The Rhesus (Rh) factor is a specific protein, technically known as the D antigen, found on the surface of red blood cells. Its presence or absence determines an individual’s Rh status and plays a significant role in blood type compatibility. If the D antigen is present, a person is considered Rh-positive; its absence means they are Rh-negative. This inherited characteristic is a fundamental part of a person’s complete blood type classification.
The Biology of the Rh D Factor
The Rh D factor is governed by the RHD gene, located on chromosome 1. Rh-positive individuals possess this gene, which codes for the D antigen protein found on the red blood cell membrane. Conversely, Rh-negative individuals typically lack a functional copy of the gene, meaning their red blood cells do not carry the D antigen.
Inheritance of the Rh D factor follows a dominant pattern; inheriting just one copy of the gene is sufficient to be Rh-positive. If both parents are Rh-negative, the child will also be Rh-negative. Approximately 85% of the human population is Rh-positive. This genetic difference is usually inconsequential unless the immune system of an Rh-negative person is exposed to Rh-positive blood.
Understanding Rh Sensitization in Pregnancy
Rh sensitization, also known as alloimmunization, is an immune response occurring when an Rh-negative person is exposed to Rh-positive red blood cells. In pregnancy, this happens when an Rh-negative mother carries an Rh-positive fetus. Although the mother’s and fetus’s blood systems are normally separate during gestation, a small amount of fetal blood can cross the placenta into the maternal bloodstream.
Blood mixing is most common during delivery, but it can also happen during procedures like amniocentesis, miscarriage, ectopic pregnancy, or abdominal trauma. When the Rh-negative mother’s immune system encounters the Rh-positive fetal red blood cells, it identifies the D antigen as foreign. The maternal immune system then produces anti-Rh D antibodies to fight this perceived invader.
The first pregnancy involving an Rh-positive fetus is typically safe because the mother’s immune system usually does not produce a significant number of antibodies until after delivery. This initial exposure sensitizes the mother, priming her immune system. In subsequent pregnancies with an Rh-positive fetus, the pre-existing maternal antibodies cross the placenta and immediately attack the fetal red blood cells, leading to complications.
Testing Protocols and Prevention Strategies
Preventing Rh sensitization is a standard and highly successful part of modern prenatal care, beginning with early screening. All pregnant women are tested at their first prenatal visit to determine their ABO blood group and Rh D type. If a woman is found to be Rh-negative, an antibody screen (indirect Coombs test) is performed to check if she has already developed anti-Rh D antibodies from a previous exposure.
If the antibody screen is negative, confirming the mother is not yet sensitized, the primary prevention strategy is the administration of Rh Immunoglobulin (RhIg), commonly known as RhoGAM. This medication is a concentrated solution of passive anti-Rh D antibodies given as an injection. RhoGAM destroys any fetal Rh-positive red blood cells that may have entered the maternal circulation before the mother’s own immune system can recognize them and mount a response.
The standard protocol involves administering a dose of RhIg proactively around the 28th week of gestation, as this timing is highly effective at preventing sensitization during the later stages of pregnancy. A second dose is given to the Rh-negative mother within 72 hours after delivering an Rh-positive baby. RhIg is also administered after any event that could cause fetal-maternal blood mixing, such as miscarriage, abortion, or invasive procedures like amniocentesis. This systematic prevention has drastically reduced the incidence of Rh-related complications in newborns.
Health Consequences for the Fetus and Newborn
If Rh sensitization occurs and is not treated, maternal anti-Rh D antibodies cross the placenta and enter the fetal bloodstream. These antibodies rapidly attach to the Rh-positive red blood cells, causing them to break down prematurely. This destruction leads to Hemolytic Disease of the Fetus and Newborn (HDFN), also known as Rh disease.
HDFN results in a range of severity, with the primary consequence being fetal anemia. The fetus attempts to compensate by rapidly producing more red blood cells, leading to an enlarged liver and spleen. Severe anemia can strain the fetal heart, causing widespread fluid accumulation in the body, a life-threatening condition known as hydrops fetalis.
After birth, the rapid breakdown of red blood cells increases the level of bilirubin, a yellow pigment the newborn’s liver struggles to process. This accumulation causes jaundice (yellowing of the skin and eyes). Very high levels of bilirubin can cross the blood-brain barrier and cause permanent brain damage known as kernicterus. For affected fetuses, advanced in utero treatment includes specialized procedures like fetal blood transfusions, where blood is delivered directly into the umbilical cord to correct the anemia.