BLOOD GROUP INCOMPATIBILITY

Rh Disease

Blood TypesLandsteiner 1900A, B, O blood groups are specific types of proteins found on the surface of RBCsAlso found in the cells and other body fluids (saliva, semen, etc)O no protein being present on RBCPossible groups include: A, B, AB,or OA, B, O groups most important for transfusions

Rh FactorProteins (antigens) occurring only on surface of RBCsRh + if proteins presentRh if proteins absent

A+, A-, B+, B-, AB+, AB-, O+, O-Most important for pregnancyInheritance is Autosomal Dominant15% Caucasian population is Rh-

Rh Factor15% Caucasian population is Rh-1954 , Mourant :Negro3-8%India3-10%China and japan1%Indonesia %

NomenclatureCorrect to say Rh(D) + or Rh blood system has other antigens: C, c, D, E, eD is by far the most common and the only preventable oneWeak D (Du) also existsAlso non Rhesus groups such as Kell, MNS, Duffy (Fy) and Kidd (Jk) exist

Rh DiseaseOccurs during pregnancy when there is an incompatibility between the blood types of the mother and fetus

Why Does Rh Status Matter?

PathophysiologyRh(D) antigen expressed by 30 d GAMany cells pass between maternal & fetal circulation including at least 0.1 ml blood in most deliveries but generally not sufficient to activate immune responseRh antigen causes > response B lymphocyte clones recognizing foreign RBC antigen are formed

Pathophysiology contInitial IgM followed by IgG in 2 wks- 6 moMemory B lymphocytes activate immune response in subsequent pregnancyIgG Ab cross placenta and attach to fetal RBCsCells then sequestered by macrophages in fetal spleen where they get hemolyzedFetal anemia

GLUCURONYL TRANSFERASE

Causes of RBC Transferabortion/ectopicpartial molar pregnancyblighted ovumantepartum bleedingspecial procedures (amniocentesis, cordocentesis, CVS)external versionplatelet transfusionabdominal traumainadvertent transfusion Rh+ bloodpostpartum (Rh+baby)

Fetus at RiskFetal anemia diagnosed by: amniocentesis cordocentesis ultrasound hydrops middle cerebral artery Doppler

Treatment: intravascular fetal transfusion preterm birth

General ScreeningABO & Rh Ab @ 1st prenatal visit@ 28 weeksPostpartumAntepartum bleeding and before giving any immune globulinNeonatal bloods ABO, Rh

Gold Standard TestIndirect Coombs:- mix Rh(D)+ cells with maternal serum- anti-Rh(D) Ab will adhere- RBCs then washed & suspended in Coombs serum (antihuman globulin)- RBCs coated with Ab will be agglutinated

Direct Coombs:- mix infants RBCs with Coombs serum- maternal Ab present if cells agglutinate

AmniocentesisCritical titre/ previous affected infantAvoid transplacental needle passageBilirubin correlates with fetal hemolysis optical density of amniotic fluid @ 450nm on spectral absorption curveData plotted on Liley curve

Liley CurveZone I fetus very low risk of severe fetal anemiaZone II mild to moderate fetal hemolysisZone III severe fetal anemia with high probability of fetal death 7-10 days

Liley good after 27 weeks98% sensitive for detecting anemia in upper zone 2/ zone 3

Infant at RiskDiagnosis: history of antibodies? early jaundice < 24 hours cord Coombs positive (due to HDN or ABO antibodies)

Treatment: Phototherapy Exchange or Direct blood transfusion

PreventionRhoGAM ( 120mcg or 300mcg)Anti-D immune globulinPreviously 16% Rh(D)- women became alloimmunized after 2 pregnancies : 2% with routine PP dose, and 0.1% with added dose @ 28 wks

Kleihauer-Betke Test% fetal RBC in maternal circulationFetal erythrocytes contain Hb F which is more resistant to acid elution than Hb A After exposure to acid, only fetal cells remain & can be identified with stain1/1000 deliveries result in fetal hemorrhage > 30mlRisk factors only identify 50%

Kleihauer CalculationsFetal red cells = MBV x maternal Hct x % fetal cells in KB newborn Hct

MBV maternal blood volume (usually 5000ml)

Fetal cells x 2 = whole blood

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Pregnancy induced DM