 29. Recognition of pregnancy at risk •First ante-natal visit check blood group, antibody screening. • If indirect coombs test is positive, the father’s Rh should be tested. • Serial maternal Anti D titers should be done every 2- 4 weeks. • If titer is less than 1/16 the fetus is not at risk. • If titer is more than 1/16 then severity of condition should be evaluated.
  • 30. Prevention • Test for excessive fetal-maternal hemorrhage after blunt trauma, abruption, cordocentesis, and bleeding with previa • Give RhoGAM for partial molar pregnancy, ectopic, chorionic villus sampling, amniocentesis, external version
  • 31. MCA Doppler and Fetal Anemia • Fetuses with anemia show an • increased peak velocity of systolic blood flow in MCA. • MCA Doppler is also used to follow fetal response to intrauterine transfusion and to assist in timing subsequent transfusions. • Non-invasive, • no risk for worsening isoimmunization
  • 32. Normal and Abnormal MCA Dopplers
  • 33. Amniocentesis - There is an excellent correlation between the amount of bilirubin in amniotic fluid and fetal hematocrit. - • - Perform serial amniocenteses • to the optical density deviation at 450 nm measures the amniotic fluid unconjugated bilirubin. • Plot values on Liley Curve at 16 weeks of gestation
  • 34. Liley Curve •Measures the level of bilirubin and predicts severity of hemolytic disease after 27 weeks
  • 35. Suggested management after amniocentesis for ΔOD 450 Serial Amniocentesis Lily zone I Lower Zone II Upper Zone II Zone III Hydramnios & Hydrops Repeat Amniocentesis every 2-4 weeks Delivery at or near term Repeat Amniocentesis in 7 days or FBS Hct < 25% Hct > 25% Intrauterine Transfusion Repeat Sampling 7to 14 days <35to 36 weeks And Fetal lung immaturity >35to 36 weeks Lung maturity present Intrauterine Transfusion Delivery
  • 36. Cordocentesis • Gold standard for detection of fetal anemia • Complications • 2.7% total risk of fetal loss • Reserved for patients with increased MCA-PSV or delta OD450
  • 37. Intrauterine transfusion
  • 38. Exchange Transfusion •.  Considered if the total serum bilirubin level is approaching 20 mg/dL and continues to rise despite intense in-hospital phototherapy.  Mortality rate 1%
  • 39. Diagnosis and Management contd.
  • 40. Review of Management for Rh Isoimmunization • Monthly indirect coombs titer (in first sensitized pregnancy) • If critical titer reached, determine paternal and fetal antigen status • Amniocentesis and delta OD450 OR MCA-PSV ** For 2nd or greater sensitized pregnancy, initiate amnio or MCA at 18-20 weeks**