Overview
Introduction
RhD alloimmunization begins when an RhD negative patient is exposed to RhD positive fetal red blood cells.
RhD alloimmunization begins when an RhD-negative patient is exposed to RhD-positive fetal red blood cells. The maternal immune system recognizes the D antigen as foreign and may produce immune anti-D IgG antibodies. Once immune anti-D antibodies exist, they can cross the placenta in a current or future RhD-positive pregnancy and bind fetal red blood cells. This causes fetal hemolysis. The fetal bone marrow and reticuloendothelial system attempt to compensate, but severe hemolysis can result in anemia, high-output cardiac failure, hydrops fetalis, stillbirth, or neonatal hyperbilirubinemia. Pathologic Step Clinical Consequence Maternal anti-D crosses placenta Fetal RBC destruction Fetal hemolysis Fetal anemia Severe anemia High-output cardiac failure Cardiac failure and hypoalbuminemia Hydrops fetalis Ongoing RBC breakdown after birth Hyperbilirubinemia Severe bilirubin toxicity Kernicterus risk RhIg is therefore a prevention medication, not a treatment for established hemolytic disease. If immune anti-D is already present, care shifts to alloimmunization management, fetal surveillance, and maternal-fetal medicine involvement. For Canadian NP practice / CNPLE-aligned preparation (Canada), items rarely announce the topic in the first sentence. Anchor to objective data, trajectory, and the safest next step for...