Prepared by : Dimalaluan, Serafin III

The Rh factor (ie, Rhesus factor) is a red blood cell surface antigen that was named after the monkeys in which it was first discovered. Rh incompatibility, also known as Rh disease, is a condition that occurs when a woman with Rh-negative blood type is exposed to Rh-positive blood cells, leading to the development of Rh antibodies.

Rh incompatibility can occur by 2 main mechanisms. The most common type occurs when an Rhnegative pregnant mother is exposed to Rh-positive fetal red blood cells secondary to fetomaternal hemorrhage during the course of pregnancy from spontaneous or induced abortion, trauma,invasive obstetric procedures, or normal delivery. Rh incompatibility can also occur when an Rh-negative female receives an Rh-positive blood transfusion. In part, this is the reason that blood banks prefer using blood type "O negative" or "type O, Rh negative," as the universal donor type in emergency situations when there is no time to type and crossmatch blood.

The most common cause of Rh incompatibility is exposure from an Rh-negative mother by Rhpositive fetal blood during pregnancy or delivery. As a consequence, blood from the fetal circulation may leak into the maternal circulation, and, after a significant exposure, sensitization occurs leading to maternal antibody production against the foreign Rh antigen. Once produced, maternal Rh immunoglobulin G (IgG) antibodies may cross freely from the placenta to the fetal circulation, where they form antigen-antibody complexes with Rh-positive fetal erythrocytes and eventually are destroyed, resulting in a fetal alloimmune-induced hemolytic anemia. Although the Rh blood group systems consist of several antigens (eg, D, C, c, E, e), the D antigen is the most immunogenic; therefore, it most commonly is involved in Rh incompatibility.

During pregnancy, red blood cells from the fetus can get

into the mother's bloodstream as she nourishes her child through the placenta. If the mother is Rh-negative, her immune system treats the Rh-positive fetal cells as if they were a foreign substance and makes antibodies against the fetal blood cells. These anti-Rh antibodies may cross the placenta into the developing baby, where they destroy the baby's circulating red blood cells. When red blood cells are broken down, they makebilirubin, which causes an infant to become yellow (jaundiced). The level of bilirubin in the infant's bloodstream may range from mild to dangerously high. First-born infants are often not affected -- unless the mother has had previous miscarriages or abortions, which could have sensitized her system -- as it takes time for the mother to develop antibodies against the fetal blood. However, second children who are also Rhpositive may be harmed. Rh incompatibility develops only when the mother is Rhnegative and the infant is Rh-positive. This problem has become uncommon in the U.S. and other places that provide good prenatal care. Special immune globulins, called RhoGAM, are now used to prevent RH incompatibility.

Factors that influence an Rh-negative pregnant female's chances of developing Rh incompatibility include the following: Ectopic pregnancy Placenta previa Placental abruption Abdominal/pelvic trauma In utero fetal death Any invasive obstetric procedure (eg, amniocentesis) Lack of prenatal care Spontaneous abortion

 Signs

and symptoms

Jaundice Motor

and mental retardation Polyhydramnios (excess amniotic fluid)

 Diagnostic Antibody

test :

screening Blood test (cbc) Amniocentesis Positive direct coombs test

 Treatment Rh

immune globulin Blood transfusion (for hemolytic anemia) RHOgam Phototherapy using bilirubin lights