3. Disorders affecting fluid-gas transport in fetus: Rh incompatibility
1. Pathophysiology - in an Rh-negative mother: Rh-positive fetal red blood cells enter the maternal circulation —» maternal antibody formation —» antibodies cross placenta and enter fetal bloodstream —» attack fetal red blood cells —» hemolysis —» anemia, hypoxia.
1. The pregnant Rh-positive mother carries her infant (Rh negative or positive) without incident.
2. The pregnant Rh-negative mother carries an Rh-negative infant without incident.
3. The pregnant Rh-negative mother usually carries her first Rh-positive child without problems unless she has been sensitized by inadvertent transfusion with Rh-positive blood. Note: Fetal cells do not usually enter the maternal bloodstream until placental separation (at abortion, abruptio placentae, amniocentesis, or birth).
2. Etiology:
1. The Rh factor is an antigen on the red blood cells of some people (these people are Rh positive); the Rh factor is dominant; a person may be homozygous or heterozygous for Rh factor.
2. An Rh-negative person is homozygous for this recessive trait - does not carry the antigen; develops antibodies when exposed to Rh-positive red blood cells (isoimmunization) through transplacental (or other) transfusion.
3. Following birth of an Rh-positive infant, if fetal cells enter the mother’s bloodstream, maternal antibody formation begins; antibodies remain in the maternal circulation.
4. At time of next pregnancy with Rh-positive fetus, antibodies cross placenta —> hemolysis. Note: Degree of hemolysis depends on amount (titer) of maternal antibodies present.
3. Possible serious complication (fetal) - rare today. Hydrops fetalis - most severe hemolytic reaction: severe anemia, cardiac decompensation, hypoxia, edema, ascites, hydrothorax; may be stillborn.
4. Assessment:
   1. Prenatal - diagnostic procedures:
      1. Maternal blood type and Rh factor.
      2. Indirect Coombs test - to determine presence of Rh sensitization (titer indicates amount of maternal antibodies).
      3. Amniocentesis - as early as 26 weeks of gestation - amount of bilirubin by-products indicates severity of hemolytic activity.
      4. RhoGAM between 28-32 wk to prevent antibody formation.
   2. Intrapartal observation of amniotic fluid (after membrane rupture).
      1. Straw-colored fluid - mild disease
      2. Golden fluid - severe fetal disease
   3. Postnatal -
5. Nursing care plan/implementation:
   1. Goal: prevent isoimmunization in Coombsnegative women
      1. Postabortion - if no evidence of Rh sensitization (antibody formation) in the Rh-negative mother, administer RhoGAM.
      2. Prenatal - if no evidence of sensitization, administer RhoGAM at 28 weeks of gestation, as ordered, to all Rh-negative women.
      3. Postpartum - if no evidence of sensitization, administer RhoGAM within 72 hr of birth to Rh-negative women who gave birth to Rh-positive baby.
         Give RhoGAM to:
         1. Rh-negative mother who gives birth to Rh-positive neonatal
         2. Rh-negative mother after spontaneous or induced abortion (>8 wk).
         3. Rh-negative mother after amniocentesis or chorionic villus sampling (CVS).
         4. Rh-negative mother between 28 and 32 weeks of gestation.
   2. Goal: health teaching.
      1. Explain, discuss that RhoGAM suppresses antibody formation in susceptible Rh-negative women carrying Rh-positive fetus. Note: Cannot reverse sensitization if already present.
      2. Required during and after each pregnancy with Rh-positive fetus.
6. Evaluation/outcome criteria:
   1. Successfully carries pregnancy to term.
   2. No evidence of Rh isoimmunization.
   3. Birth of viable infant.