document 020 : Anemia Hemolysis

Hemolysis: 

• Rh incompatibility - erythroblastosis fetalis.  Fetal blood cells containing Rh antigen (positive) enter the maternal circulation; maternal RBCs have no antigen (negative); maternal immune system produces antibodies against the foreign fetal antigens; in subsequent pregnancies maternal antibodies enter fetal circulation and destroy RBCs.
• Maternal antibodies to subsequent pregnancies.  Destroy fetal RBCs.
• Predisposing factors - previous pregnancy or abortion, fetal-maternal hemorrhage during pregnancy, delivery, amniocentesis, external version, manual removal of the placenta.
• Infant presentation - anemia, hypoxia/acidosis (decreased RBC count and decreased oxygen carrying capacity of immature cells), CHF/hydrops (fetus attemps to expand blood volume and cardiac output, resulting in generalized edema), ascites/plural effusion (fluid collecting in large cavities).  Hepatosplenomegaly, petechia, hypoglycemia (increased RBC destruction stimulates insulin secretion, resulting in hyperplasia of pancreatic islets and hyperinsulinemia).  Positive coombs test result.

• Rhogam:  anti-D immune globulin.  Destruction of fetal RBCs in maternal circulation-block maternal antibody production.

• ABO Incompatibility:
• More frequent, but less severe than Rh incompatibility
• Most often seen with mothers who have O type carrying fetus with A or B.
• Maternal exposure to naturally occuring A/B antigens in food, bacteria, pollen stimulates anti-a/b antibodies.
• Infant presentation
• Mild hemolysis, anemia, reticulocytosis.
• Hyperbilirubinemia(occ requiring exchange)
• G6PD:
• Enzymatic disorder, X-linked (mainly male), hemolysis/shortened erythrocyte life.
• Common in African American as well as of Mediterranean, African, and Asian Descent.