Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (1159 page)

   Antibody Screening

   Antibody screening is used to detect the presence of unexpected alloantibodies in the recipient’s serum, directed against non-ABO blood group antigens (e.g., Kell, Duffy, and Kidd). This is accomplished by using commercially available screening RBCs. Generally, an IAT is performed using the patient’s serum and two or three group O RBCs with known but varied blood group antigens.

   If agglutination is detected in the antibody screen, the antibody must be identified and antigen-negative RBCs must be selected for transfusion.

   Crossmatching

   The crossmatch assay involves testing the patient’s serum with the donor RBC taken from a segment attached to the selected blood unit. Unless there is a very urgent need for blood, crossmatching is mandatory. The method used must be able to demonstrate incompatibility to ABO and other clinically significant RBC antibodies.

   If the recipient/patient has a negative antibody screen, an abbreviated (immediate spin) crossmatch is adequate. However, if the patient has a positive antibody screen or there is a previous history of alloimmunization, antigennegative donor units must be selected and a full Coombs crossmatch must be performed (by incubating the patient’s plasma and the donor red cells at body temperature and then adding AHG).

   An immediate spin crossmatch is one additional means of ensuring that the patient receives ABO compatible red cells as ABO antibodies will cause agglutination without incubation at body temperature and addition of AHG.

   In order to detect many of the clinically significant non-ABO antibodies, a Coombs crossmatch is necessary as agglutination will not be seen without incubation at body temperature and addition of AHG.

   Limitations

   Acquired antigens, such as “acquired B” antigens in group A individuals.

   Forward and reverse typing discrepancies. When they occur, the cause must be immediately investigated. The most common cause is a patient who is a subgroup of A and who has formed anti-A
₁
antibodies (80% of group A patients are subgroup A
₁
. Most of the remainder are A
₂
and may develop anti-A
₁
antibodies.

   Warm and cold autoantibodies can interfere with pretransfusion testing.